title: TF ChIP-seq from whole organism (ENCSR118TAH)

summary:
ChIP-seq on transgenic flies expressing -eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR195OCT)

status: Public on Feb 27 2024

city: Stanford

first: ENCODE

last: DCC

state: CA

address: 300 Pasteur Dr

country: USA

institute: ENCODE DCC

type: Genome binding/occupancy profiling by high throughput sequencing

summary:
Input control for ChIP-seq on transgenic flies expressing NK7.1-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR194XZB)

summary:
This is the ChIP-seq control of transgenic worms expressing CEH-24-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR116ZCQ)

summary:
Input control for ChIP-seq on transgenic flies expressing REPTOR-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR117TRB)

summary:
ChIP-seq on transgenic worms expressing lin-54-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR117BAW)

summary:
ChIP-seq on transgenic worms expressing D2030.7-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR195DZI)

summary:
Input control for ChIP-seq on transgenic flies expressing CG17361-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR194MGU)

summary:
Input control for ChIP-seq on transgenic flies expressing Rfx-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR286EOA)

summary:
ChIP-seq on transgenic flies expressing mirr-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR194OUP)

summary:
This is the ChIP-seq control of transgenic worms expressing LIM-6-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR116MEY)

summary:
Input ChIP-seq in L2 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR117DIE)

summary:
Input ChIP-seq in L1 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR116BMC)

summary:
This is the ChIP-seq control of transgenic worms expressing NFYA-1-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR114XOX)


title: TF ChIP-seq from whole organism (ENCSR115ZDZ)

summary:
ChIP-seq on transgenic worms expressing sup-37-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR114JYK)

summary:
Input control for ChIP-seq on transgenic flies expressing insv-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR114LFX)

summary:
ChIP-seq on transgenic flies expressing CG4707-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR113XNT)

summary:
This is the ChIP-seq control of transgenic worms expressing HLH-30-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR194HLU)

summary:
Input control for ChIP-seq on transgenic flies expressing ttk-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR113ROD)

summary:
This is the ChIP-seq control of transgenic worms expressing ekl-4-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR113XIS)

summary:
This is the ChIP-seq control of transgenic worms expressing ceh-19-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR113DVD)

summary:
ChIP-seq on transgenic worms expressing mxl-2-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR193TLR)

summary:
Input control for ChIP-seq on transgenic flies expressing bowl-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR112URX)

summary:
ChIP-seq against eGFP-mab-5 in mixed stage (embryonic) worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR112GYX)

summary:
Input ChIP-seq in late-embryonic stage worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR193QEM)

summary:
ChIP-seq on transgenic worms expressing ceh-44-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR111RAO)

summary:
Input control for ChIP-seq on transgenic flies expressing trem-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR111CQR)

summary:
Input control for ChIP-seq on transgenic flies expressing CG8944-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR111LGE)

summary:
ChIP-seq of transgenic worms expressing F13H6.1-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR010CSQ)

summary:
Input control for ChIP-seq on transgenic flies expressing CG11456-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR194LIS)

summary:
ChIP-seq on transgenic flies expressing CG18476-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR009STJ)

summary:
Input control for ChIP-seq on transgenic flies expressing CG6163-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR110JFN)

summary:
Input control for ChIP-seq on transgenic flies expressing schlank-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR110JOZ)

summary:
ChIP-seq on transgenic flies expressing Lim3-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR109XBO)

summary:
This is the ChIP-seq control of transgenic worms expressing ZTF-16-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR009EUK)

summary:
This is the ChIP-seq control of transgenic worms expressing sea-2-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR008NYP)

summary:
ChIP-seq on transgenic flies expressing sug-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR109RMR)

summary:
ChIP-seq on transgenic flies expressing tap-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR007MVL)

summary:
ChIP-seq against eGFP-jun-1 in L3 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR110QRS)

summary:
ChIP-seq on transgenic flies expressing Dip3-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR108PJB)

summary:
This is the ChIP-seq control of transgenic worms expressing egl-18-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR008GMV)

summary:
Input ChIP-seq in young adult worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR107BQR)

summary:
ChIP-seq of transgenic worms expressing NHR-85-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR106DTT)

summary:
This is the ChIP-seq control of transgenic worms expressing CEH-48-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR191UXN)

summary:
Input control for ChIP-seq on transgenic flies expressing CG12236-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR190ONG)

summary:
This is the ChIP-seq control of transgenic worms expressing DSC-1-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR190GMM)

summary:
Input control for ChIP-seq on transgenic flies expressing CG3726-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR007HUT)

summary:
ChIP-seq on transgenic flies expressing cyc-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR112EFN)

summary:
Input control for ChIP-seq on transgenic flies expressing Sox102F-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR105NBC)

summary:
ChIP-seq on transgenic flies expressing knrl-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR105HNS)

summary:
Input control for ChIP-seq on transgenic flies expressing fd59A-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR190CJZ)

summary:
ChIP-seq on transgenic flies expressing CG9609-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR284YMU)

summary:
Input control for ChIP-seq on transgenic flies expressing HLH4C-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR189NRY)

summary:
ChIP-seq on transgenic flies expressing Hsf-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR189IPH)

summary:
ChIP-seq on transgenic flies expressing onecut-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR009OQO)

summary:
Input ChIP-seq in L3 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR284UJF)

summary:
Input control for ChIP-seq on transgenic flies expressing nerfin-2-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR284TTZ)

summary:
This is the ChIP-seq control of transgenic worms expressing ODD-2-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR188ZKB)

summary:
ChIP-seq on transgenic flies expressing -eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR283MGP)

summary:
ChIP-seq on transgenic flies expressing CG10669-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR283FJI)

summary:
This is the ChIP-seq control of transgenic worms expressing ham-2-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR283RSJ)

summary:
Input ChIP-seq in L2 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR187HHD)

summary:
This is the ChIP-seq control of transgenic worms expressing ETS-4-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR187ZBO)

summary:
ChIP-seq against eGFP-nhr-6 in L4 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR187IVR)

summary:
ChIP-seq on transgenic flies expressing CG14711-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR006GXP)

summary:
Input ChIP-seq in L1 larva worms grown at 26C.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR283CFB)

summary:
ChIP-seq on transgenic flies expressing ara-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR186QCV)

summary:
Input control for ChIP-seq on transgenic flies expressing Poxn-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR283AVD)

summary:
Input control for ChIP-seq on transgenic flies expressing CG4282-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR283UXP)

summary:
ChIP-seq on transgenic flies expressing Slp2-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR191QNY)

summary:
Input ChIP-seq in L4 worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR103JYD)

summary:
Input control for ChIP-seq on transgenic flies expressing Six4-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR103OZL)

summary:
ChIP-seq on transgenic flies expressing gsb-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR101ZRY)

summary:
This is the ChIP-seq control of transgenic worms expressing FKH-8-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR102QDH)

summary:
Input control for ChIP-seq on transgenic flies expressing Hand-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR005MLL)

summary:
ChIP-seq on transgenic flies expressing Pdp1-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR104XOO)

summary:
ChIP-seq on transgenic flies expressing trem-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR004RJS)

summary:
ChIP-seq on transgenic flies expressing CG9876-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR005SGO)

summary:
ChIP-seq against eGFP-ces-1 in L4 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR101VVI)

summary:
This is the ChIP-seq control of transgenic worms expressing SMA-3-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR004EEK)

summary:
Input control for ChIP-seq on transgenic flies expressing vfl-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR100ITO)

summary:
Input control for ChIP-seq on transgenic flies expressing HLH54F-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR100SUV)

summary:
Input control for ChIP-seq on transgenic flies expressing CG4854-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR186ZKW)

summary:
ChIP-seq on transgenic flies expressing -eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR004JBX)

summary:
ChIP-seq against eGFP-ceh-16 in L2 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR000WON)

summary:
Input control for ChIP-seq on transgenic flies expressing CG4820-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR002EBG)

summary:
Input ChIP-seq in L2 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Control ChIP-seq from whole organism (ENCSR001UTJ)

summary:
Input ChIP-seq in L4 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR101LNT)

summary:
ChIP-seq on transgenic flies expressing CG3065-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: TF ChIP-seq from whole organism (ENCSR002FCO)

summary:
ChIP-seq of transgenic worms expressing CEH-36-eGFP fusion proteins. The IP was performed using an anti-GFP antibody.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: An activity-specificity trade-off encoded in human transcription factors

city: Berlin

first: Alexandre

middle: P

last: Magalhaes

address: Ihnestrasse 63-73

country: Germany

institute: Max Planck Institute for Molecular Genetics

type: Expression profiling by high throughput sequencing

summary: Transcription factors play essential roles in cell type specification during differentiation, and small sets of transcription factors can reprogram cell identity. Therefore, we tested the impact of increasing periodicity of aromatic residues on the ability of transcription factors to reprogram cells.

