SP1 acts as a key factor, contributes to upregulation of ADAM23 expression under serum deprivation.
ADAM23 modulates many cellular functions, alteration of expression causes a number of tumor types; however, the mechanisms controlling ADAM23 expression remain unknown. Here we have identified a SP1 binding site (-202/-190) that binds SP1 at the proximal promoter of human ADAM23 gene; furthermore, serum deprivation enhances open chromatin accessibility and help expose the SP1 binding site; finally, SP1 binding recruits RNA polymerase II, which in turn results in upregulation of endogenous ADAM23 expression. Therefore, the present study delineates the fundamental elements of a core promoter structure that will be helpful for future studies of the regulation of ADAM23 gene.
Pan
Qiuhui
Q
The Central Laboratory, People's 10th Hospital, Shanghai 200072, PR China.
Yang
Songhai
S
Wei
Youzhen
Y
Sun
Fenyong
F
Li
Zhi
Z
D051722:ADAM Proteins / Q000235:genetics*; D001665:Binding Sites; D002460:Cell Line; D047369:Chromatin Immunoprecipitation; D005786:Gene Expression Regulation; D006801:Humans; D011401:Promoter Regions, Genetic; D012319:RNA Polymerase II / Q000378:metabolism; D044967:Serum / Q000378:metabolism*; D016329:Sp1 Transcription Factor / Q000378:metabolism*; D015854:Up-Regulation
D016329:Sp1 Transcription Factor; D012319:RNA Polymerase II; D051722:ADAM Proteins; C114633:ADAM23 protein, human