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: We performed multiple RNAseq, scRNAseq, TTSlamSeq, and ChIPseq of the cells expressing the WT, "AroLITE" and "AroPERFECT" of  CEBPa, HOXD4, NGN2, and MYOD1 proteins after transgene induction to measure differentiation of specific cell lines.

first: Julian

last: Naderi

last: P Magalhaes

first: Gregoire

last: Stik

first: Thomas

last: Graf

first: Denes

last: Hnisz


title: Succinate dehydrogenase (SDH)-Complex II regulates skeletal muscle cellular respiration and fatigue but not muscle mass in genetically induced pulmonary emphysema [20 wk]

status: Public on Feb 24 2024

city: Albany

first: Ariel

last: Jaitovich

email: balnisj@amc.edu, jaitova@amc.edu

state: NY

address: 47 New Scotland Ave.

department: MCP

institute: Albany Medical College

summary: Skeletal muscle wasting and reduced oxidative capacity coexist in patients with COPD/pulmonary emphysema and are independently associated with higher mortality. Whether reduced respiration contributes to muscle atrophy in that setting remains unknown. We have previously shown that a mouse with genetically induced COPD/pulmonary emphysema recapitulates muscle dysfunction features present in patients’ muscles, including reduced expression and activity of succinate dehydrogenase (SDH), which are partially reversed by genetic gain of SDH function. Previous research suggests that succinate accumulation, a by-product of SDH inhibition, can increase respiratory capacity of skeletal muscle. Here, we generated an inducible, muscle-specific SDH-C knockout mouse which demonstrates lower mitochondrial oxygen consumption and oxidative fibers’ contractility, associated with overall reduced exercise endurance. These changes are partially offset by mitochondrial complex I-dependent respiration, a respiratory pattern replicated in the muscles from the COPD/pulmonary emphysema genetic model. Moreover, while mice skeletal muscle SDH-C knockout causes an early succinate accumulation associated with a downregulated transcriptome, these changes do not correlate with the proteomic landscape; and animals muscle mass, fiber-type composition, and dry body mass constituents remain unaltered. We preset the first conditional, skeletal muscle-specific SDH-C knockout animal and demonstrate that while SDH-C regulates fibers respiration in genetically induced pulmonary emphysema, it does not control muscle mass.

overall_design: Differential expression of genes (mRNA) isolated from tibialis anterior (TA) skeletal muscle; 20 wk post induction WT vs. skeletal muscle SDHC-KO mice.

first: Joseph

last: Balnis


title: Succinate dehydrogenase (SDH)-Complex II regulates skeletal muscle cellular respiration and fatigue but not muscle mass in genetically induced pulmonary emphysema [3 wk]

overall_design: Differential expression of genes (mRNA) isolated from tibialis anterior (TA) skeletal muscle; 3 wk post induction WT vs. skeletal muscle SDHC-KO mice.


title: Combined analysis of ATAC-Seq and RNA-Seq reveal a potential role of WRKY34 in tomato response to cold stress [ATAC]

status: Public on Feb 23 2024

city: 杭州市

first: Mingyue

last: Guo

state: 浙江省

address: 浙江大学紫金港校区

country: China

institute: 浙江大学

summary: To further clarify the differences in the potential regulatory mechanisms of cold tolerance between wild and cultivated tomatoes, we subjected cold-sensitive cultivated tomato (Solanum lycopersicum) Ailsa Craig (AC) and cold-tolerant wild tomato (S. habrochaites) LA1777 to cold stress for 6 h, and performed ATAC-Seq and RNA-Seq, respectively.

sample_organism:
Solanum lycopersicum
Solanum habrochaites

overall_design: We subjected cold-sensitive cultivated tomato (Solanum lycopersicum) Ailsa Craig (AC) and cold-tolerant wild tomato (S. habrochaites) LA1777 to cold stress for 6 h, and performed ATAC-Seq.

first: Fengjun

last: Yang

first: Lijuan

last: Zhu

first: Jie

last: Zhou


title: Ebf1 is a mouse deafness gene and deletion causes a dramatic increase in hair cells and support cells of the organ of Corti

status: Public on Feb 26 2024

city: Seattle

first: Olivia

last: Bermingham-McDonogh

state: WA

address: 1959  NE Pacific St box 357420

department: Biological Structure

institute: University of Washington

summary: Following up on our previous observation that early B cell factor (EBF) sites are enriched in open chromatin of the developing sensory epithelium of the mouse cochlea, we investigated the effect of deletion of Ebf1 on inner ear development. We used a Cre driver to delete Ebf1 at the otocyst stage prior to development of the cochlea. These animals survived and were fertile. We examined the cochlea at postnatal day (P) 1 and found that the sensory epithelium had doubled in size but the length of the cochlear duct was unaffected. We also found that deletion of Ebf1 led to ectopic sensory patches in the Kölliker’s organ. Innervation of the developing organ of Corti was disrupted with no obvious spiral bundles. The ectopic patches were also innervated. All the extra hair cells (HCs) within the sensory epithelium and Kölliker’s organ contained mechanoelectrical transduction channels as indicated by rapid uptake of FM1-43. The excessive numbers of HCs were still present in the adult Ebf1 conditional knockout (cKO) animal. The animals had no detectable auditory brainstem response (ABR) suggesting that this gene is essential for hearing development.

overall_design: Sox2-GFP cells were Facs purified from mouse cochlear ducts at E12.5, E14.5 and E16.5.  The cells were then made into single cells sequencing libraries using 10X genomics protocol

first: Brent

middle: A

last: Wilkerson


title: Effects of PCB 52 Exposure Via Sub-Acute Nose-Only Inhalation on Gene Expression in Livers of Adolescent Rats

city: Iowa City

first: Aloysius

middle: John

last: Klingelhutz

state: IA

address: 3-604 BSB, 51 Newton Road

department: Microbiology and Immunology

institute: University of Iowa

summary: Polychlorinated biphenyls (PCBs) are persistent environmental toxicants that pose a variety of health risks in humans. PCB 52 has been found in the indoor air of schools where adolescent students and staff are being actively exposed. This study examined the livers of adolescent Sprague-Dawley rats after sub-acute exposure to PCB 52 via nose-only inhalation. Rats were exposed for 4 hours daily for 28 consecutive days. RNA extracted from both male and female livers were submitted for RNA sequencing to compare the effects of PCB 52 on the expression of genes in the liver.

overall_design: To determine the gene expression alterations following PCB 52 inhalation exposure in adolescent rats, male and female livers were processed for RNA sequencing. (N = 6 per sex)

first: Brynn

middle: K

last: Helm-Kwasny

first: Amanda

last: Bullert

first: Hui

last: Wang

first: Michael

middle: S

last: Chimenti

first: Andrea

last: Adamcakova-Dodd

first: Xuefang

last: Jing

first: David

last: Meyerholz

first: James

last: Ankrum

first: Peter

last: Thorne

first: Hans-Joachim

last: Lehmler

middle: J


title: Sin3B loss enhances the T-cell inflamed tumor microenvironment through the redistribution of H3K27Ac signals in pancreatic cancer [CUT&Tag]

status: Public on Feb 20 2024

city: Shanghai

first: Zhengyan

last: Zhang

address: State Key Laboratory of Systems Medicine for Cancer, Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Cancer Institute, Shanghai Jiao Tong University,

summary: Pancreatic ductal adenocarcinoma (PDAC) displays a poor response to immunotherapy. This poor response is predominantly attributed to the highly immunosuppressive tumor microenvironment (TME), characterized by a scarcity and dysfunction of infiltrating CD8+ T cells. Epigenetic regulators have recently been implicated in immune escape and immunotherapy sensitivity, presenting an appealing approach for directly targeting epigenetic factors or combining epigenetic therapies with immunotherapy in PDAC. Our study is the first to delineate the regulatory function of the epigenetic factor Sin3B in the tumor immune microenvironment (TIME) of PDAC. Using murine PDAC models, we discovered that intrinsic Sin3B loss in tumor cells reshapes the TIME, manifested by increased CD8+ T cell infiltration into tumors through enhanced secretion of  CXCL9 and CXCL10. This was accompanied by an increase in the cytotoxicity of CD8+ T cells, as evidenced by elevated Granzyme B (GzmB) and IFNγ production. Furthermore, Sin3B-deficient tumor cells exhibited heightened secretion of CXCL9/10 in response to IFNγ, creating a positive feedback loop via the CXCL9/10-CXCR3 axis and thus intensifying immune response against PDAC. Additionally, loss of Sin3B increased PDAC susceptibility to anti-PD1 therapy in mice. Corroborating our findings in the mouse model, analysis of human PDAC samples demonstrated a significant inverse correlation between Sin3B levels and both CD8+ T cell presence and CXCL9/10 expression. Notably, PDAC patients with lower Sin3B expression exhibited a more favorable response to anti-PD1 therapy. Concerning the mechanism, we systematically uncovered the extensive epigenetic regulation employed by Sin3B loss via the modulation of H3K27Ac redistribution in PDAC cells. Sin3B deficiency resulted in an uptick of H3K27Ac peaks concentrated in the promoter and enhancer regions. Under the treatment of IFNγ, Sin3B loss leads to the enrichment of H3K27Ac peaks in promoter regions of ISG-related genes such as CXCL9 and CXCL10, thereby boosting their expression. Collectively, our research outcomes propose a potential target for enhancing the accessibility of cytotoxic T cells to the tumor site and improving immunotherapy in the challenging landscape of PDAC.

overall_design: To investigate the function of Sin3B regulating chemokines, wo conducted Sin3B KO and WT cell lines. Then, we performed CUT&Tag sequencing to analyse how Sin3B regulates Redistribution of H3K27Ac. Markers are :Sin3B, H3K27ac, HDAC1.

first: Yingying

last: Tang

first: Junyi

last: Xu

first: Jing

last: Xue


title: Identification of robust cellular programs using reproducible LDA that impact sex-specific disease progression in different genotypes of a mouse model of AD

city: Irvine

first: Narges

last: Rezaie

state: California

address: 2218 Biological Sciences III

institute: University of California, Irvine

summary: The gene expression profiles of distinct cell types reflect complex genomic interactions among multiple simultaneous biological processes within each cell that can be altered by disease progression as well as genetic background. The Identification of these active cellular programs is an open challenge in the analysis of single-cell RNA-seq data. Latent Dirichlet Allocation (LDA) is a generative method used to identify recurring patterns in counts data, commonly referred to as topics that can be used to interpret the state of each cell.  However, LDA's interpretability is hindered by hyperparameter selection of the number of topics as well as the variability in topic definitions due to random initialization. We developed Topyfic, a Reproducible LDA (rLDA) package, to accurately infer the identity and activity of cellular programs in single-cell data, providing insights into the relative contributions of each program in individual cells. We apply Topyfic to brain single-cell and single-nucleus datasets of two 5xFAD mouse models of Alzheimer’s disease crossed with C57BL6/J or CAST/EiJ mice to identify distinct cell types and states in cell types such as microglia. We find that 8-month 5xFAD/Cast F1 males show higher level of microglial activation than matching 5xFAD/BL6 F1 males, whereas female mice show similar levels of microglial activation. We show that regulatory genes such as TFs, microRNA host genes, and chromatin regulatory genes alone capture cell types and cell states. Our study highlights how topic modeling with a limited vocabulary of regulatory genes can identify gene expression programs in single-cell data to quantify similar and divergent cell states in distinct genotypes.

overall_design: Cortex and hippocampus of Tthe 5xFAD mouse model of Alzheimer's disease and matching wildtype (C57BL/6J) 8 month mice of box sexes  were dissect and processed for single cell and single nucleus RNA-sequencing

first: Ali

last: Mortazavi


title: Control ChIP-seq from whole organism (ENCSR101SVT)

first: ENCODE

last: DCC


title: Deciphering the Links: Fragmented Polystyrene as a Driver of Skin Inflammation

status: Public on Feb 19 2024

city: seoul

first: sungguan

last: hong

address: 84, Heukseok-ro, Dongjak-gu, Seoul, 104-407

department: Chemistry

country: South Korea

institute: Chung-Ang

summary: Recent studies have identified the pervasive presence of nano- and microplastics (NMP) in atmospheric air, leading to inevitable human exposure. Human skin, with an extensive surface area of 1.5-2 m², is constantly exposed to airborne NMP, yet the dermal implications of such exposure remain elusive. Our investigation employed fragmented polystyrene (fPS), a plastic commonly found in the air, to evaluate dermal penetration using various skin models. We utilized pyrolysis-gas chromatography/mass spectrometry (py-GC/MS) to quantify fPS that had penetrated the skin model. Furthermore, we examined the biological alterations in skin keratinocytes consequent to fPS exposure and analyzed the regulation of inflammatory response markers. Our findings reveal deleterious effects on skin keratinocytes, underlining the potential risks posed by short-term fPS exposure. This multifaceted skin model study offers new perspectives on the toxicological impacts of NMP.

overall_design: To investigate the effects of fPS exposure on skin keratinocytes, we established HaCaT cells, a human-derived keratinocyte cell line.

first: Gyeong

middle: B

last: Song

first: Jisoo

last: Nam

first: Sangmin

last: Ji

first: Gijeong

last: Woo

first: Soojeong

last: Park

first: Bokyung

last: Kim

first: Jeein

last: Hong

first: Myung

middle: G

last: Choi

first: Seokheon

first: Wonchul

last: Lim

first: Sangwoon

last: Yoon

first: Woo

first: Mi

first: Hye

middle: R

last: Koh

first: Tae-Gyu

first: Sungguan


title: Control ChIP-seq from whole organism (ENCSR100NPZ)

first: ENCODE

summary:
This is the ChIP-seq control of transgenic worms expressing madf-6-eGFP fusion proteins.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: p16-dependent upregulation of PD-L1 impairs immunosurveillance of senescent cells [RNA-seq: Lung Epithelial Cells]

status: Public on Feb 14 2024

city: Rehovot

first: Valery

last: Krizhanovsky

state: Israel

address: 234 Herzl St.

department: Molecular Cell Biology

country: Israel

institute: Weizmann Institute of Science

summary: The accumulation of senescent cells promotes aging, but a molecular mechanism that senescent cells use to evade immune clearance and accumulate remains to be elucidated. Here, we report that p16-positive senescent cells upregulate the immune checkpoint protein programmed death-ligand 1 (PD-L1) to accumulate in aging and chronic inflammation. p16-mediated inhibition of CDK4/6 promotes PD-L1 stability in senescent cells via the downregulation of ubiquitin-dependent degradation. p16 expression in infiltrating macrophages induces an immunosuppressive environment that can contribute to an increased burden of senescent cells. Treatment with immunostimulatory anti-PD-L1 antibody enhances the cytotoxic T cell activity and leads to the elimination of p16, PD-L1-positive cells. Our study uncovers a molecular mechanism of p16-dependent regulation of PD-L1 protein stability in senescent cells and reveals the potential of PD-L1 as a target for treating senescence-mediated age-associated diseases.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for mouse lung epithelial cells chronically exposed to LPS (chronic inflammation) or PBS (control).

first: Julia

last: Majewska

first: Amit

last: Agrawal

first: Avi

last: Mayo

first: Lior

last: Roitman

first: Rishita

last: Chatterjee

first: Jarmila

last: Kralova

first: Tomer

last: Landsberger

first: Yonatan

last: Katzenelenbogen

last: Meir-Salame

first: Efrat

last: Hagai

first: Nemanja

last: Stanojevic

first: Ido

last: Amit

first: Uri

last: Alon


title: Transcriptome analysis of the Rhodobacter sphaeroides RNase III mutant (inactivated enzyme) by total RNA sequencing

city: Gießen

first: Gabriele

last: Klug

address: Heinrich-Buff-Ring 26-32

department: Molecular- and Microbiology

institute: Justus-Liebig University Gießen

summary: RNase III is an important and highly conserved endoribonuclease known to impact rRNA, mRNA and ncRNA abundances by RNA processing. In this study we analyzed the effects of an inactivation of RNase III (inactivated through substitution of two strictly conserved amino acids within the active enzyme center) on the  transcriptome of the facultative phototrophic model organism Rhodobacter sphaeroides.

overall_design: Comparative gene expression profiling analysis of RNAseq data of independent biological triplicates of the Rhodobacter sphaeroides RNase III (rnc) mutant strain under three different growth conditions (aerobic, microaerobic or phototrophic).

first: Janek

last: Börner

first: Tobias

last: Friedrich


title: p16-dependent upregulation of PD-L1 impairs immunosurveillance of senescent cells [RNA-seq: Lung Alveolar Macrophages]

last: Krizhanovsky

overall_design: Comparative gene expression profiling analysis of RNA-seq data for mouse lung alveolar macrophages (positive or negative for p16) chronically exposed to LPS (chronic inflammation) or PBS (control).


title: p16-dependent upregulation of PD-L1 impairs immunosurveillance of senescent cells

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: Comparative analysis of RNA interference and pattern-triggered immunity induced by dsRNA in response to virus infection

status: Public on Feb 12 2024

city: Madrid

first: Francisco

last: Tenllado

address: Ramiro de Maeztu, 9

country: Spain

institute: CSIC

summary: The main goal of this study was to compare the differential efficiency of the antiviral activity triggered by externally delivered virus-specific and nonspecific dsRNAs in plants. RNAi mediated by virus-specific dsRNA is the main antiviral defense mechanism in plants, but nonspecific dsRNA-triggered responses have been documented to play a role in antiviral defense. Using PVX as a model, we have determined that co-inoculation with either virus-specific or nonspecific dsRNA reduced virus accumulation in both inoculated and systemic leaves although at different extent. While the administration of dsRNA specific for the targeted virus induced a potent RNAi-based antiviral response that resulted in highly effective control of viral disease, the degree of interference with PVX-GFP infection afforded by nonspecific dsRNA (PTI) was limited. To identify early biological processes and pathways associated with dsRNA-based immunity, we conducted a global transcriptome RNAseq assay from N. benthamiana leaves inoculated with four different treatments, i.e., dsGFP alone (dsG), PVX-GFP combined with dsGFP (dsG_VG), wild-type (Wt) PVX combined with dsGFP (dsG_V) and bacterial nucleic acid extracts not expressing dsRNA as a control (Ctr). KEGG analysis of differentially expressed genes showed a significant enrichment of terms related to plant-pathogen signaling pathways (KEGG terms Plant-pathogen interaction and MAPK signaling) in all the three treatments with dsRNA. Our results further indicate that the transcriptomic response triggered by dsRNA alone includes canonical immune pathways or genes known to be involved in defense responses, i.e., Ca+2 signaling, ethylene signaling, MAPK signaling, WRKY transcription factors, PR transcriptional factors, NBS-LRR resistance genes, EDS1, and LRR receptor-like kinases, many of which are typical of antimicrobial PTI . Moreover, the transcriptomic response to the homologous combination (dsGFP plus PVX-GFP) had a greater overrepresentation of genes involved in plant-pathogen signaling pathways than the heterologous combination (dsGFP plus Wt PVX), highlighting a quantitative difference between RNAi and PTI immune responses.

overall_design: Comparative gene expression profiling analysis of RNA-seq data from Nicotiana bentamina leaves inoculated with four different treatments, i.e., dsGFP alone (dsG), PVX-GFP combined with dsGFP (dsG_VG), PVX combined with dsGFP (dsG_V) and bacterial nucleic acid extracts not expressing dsRNA as a control (Ctr).  Three biological replicates were analyzed for each treatment.

first: Khouloud

last: Necira


title: Dynamic Hippo pathway activity underlies mesenchymal differentiation during lung alveolar morphogenesis

status: Public on Feb 10 2024

city: Philadelphia

first: Sylvia

middle: N

last: Michki

state: PA

address: 3615 Civic Center Blvd

department: Pulmonary & Sleep Medicine

institute: Children's Hospital of Philadelphia

summary: Alveologenesis, the final stage in lung development, substantially remodels the distal lung, expanding the alveolar surface area for efficient gas exchange. Secondary crest myofibroblasts (SCMF) exist transiently in the neonatal distal lung and are critical for alveologenesis. However, the pathways that regulate SCMF function, proliferation, and temporal identity remain poorly understood. To address this, we purified SCMFs from reporter mice, performed bulk RNA-sequencing, and found dynamic changes in Hippo-signaling components during alveologenesis. We deleted Hippo effectors, Yap/Taz, from Acta2-expressing SCMFs at the onset of alveologenesis, causing a significant arrest in alveolar development. Using scRNA-seq, we identified a distinct cluster of cells in mutant lungs with altered expression of marker genes associated with proximal mesenchymal cell types, airway smooth muscle (ASM), and alveolar duct myofibroblasts (DMF). Using lineage tracing, we show that neonatal Acta2-expressing SCMFs give rise to adult DMFs and that Yap/Taz mutants have an increase of persisting DMF-like cells in the alveolar ducts. Our findings identify aberrant differentiation of neonatal lung myofibroblasts and demonstrate that Yap/Taz are critical for maintaining lineage commitment.

overall_design: 10Xv3 3’-biased scRNA-seq of cells from whole lung in mice, either a) with/without Acta2-CreERT2-driven YAP/TAZ deletion, or b) with Acta2-CreERT2-driven R26R-LSL-tdTomato lineage tracing and no other genetic manipulation.

first: Fatima

last: Chaudhry

first: Dain

middle: L

last: Shirmer

first: Sharon

last: Mcgrath-Morrow

first: Lisa

last: Young

first: David

last: Frank

first: Jarod

last: Zepp


title: Dynamic Hippo pathway activity underlies mesenchymal differentiation during lung alveolar morphogenesis [bulk RNA-seq]

overall_design: Bulk RNA-seq of Acta2-dsRed+, Pdgfra-GFP+ cells from whole mouse lung at E17.5, P3, P7, and P10


title: Expression data of NIT-1 cells treated with CdSO4

status: Public on Feb 09 2024

city: Dali

first: Yahao

last: MOU

address: No. 22, Wanhua Road

institute: Dali University

summary: Cadmium is a widespread environmental heavy metal pollutant as well as a strong endocrine disruptor. Epidemiologic evidence shows a positive correlation between cadmium levels in humans and the incidence of diabetes mellitus.Moreover,  cadmium can accumulate in pancreatic islet and induce oxidative damage, apoptosis and decreased insulin.However, the specific mechanisms involved have not been completely elucidated.We hope to use microarrays to explore the mechanism by analyzing the changes of genes during the process of cadmium damage in islet β-cells.

overall_design: After treatment of NIT-1 cells with 4 μmol/L CdSO4 to induce oxidative damage, total RNA was collected from the experimental and control groups.

first: Shiyan

last: GU


title: RNAseq of Group A Streptococcus clinical isolates

status: Public on Feb 02 2024

city: Greenville

first: Weihua

last: Huang

state: North Carolina

address: 600 Moye Blvd, Brody 7S-24

department: Pathology

institute: East Carolina University

summary: We compared differential gene expression in ST399/EMM-77, invasive ST28/EMM-1 and non-invasive ST28/EMM-1, 4 isolates in each group.

overall_design: RNAseq for grouped differential gene expression analysis


title: Expanded repertoire of RNA-editing-based detection for RNA binding protein interactions (4)

city: La Jolla

first: Brian

last: Yee

address: 9500 Gilman Dr

department: Health

institute: UCSD

summary: RNA binding proteins (RBPs) are key regulators of RNA processing and cellular function. Technologies to discover RNA targets of RBPs such as TRIBE (targets of RNA binding proteins identified by editing) and STAMP (surveying targets by APOBEC1 mediated profiling) utilize fusions of RNA base-editors (rBEs) to RBPs to circumvent the limitations of immunoprecipitation (CLIP)-based methods that require enzymatic digestion and large amounts of input material. To expand the collection of rBEs suitable for editing-based RBP-RNA interactome studies, we developed experimental and computational assays to systematically evaluate the editing activities of over thirty A-to-I and C-to-U rBEs in human cells. We identify rBEs that outperform Drosophila ADAR (TRIBE) and mammalian APOBEC1 (STAMP) in the characterization of the binding patterns of sequence-specific and broad-binding RBPs and recommend rBEs that pair effectively in dual-RBP-based applications. We demonstrate that the optimal choice of single or multiple rBEs to fuse to a given or pair of RBPs depends on the editing biases of the rBEs and the binding preferences of the RBPs. Our framework ENGRAVe (Editing nucleotides with general RNA-base-editor variants) frames the use of and expands the choices of rBEs for the next generation of RBP-RNA target discoveries.

overall_design: Plasmids encoding RPS2-rBE fusions were transiently transfected into HEK293XT cells. Then, 24 hrs after transfection, construct expression was induced by the addition of doxycycline (Dox) at 2 µg/mL for 24 hrs. After, Torin-1 (100 nM final concentration in the wells) dissolved in DMSO or DMSO without Torin-1 (vehicle) was added, and the cells were incubated for 48 hrs before extraction of DNA-free total RNA and sequencing library preparation.

first: Hugo

middle: C

last: Medina-Munoz

first: Eric

last: Kofman

first: Pratibha

last: Jagannatha

first: Evan

last: Boyle

first: Tao

last: Yu

first: Krysten

last: Jones

first: Jasmine

last: Mueller

first: Grace

middle: D

last: Lykins

first: Brodie

last: Ranzau

first: Rahul

middle: M

last: Kohli

first: Alexis

last: Komor

first: Gene

middle: W

last: Yeo


title: Expanded repertoire of RNA-editing-based detection for RNA binding protein interactions (5)

overall_design: MCP-C-to-U and PP7-A-to-I rBEs were expressed together in HEK293XT cells with one of three reporter mRNAs, each bearing a different MS2 and PP7 stem-loops distribution in the 3'UTR. After, total RNA was extracted, and libraries were sequenced to analyze the editing profiles.


title: TF ChIP-seq from whole organism (ENCSR100DTS)

first: ENCODE

last: DCC

summary:
ChIP-seq against eGFP-mef-2 in L1 larva worms.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Expanded repertoire of RNA-editing-based detection for RNA binding protein interactions (2)

summary: RNA binding proteins (RBPs) are key regulators of RNA processing and cellular function. Technologies to discover RNA targets of RBPs such as TRIBE (targets of RNA binding proteins identified by editing) and STAMP (surveying targets by APOBEC1 mediated profiling) utilize fusions of RNA base-editors (rBEs) to RBPs to circumvent the limitations of immunoprecipitation (CLIP)-based methods that require enzymatic digestion and large amounts of input material. To expand the collection of rBEs suitable for editing-based RBP-RNA interactome studies, we developed experimental and computational assays to systematically evaluate the editing activities of over thirty A-to-I and C-to-U rBEs in human cells. We identify rBEs that outperform Drosophila ADAR (TRIBE) and mammalian APOBEC1 (STAMP) in the characterization of the binding patterns of sequence-specific and broad-binding RBPs and recommend rBEs that pair effectively in dual-RBP-based applications. We demonstrate that the optimal choice of single or multiple rBEs to fuse to a given or pair of RBPs depends on the editing biases of the rBEs and the binding preferences of the RBPs. Our framework ENGRAVe (Editing nucleotides with general RNA-base-editor variants) reframes the use of and expands the choice of rBEs for the next generation of RBP-RNA target discoveries.

overall_design: The experiment is Poly(A) RNA sequencing of samples corresponding to MS2 coat-protein (MCP)-rBE fusions demonstrating favorable editing profiles on the MCP binding site-containing reporter mRNA. The approach simultaneously detects edits on the reporter mRNA (on-target) and endogenous transcripts (off-target). Editing on endogenous transcripts is considered "off-target" because those RNAs lack MS2 coat protein (MCP) binding sites.


title: Blocker-SELEX: A Structure-Guided Strategy for Developing Inhibitory Aptamers Disrupting Transcription Factor Interactions

status: Public on Feb 01 2024

city: Hangzhou

first: Xueying

last: Liu

address: No. 150 Dongfang Road, Qiantang District

institute: Hangzhou lnstitute of Medicine Chinese Academy of Sciences

summary: Despite the well-established significance of transcription factors (TFs) in pathogenesis, their utilization as pharmacological targets has been limited by the inherent challenges mainly associated with modulating their protein-protein and protein-DNA interactions. The lack of defined small-molecule binding pockets and the nuclear localization of TFs makes neither small molecule inhibitors nor neutral antibodies suitable in blocking TF interactions. Aptamers are short oligonucleotides exhibiting high affinity and specificity for a diverse range of targets. The large molecular weights, expansive blocking surfaces and efficient cellular internalization make aptamers as a compelling molecular tool for traditional TF interaction modulators. Here, we report a structure-guided design strategy called Blocker-SELEX for developing inhibitory aptamers (iAptamer) that selectively block TF interactions. Our approach led to the discovery of an iAptamer that cooperatively disrupts SCAF4/SCAF8-RNA Polymerase II (RNAP2) interactions, thus dysregulates RNAP2 dependent gene expression and splicing, leading to the impairing of cell proliferation. This approach was further applied to develop iAptamers efficiently block WDR5-MYC interaction. Together, our study highlights the potential of Blocker-SELEX in developing iAptamers that effectively disrupt TF interactions, and the generated iAptamers hold promising implications as chemical tools in studying biological functions of TF interactions and the potential for nucleic acids drug development.

overall_design: To validate the targeted effect of SRiApt-1 on gene transcription and mRNA splicing by inhibiting the interaction between RNAP2 and SCAF4/SCAF8 proteins at the cellular level, we first optimized the stability of SRiApt-1 by introducing two 2'-O-Me modifications, resulting in SRiApt-1_m (5'-G(2'-O-Me)GGGTGGGGA(2'-O-Me)G-3') . Subsequently, mRNA sequencing was conducted on HCT116 cells cell line treated with SRiApt-1_m or control aptamers for 24 hours. Analysis of the RNA-seq data revealed significant alterations in the transcriptome of HCT116 cells upon SRiApt-1_m aptamer treatment.

first: Tongqing

last: Li

first: Yong

last: Wei

first: Qin

last: Wu


title: Expanded repertoire for RNA-editing-based detection for RNA binding protein interactions (3)

first: Brian

last: Yee

overall_design: rBEs were expressed in HEK293XT cells as fusions to RBFOX2 (RBFOX2-rBE) or without being fused to an RBP. The editing profiles with and without the RBP were examined.

first: Hugo

last: Medina-Munoz


title: Gut bacteria-derived serotonin promotes immune tolerance in early life through regulation of neonatal gut T cells  II

status: Public on Jan 31 2024

city: New York

first: Katherine

last: Sanidad

address: 413 E69th St

institute: Weill Cornell Medicine

summary: The gut microbiota promotes immune system development in early life, but the interactions between the gut metabolome and immune cells in the neonatal gut remains largely undefined. Here, we demonstrate that the neonatal gut is uniquely enriched with neurotransmitters, including serotonin; specific gut bacteria produce serotonin directly while downregulating monoamine oxidase A to limit serotonin breakdown. Serotonin directly signals to T cells to increase intracellular indole-3-acetaldehdye to inhibit mTOR activation and thereby promotes the differentiation of regulatory T cells, both ex vivo and in vivo in the neonatal intestine. Oral gavage of serotonin into neonatal mice leads to long-term T cell-mediated antigen-specific immune tolerance towards both dietary antigens and commensal bacteria. Together, our study has uncovered an important role for unique gut bacteria to increase serotonin availability in the neonatal gut and a novel function of gut serotonin to shape T cell response to dietary antigens and commensal bacteria to promote immune tolerance in early life.

overall_design: WT neonatal mice were given 50 μL of 5-HT (12.5 μg/mL) or vehicle (PBS) at P8 and P9 via oral gavage. The mice were then sacrificed at P14 and SI and colon luminal contents were collected for 16S sequencing. DNA was extracted from luminal contents and the V4-V5 region of the 16S rRNA gene was amplified using universal primers and sequenced on an Illumina MiSeq sequencer.

middle: Z

first: Stephanie

last: Rager

first: Hannah

last: Carrow

first: Aparna

last: Ananthanarayanan

first: Ryann

last: Callaghan

first: Lucy

last: Hart

first: Tingting

first: Purnima

last: Ravisankar

first: Julia

last: Brown

first: Mohammed

last: Amir

first: Jenny

last: Jin

first: Alexandria

last: Savage

first: Ryan

last: Luo

first: Florencia

last: Rowdo

first: M

last: Martin

first: Randi

last: Silver

first: Chun-Jun

last: Guo

first: Jan

last: Krumsiek

first: Naohiro

last: Inohara

first: Melody

middle: Y

last: Zeng


title: Gut bacteria-derived serotonin promotes immune tolerance in early life through regulation of neonatal gut T cells I

first: Katherine

last: Sanidad

overall_design: Small intestine luminal contents were harvested from adult (8 weeks) and neonatal (14 days) mice. DNA was extracted from luminal contents and the V4-V5 region of the 16S rRNA gene was amplified using universal primers and sequenced on an Illumina MiSeq sequencer.

first: Stephanie

last: Rager

first: Hannah

last: Carrow

first: Aparna

last: Li


title: Expanded repertoire of RNA-editing-based detection for RNA binding protein interactions (1)

first: Brian

last: Yee

overall_design: A variety of RBP-rBE fusions were first expressed together with a reporter mRNA to assess the corresponding editing profiles.

first: Hugo

last: Medina-Munoz

first: Eric

last: Kofman

first: Pratibha

last: Jagannatha

first: Evan

last: Boyle

first: Tao

last: Yu

first: Krysten

last: Jones

first: Jasmine

last: Mueller

first: Grace

last: Lykins

first: Brodie

last: Ranzau

first: Rahul

last: Kohli

first: Alexis

last: Komor

first: Gene

last: Yeo


title: Gut bacteria-derived serotonin promotes immune tolerance in early life through regulation of neonatal gut T cells III

first: Katherine

last: Sanidad

overall_design: GF WT neonatal mice were given 50 μL of 5-HT (12.5 μg/mL) or vehicle (PBS) at P8 and P9 via oral gavage. The mice were then sacrificed at P14 and small intestine tissue was harvested. Total RNA was isolated and bulk RNA-seq performed using an Illumina NovaSeq 6000 sequencer. LEfSe followed by multiple hypotheses correction using signal-to-noise rate and false discovery rate analyses was used to discover genes with differential abundance. Differences at LEfSe p < 0.05  and FDR < 0.05 were considered significant.

last: Ananthanarayanan

first: Ryann

last: Callaghan

first: Lucy

last: Hart

first: Tingting

first: Purnima

last: Ravisankar

first: Julia

last: Brown

first: Mohammed

last: Amir

first: Jenny

last: Jin

first: Alexandria

last: Savage

first: Ryan

last: Luo

first: Florencia

last: Rowdo

first: M

last: Martin

first: Randi

last: Silver

first: Chun-Jun

last: Guo

first: Jan

last: Krumsiek

first: Naohiro

last: Inohara

first: Melody

last: Zeng


title: Neuronal IL-17 controls C. elegans developmental diapause through p53/CEP-1

status: Public on Jan 30 2024

city: Buffalo

first: Johnny

last: Cruz Corchado

address: Elm & Carlton Streets Buffalo,L3-L125

department: Cell Stress

institute: Roswell Park Comprehensive Cancer Institue

summary: Metazoan growth and development requires the coordination of cell cycle progression and metabolism with nutrient availability1-3. Here, we show that in C. elegans, amphid neurons regulate the animals’ developmental decision to continue reproductive growth or arrest as quiescent dauer larvae in response to food, by controlling the activity of C. elegans p53-like ortholog, CEP-1. Specifically, upon food availability, larval neurons secrete a mammalian IL-17 ortholog, ILC-17.1, and ILC-17.1 signaling is needed for C. elegans to progress through development into reproductive adults. ILC-17.1 deficiency activates CEP-1/p53 in larval blast cells, and causes larvae to arrest as stress-resistant, quiescent dauers by activating DAF-16/FOXO, decreasing cytochrome C levels, decreasing glucose utilization and upregulating cell cycle inhibitors. Increasing ILC-17.1 levels represses CEP-1/p53 and promotes anabolic growth, but also inhibits apoptosis upon genotoxic stress. IL-17 also represses p53 in human epithelial cells. These studies describe a role for the tumor suppressor p53-like proteins in controlling developmental quiescence of a metazoan in response to neuronal activity and immunometabolic signals and are relevant to our understanding of neuroimmune mechanisms in cancer. This novel role for p53-like proteins in C. elegans supports the argument that their developmental function was a main driving force in their evolution4,5.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for  C. elegans larvae of the following gennotypes wild type (N2), ilc-17.1(syb5296) X and praEx022 (unc-54p::ilc-17.1 cDNA::3XFLAG::tbb-2 3’UTR; pdat-1::GFP::unc-54 3’UTR).

last: Cruz

first: Abhishiktha

last: Godthi

first: Srijit

last: Das

first: Venna

last: Prahlad


title: Gut bacteria-derived serotonin promotes immune tolerance in early life through regulation of neonatal gut T cells

first: Katherine

last: Sanidad


title: Proteomic profiling Proteogenomic landscape of multiple myeloma reveals CDK6 upregulation as a targetable resistance mechanism for lenalidomide in multiple myeloma

city: Berlin

first: Anna

last: Dolnik

address: Augustenburger Platz 1

department: Campus Virchow-Klinikum (CVK)

institute: Charité Universitätsmedizin Berlin

summary: Multiple myeloma is a plasma cell malignancy of the bone marrow. Despite therapeutic advances in multiple myeloma, it remains incurable and better risk stratification as well as new therapies are therefore highly needed. While genetics and gene expression have been extensively studied leading to new insights in disease biology and improved prognostic models, the proteome of multiple myeloma has not been systematically assessed. Here, we provide a comprehensive multi-omic analysis including deep tandem mass tags (TMT)-based quantitative global (phospho)proteomics, RNA sequencing and nanopore DNA sequencing of 138 primary patient-derived plasma cell malignancy samples, including treatment-naive multiple myeloma cases selected for clinical trials, plasma cell leukemia, and the premalignancy MGUS, as well as healthy controls. We found that the (phospho)proteome of malignant plasma cells is highly deregulated as compared to healthy cells and is both defined by chromosomal alterations and extensive post-transcriptional regulation. A protein signature consisting of 8 proteins was identified that is associated with aggressive disease and highly predictive for outcomes in newly diagnosed multiple myeloma. Integration with functional genetics and single-cell sequencing revealed generally and genetic subtype-specific deregulated proteins and pathways in plasma cell malignancies that include novel potential targets for (immuno)therapies. Our study provides a unique resource for investigating biology and new therapeutic approaches in multiple myeloma and associated diseases and highlights the broad implications of proteomic studies in cancer.

overall_design: mRNA profiles of CD138+ or bone marrow with the content of CD138+ >75% (Multiple Myelom) were generated using TruSeq RNA Exome (TruSeq RNA Access Kit) (Illumina) followed by sequencing with 50 bp single-end reads on NextSeq; Two samples were sequenced on HiSeq 2000 as indicated in column "instrument model".

first: Evelyn

last: Ramberger

last: Krönke


title: Cardiotoxic effects of mycotoxin citrinin on mammalian cells revealed by transcriptome profiling

city: Taipei

first: Jui-Feng

last: Tsai

address: No. 1, Sec. 1, Ren'Ai Rd,

department: Graduate Institute of Toxicology

country: Taiwan

institute: National Taiwan University

summary: Mycotoxin citrinin (CTN) is widely found in multiple types of grains in foods and feeds globally. CTN also contaminates Monascus-derived health supplements such as red yeast rice and red yeast extracts during the fermentation process, which are originally used for preventing cardiovascular diseases. A previous study has reported that CTN is cardiotoxic to zebrafish embryos during their development by interfering some cardiogenic genes and pathways, showing a potential risk of consuming CTN-contaminated foods and products. However, the cardiotoxic effects and the underlying mechanisms of CTN on mammalian cardiomyocytes remain unclear and need to be ellucidated. In this study, we performed RNA-seq experiments in order to investigate the transcriptomic alterations induced by CTN-exposed rat H9c2 cardiomyocytes. The transcriptome profiling we obtained may reveal some evidence regarding the toxic effects of CTN on cardiac phenotypes, chromosome segregation, tubulin arrangement, mitochondrial functioning, and stress responses, etc.

overall_design: RNA-seq analysis was performed for CTN-exposed cardiac cells. Rat cardiomyoblast H9c2 cells were treated with vehicle (CTN_0) and 50 μM of CTN (CTN_50) for 48 h.  Four biological replicates were pooled for one batch; two independent batches of samples were sent for RNA-seq.

first: Biing-Hui

last: Liu


title: The Tabulae Paralytica: Multimodal single-cell and spatial atlases of spinal cord injury

city: Geneve

first: Alan Yue Yang

last: Teo

address: Chem. des Mines 9, Campus Biotech

department: SV

country: Switzerland

institute: EPFL

summary: This submission is a dataset of two modalities, single-nucleus transcriptomics and single-nuclei spatial transcriptomics in the spinal cords of mice. The single-nuclei transcriptomics data is harvested and profiled using 10x Genomics Chromium Single Cell Kit Version. The single-nuclei spatial transcriptomics data is harvested and profiled using Visium Spatial Gene Expression.

overall_design: We used single-nucleus RNA-sequencing and spatial transcriptomics to profile the mid thoracic spinal cord of mice over various conditions spanning from age, spinal cord injury (SCI) severity, drug treatments, time after SCI, sex and injury models

first: Michael

last: Skinnider

first: Matthieu

last: Gautier

first: Alan

first: Claudia

last: Kathe

first: Thomas

middle: H

last: Hutson

first: Achilleas

last: Laskaratos

first: Alexandra

last: de Coucy

first: Nicola

last: Regazzi

first: Viviana

last: Aureli

first: Nicholas

last: James

first: Bernard

last: Schneider

middle: V

last: Sofroniew

first: Quentin

last: Barraud

first: Jocelyne

last: Bloch

first: Mark

last: Anderson

first: Jordan

last: Squair

first: Grégoire

last: Courtine


title: Il-17 p53 Developmental Series

first: Johnny

last: Cruz Corchado

summary: Here, we show that the activity of the tumor suppressor p53 in the metazoan C. elegans switches organismal development between reproductive growth and dormancy by responding to nutrient availability signaled by the cytokine, ILC-17.1. ILC-17.1-dependent repression of the C. elegans p53 ortholog CEP-1 is required for larval growth and development; ILC-17.1 deficiency activates CEP-1/p53 in post-embryonically dividing progenitor blast cells, decreases glucose utilization and cytochrome C levels, upregulates cell cycle inhibitors, and causes larvae to arrest as stress-resistant, quiescent dauers.

overall_design: Comparative gene expression profiling analysis of RNA-seq data at two different developmental time points(15 hrs and 32 hrs) of C. elegans larvae in  the following gennotypes wild type (N2), ilc-17.1(syb5296) X,unc-119 (ed4); gtIs1 [CEP-1::GFP + unc-119 (+)],ilc-17.1 (syb5296)X; cep-1 (gk138) I

last: Cruz

first: Abhishiktha

last: Godthi

first: Venna

last: Prahlad


title: Expanded palette of RNA base editors for comprehensive RBP-RNA interactome studies

first: Brian

last: Yee

overall_design: Refer to individual Series


title: Effects of renal ischemia-reperfusion injury in Azin1 A-to-I locked and uneditable mice

status: Public on Jan 20 2024

city: Indianapolis

first: Takashi

last: Hato

state: IN

address: 950 W. Walnut St. R2 202

department: Medicine

institute: Indiana University

summary: We generated two mouse models of Azin1 A-to-I editing. In the first model, the editing site is locked in the edited state (AGC serine to GGC glycine). In the second model, the editing site is disrupted while preserving the codon composition (AGC serine to TCC serine). Bulk total RNA-seq was performed on kidney tissues under basal conditions and 24 hours after 20 min bilateral renal ischemia-reperfusion injury.

overall_design: Ischemia-reperfusion injury was performed under isoflurane anesthesia. Prior to surgery, mice were given extended-release buprenorphine at a dose of 3.25 mg/kg. The mice were subjected to a 20-minute bilateral renal pedicle clamp followed by reperfusion. Tissues were harvested 24 hours after surgery. A heating pad was used to ensure their rectal temperature remained above 36 °C throughout the surgical procedure. No antibiotics or fluid resuscitation were administered.


title: Identification of FDA-Approved Drugs that Induce Heart Regeneration in Mammals [RNA]

status: Public on Jan 18 2024

city: Dallas

first: Hesham A.

last: Sadek

state: TX

address: 6000 Harry Hines Blvd

institute: UT Southwestern Medical Center

summary: The inability of the adult human heart to regenerate lost or damaged myocardial tissue has created one of the most pressing public health dilemmas due to the devastating impact of heart failure. Our group and others have outlined several regulators of cardiomyocyte mitosis that may impact the regenerative capacity of the adult myocardium in mammals. Recently, we reported that the transcription factors Meis1 and Hoxb13 regulate postnatal cardiomyocyte cell cycle arrest, where concomitant deletion of both genes induced cardiomyocyte proliferation and myocardial regeneration following ischemic injury. These studies suggest that pharmacological targeting Meis1 and Hoxb13 transcriptional activity could be a viable path towards heart regeneration.  Therefore, we performed an in-silico screen to identify FDA-approved drugs that can inhibit Meis1 and Hoxb13 transcriptional activity based on the published crystal structure of Meis1 and Hoxb13 bound to DNA. Our screen yielded several candidates based on binding profiles to either Meis1 DNA binding domain, Hoxb13 DNA binding domain, or the interface between Meis1 and Hoxb13, as well as safety and side effect profiles. Out of the shortlist of top hits, paromomycin and neomycin induced proliferation of neonatal rat ventricular myocytes in vitro and displayed dose-dependent inhibition of Meis1 and Hoxb13 transcriptional activity by luciferase assay, and disruption of DNA binding by EMSA. X-ray crystal structure revealed that both paromomycin and neomycin bind to Meis1 near the Hoxb13 interaction site where they interact with 3 out of the 5 Meis1 amino acids that participate in DNA-binding. The crystal structure also demonstrates that both drugs bind at the interface of Meis1 homodimer, therefore placing one of the Meis1 monomers in a position incompatible with DNA-binding. Importantly, administration of paromomycin-neomycin combination by intraperitoneal injection in mice induced cardiomyocyte proliferation, improved left ventricular (LV) systolic function and decreased scar formation in two models of ischemic reperfusion injury in mice. Finally, dual intravenous administration of the paromomycin-neomycin combination in Yorkshire pigs following cardiac ischemia/reperfusion injury induced cardiomyocyte proliferation, improved LV systolic function, and decreased scar formation. Collectively, we identified paromomycin and neomycin as FDA-approved drugs with therapeutic potential for induction of heart regeneration in humans.

overall_design:
To investigate the alternative gene expression in Paro/Neo-suppressed Meis1/Hoxb13 activity, we performed bulk RNA-Seq in a vehicle and Paro/Neo—treated mice.
We performed gene expression profiling analysis using data obtained from RNA-Seq of 3 mouse ventricles for a vehicle or Paromyomycin/Neomycin combination treatment.
Comparative gene expression profiling analysis of RNA-seq data for Paromomycin/Neomycin combination treatment and its vehicle control.

first: Hesham

middle: A

first: NgocUyenNhi

last: Nguyen

first: Mahmoud

last: Ahmed

first: Chao

last: Xing

first: Yan

last: Liu


title: Identification of FDA-Approved Drugs that Induce Heart Regeneration in Mammals [ChIP]

overall_design: Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for Meis1 or Hoxb13 in postnatal day (p) 15 murine hearts that underwent 7 days of combination Paromomycin and Neomycin injection from p7.

first: NUN


title: Identification of FDA-Approved Drugs that Induce Heart Regeneration in Mammals

status: Public on Jan 19 2024

summary: This SuperSeries is composed of the SubSeries listed below.


title: RNase-mediated reprogramming of Yersinia virulence

status: Public on Jan 23 2024

city: Münster

first: Ileana

last: Salto

state: Nordrhein-Westfalen

address: Von-Esmarch-Str. 56

institute: Institute für Infektiologie. ZMBE. Münster

summary: RNA degradation is an essential process that allows bacteria to regulate gene expression and has emerged as an important mechanism for controlling virulence. However, the individual contributions of RNases in this process are mostly unknown. Here, we report that of 11 tested potential RNases of the intestinal pathogen Yersinia pseudotuberculosis, two, the endoribonuclease RNase III and the exoribonuclease PNPase, repress the synthesis of the master virulence regulator LcrF. LcrF activates the expression of virulence plasmid genes encoding the type III secretion system (Ysc-T3SS) and its substrates (Yop proteins), that are employed to inhibit immune cell functions during infection. Loss of both RNases led to an increase in lcrF mRNA levels and stability. Our work indicates that PNPase exerts its influence through YopD, known to accelerate lcrF mRNA degradation. Loss of RNase III results in the downregulation of the CsrB and CsrC RNAs, leading to increased availability of active CsrA, which has previously been shown to enhance lcrF mRNA translation and stability. Other factors that influence the translation process and were found to be differentially expressed in the RNase III-deficient mutant could support this process.  Transcriptomic profiling further revealed that Ysc-T3SS-mediated Yop secretion leads to global reprogramming of the Yersinia transcriptome with a massive shift of the expression from chromosomal towards virulence plasmid-encoded genes. A similar extensive transcriptional reprogramming was also observed in the RNase III-deficient mutant under non-secretion conditions. This illustrated that RNase III enables immediate coordination of virulence traits, such as Ysc-T3SS/Yops, with other functions required for host-pathogen interactions and survival in the host.

overall_design: RNA sequencing  was used to determine the global transcriptome of the wild-type (YPIII) and YP356 (RNase III-deficient mutant) grown under different conditions. For this purpose, cells were grown O/D for 2 h at 25°C with a subsequent shift to 37°C. Samples were taken in triplicates before and at different time points after the shift to 37°C and total RNA was isolated using hot-phenol RNA extraction. A first set of samples was taken after 2 h at 25°C (Time 0) before the shift to 37°C. The second and third sample were taken 1 h (Time 1) and 4 h (Time 2) after the shift to 37°C, either with (“-Ca2+”) or without (“37°C”) induction of secretion. Five independent cultures (10 ml each) were prepared from independent O/N cultures in LB medium for each sample and pooled for RNA extraction. Harvesting of the cultures took place at 4,000 rpm for 3 min  with the centrifuge set to the respective cultivation temperature. Triplicates for all time points were prepared for the wild-type (YPIII) and YP356 (RNase III-deficient mutant)

first: Ines

last: Meyer

first: Marcel

last: Volk

first: Moesser

last: Theresa

first: Anne-Sophie

last: Herbrüggen

first: Manfred

last: Rohde

first: Michael

last: Beckstette

first: Ann

middle: K

last: Heroven

first: Petra

last: Dersch


title: RNA sequencing/Gene expression studies of G⍺13 signaling in lymphoma [RNA-seq]

status: Public on Jan 17 2024

city: Bethesda

first: David

last: Huang

state: Maryland

address: 9000 Rockville Pike

institute: National Cancer Institute

summary: We determined that loss of G⍺13 signaling promotes oncogenic signaling in aggressive B-cell lymphomas. We sought to measure gene expression change in aggressive B-cell lymphoma cells by RNA-sequencing following G⍺13 stimulation.

overall_design: RNA sequencing to determine gene expression in NUDUL1 lymphoma cells (Control or GNA13-deficient) treated with U46619 10nM for 24 hours

first: Hang

middle: T

first: Jagan

last: Muppidi


title: Transcriptomic and epigenetic dissection of  spinal ependymoma (SP-EPN) identifies clinically relevant subtypes enriched for tumors with and without NF2 mutations

status: Public on Jan 26 2024

city: Hamburg

first: Karoline

last: Hack

address: Martinistraße 52

department: Children's Cancer Center Hamburg

institute: University Medical Center Hamburg-Eppendorf

type: Methylation profiling by genome tiling array


title: RNA sequencing/Gene expression studies of G⍺13 signaling in lymphoma [scRNA-seq]

summary: We determined that loss of G⍺13 signaling promotes oncogenic signaling in aggressive B-cell lymphomas. We sought to measure gene expression change in control and G⍺13-deficient germinal center (GC) B cells  by RNA-sequencing

overall_design:
Mesenteric LN (mLN) and peripheral LN (pLN) GC B cells from control and G⍺13-deficient mice  were isolated by Fluorescence-activated cell sorting (FACS) and analyzed using scRNAseq
***Submitter declares that the raw data will be deposited in SRA***
Additonal information can be found at: https://lymphochip.nih.gov/local/GNA13_Proliferation/


title: RNA sequencing/Gene expression studies of G⍺13 signaling in lymphoma


title: Disruption of the Uty epigenetic regulator locus in hematopoietic cells phenocopies the profibrotic attributes of Y chromosome loss in heart failure

status: Public on Jan 22 2024

city: Charlottesville

first: Nicholas

last: Chavkin

address: 415 Lane Road

institute: University of Virginia

summary: Heart failure is a prevalent condition that affects millions of people worldwide with men exhibiting a higher incidence than women. However, the mechanisms underlying this sex difference remain poorly understood. Our previous work has shown that the presence of mosaic loss of Y chromosome (LOY) in leukocytes is causally associated with increased risk for heart failure. In the current study, we show that LOY macrophages from the failing hearts of humans with dilated cardiomyopathy exhibit widespread changes in gene expression that correlate with fibroblast activation in the myocardium, and we identify the ubiquitously transcribed tetratricopeptide Y linked (Uty) gene in leukocytes as a causal locus for accelerated progression of heart failure in male mice with LOY. Using single-cell multiomics analysis, we demonstrate that Uty disruption leads to epigenetic alterations in both monocytes and macrophages, increasing the propensity of differentiation into pro-fibrotic macrophages that can contribute to cardiac fibrosis and dysfunction. These findings shed light on the mechanisms that contribute to the higher incidence of heart failure in males and suggest potential targets for treatment of heart failure patients with LOY in leukocytes.

overall_design: Cardiac immune cells derived from BMT were isolated by tissue digestion and single cell dissociation of cardiac tissue 7 days post-TAC. Briefly, hearts from Control or UTYGT BMT mice were isolated 7 days post-TAC from three mice in each condition, cardiac tissue was digested using a digestion solution containing collagenase I (450 U/ml), collagenase XI (125 U/ml), hyaluronidase (450 U/ml), and DNAseI (60 U/ml) with subsequent homogenization, and live BMT-derived cardiac immune cells were isolated by FACS for the DAPI-CD45.2+ population. Single cell suspensions were then pooled between three mice at equal proportions.

first: Kenneth

last: Walsh

first: Soichi

last: Sano


title: The Host Modulates Transcriptional Profile and Phenotypic Heterogeneity in Symbionts

city: Hefei

first: Ziguang

last: Wang

state: Anhui

address: Changjiang West Road

department: School of Plant Protection

institute: Anhui Agricultural University

summary: Host-microbe interactions are virtually bidirectional, benefiting both the host and microbial sides. It is becoming increasingly recognized the influence of the microbe on many aspects of host physiology and diseases, but whether/how the host affects their symbionts is poorly characterized. Here, we reported that the host acts as a critical factor to shape the lifestyle of their symbionts in the Drosophila and bacteria model system. First, we observe that Drosophila larvae play a pivotal role in competing with pathogenic symbionts in the co-existing niche. More specifically, host larvae antagonize symbionts by deconstructing the surface slick, preventing outgrowth and antagonizing the pathogenicity of S. marcescens. Furthermore, Drosophila larvae cause the shift in the transcriptomic profile of S. marcescens, characterized with the upregulated expression of genes related to bacterial proliferation and growth and the downregulated expression of genes related to bacterial pathogenicity. More importantly, advances in bacterial single-cell RNA sequencing provide opportunities to reveal transcriptional variation, including toxic factors, across individual cells and a subpopulation clustering of isogenic bacterial populations. Finally, we found that AMPs from larvae recapitulated the response of S. marcescens to the presence of Drosophila larvae. Altogether, these findings provide an insight into the pivotal roles of the host in influencing the potential pathogens' lifecycle switching from commensalism to pathogenicity, opening the door to a better understanding of the ecological relationships between the host and microbe.

overall_design: First, the single cultivation and heat shock group was detected to test single-cell bacteria sequencing technology. And then the Larvae, Force and control groups  was detected. Single cell transcription profiling was compared between the Larvae, Force and control groups to explore the influence of host on serratia marcescens.

first: Shuai

last: Li

first: Yirong

first: Wei


title: The Host Modulates Transcriptional Profile and Phenotypic Heterogeneity in Symbionts.

overall_design: The serratia marcescens in the control group were cultured alone.The serratia marcescens and larvae were co-cultured in the experimental group.And then transcription profiling was then compared between the experimental and control groups to explore the influence of host on serratia marcescens.

last: Liu


title: Single-cell division tracing and transcriptomics reveal cell types and differentiation paths in the regenerating lung

status: Public on Jan 16 2024

city: Heidelberg

first: Cihan

last: Erkut

address: Im Neuenheimer Feld 581

department: Applied Functional Genomics

institute: German Cancer Research Center

summary: Understanding the molecular and cellular processes involved in lung epithelial regeneration may fuel the development of therapeutic approaches for lung diseases. We combine mouse models allowing diphtheria toxin-mediated damage of specific epithelial cell types and parallel GFP-labeling of functionally dividing cells with single-cell transcriptomics to characterize the regeneration of the distal lung. We uncover cell types, including Krt13+ basal and Krt15+ club cells, detect an intermediate cell state between basal and goblet cells, reveal goblet cells as actively dividing progenitor cells, and provide evidence that adventitial fibroblasts act as supporting cells in epithelial regeneration. We also show that diphtheria toxin-expressing cells can persist in the lung, express specific inflammatory factors, and transcriptionally resemble a previously undescribed population in the lungs of COVID-19 patients. Our study provides a comprehensive single-cell atlas of the distal lung that characterizes early transcriptional and cellular responses to concise epithelial injury, encompassing proliferation, differentiation, and cell-to-cell interactions.

overall_design: Epithelial and/or mesenchymal  cells were sorted from uninjured mouse lungs or from mouse lungs were club or AT2 and club cells were killed via DTA expression.  Dividing cells and rare cell types  were enriched during sorting.

first: Leila

last: Martins

first: Lina

last: Sieverling

first: Michelle

last: Michelhans

first: Lars

last: Velten


title: A Genome-Wide CRISPR Screen Identifies BRD4 as a Regulator of Cardiomyocyte Differentiation [CUT&RUN]

city: San Francisco

first: Angelo

last: Pelonero

address: 1650 Owens Street

department: Cardiovascular Disease Institute

institute: Gladstone Institutes (UCSF)

summary: We employed bulk Cut & Run sequencing to interrogate the consequence of BRD4 deletion in cardiac progenitor cells

overall_design: Bulk accessibility analysis of hiPSC-derived cardiac progenitor cells, including a novel cell line w/ biallelically appended 3XFLAG epitope tag at the N-terminus of BRD4

first: Arun

last: Padmanabhan

first: Deepak

last: Srivastava


title: Morphological diversification and functional maturation of human astrocytes in glia-enriched cortical organoids transplanted in the mouse brain

city: San Diego

first: April

middle: Elizabeth

last: Williams

address: 10010 N Torrey Pines Rd

department: IGC

institute: Salk Institute for Biological Studies

summary: Astrocytes, the most abundant glial cell type in the brain, are underrepresented in traditional cortical organoid models due to the delayed onset of cortical gliogenesis. Here, we introduce a novel glia-enriched cortical organoid model that exhibits accelerated astrogliogenesis. We demonstrated that induction of a gliogenic switch in a subset of progenitors enabled rapid derivation of astroglial cells, which account for 25-31% of the cell population within eight to ten weeks of differentiation. Intracerebral transplantation of these organoids reliably generated a diverse repertoire of cortical neurons and anatomical subclasses of human astrocytes. Spatial transcriptome profiling identified layer-specific expression patterns among distinct subclasses of astrocytes within the organoid transplants. Using an in vivo acute neuroinflammation model, we identified a subpopulation of astrocytes that rapidly activates proinflammatory pathways upon cytokine stimulation. Additionally, we demonstrated that CD38 signaling plays a crucial role in mediating metabolic and mitochondrial stress in reactive astrocytes. This model provides a robust platform for investigating human astrocyte function.

overall_design:
Single-nucleus RNA-Seq
Single-cell RNA-Seq

first: Meiyan

first: Maxim

last: Shokhirev

first: Jingting

last: Yu

first: Fred

last: Gage

first: Lei

last: Zhang


title: Deciphering Fatty Acid Biosynthesis-Driven Molecular Subtypes in Pancreatic Ductal Adenocarcinoma with Prognostic Insights

city: Shanghai

first: jun yi

last: Xu

state: Shanghai

address: 160 Pujian Rd

institute: Shanghaijiaotong university

summary: Pancreatic ductal adenocarcinoma (PDAC) poses a significant challenge due to its high heterogeneity and aggressiveness. Recognizing the urgency to delineate molecular subtypes, our study focused on the emerging field of lipid metabolism remodeling in PDAC, particularly exploring the prognostic potential and molecular classification associated with fatty acid biosynthesis. Here we identified a 7-gene signature associated with fatty acid biosynthesis-related genes (FRGs), providing a robust tool for survival prediction. The high- FRGs score group displayed a poorer prognosis, lower immune infiltration abundance, and a higher tumor mutational burden.  Notably,  ACSL5,  a key gene in 7-gene signature panel  was upregulated in PDAC. The biological function of ACSL5 were validated with in vitro assay.  Finally, we unveiled that ACSL5 played a crucial role in pancreatic cancer progression, promoting tumor initiation, metastasis, and immune evasion.

overall_design: To investigate the function of ACSL5 in the progression of PDAC, we examined ACSL5 knockdown and WT cell lines. Then, we performed RNA sequencing to analyze gene expression profile of ACSL5 knockdown and WT cells.

first: Junyi

first: Mingzhu

first: Jing

last: Xue

first: Ping

last: Lu


title: Gene expression profiling of Staphylococcus aureus strain Newman and gene asp23 deletion mutant

status: Public on Jan 14 2024

city: Chongqing

first: Keting

last: Zhu

address: Shapinba Main Street

department: Department of Emergency Medicine

institute: Army Medical University

summary: RNA samples were extracted from both the WT and isogenic mutant NMΔasp23, respectively, and then subjected to RNA-seq analysis.

overall_design: Total cellular RNA isolation and RNA-seq Overnight cultures of Newman and mutant NMasp23

first: Jia

last: Li