The 3' UTR of the human CTLA4 mRNA can regulate mRNA stability and translational efficiency.
T cell activation results from the integration of signals generated through the T cell antigen receptor-CD3 complex with those from additional positive and negative regulatory pathways mainly mediated by the engagement of costimulatory receptors on T cells. Disruption of this balance leads to a defective immune response or alternative over-activation of the immune system. CTLA-4 plays a critical role in downregulating T cell responses. Autoimmune diseases have shown genetic linkage to the CTLA4 locus. In this report we demonstrate that the 3' UTR of CTLA4 regulates firefly luciferase reporter gene expression, can confer instability to CTLA4 mRNA and can influence its translation efficiency in vitro.
Malquori
Lorenzo
L
Istituto di Biologia Cellulare, Consiglio Nazionale delle Ricerche, Campus Adriano Buzzati-Traverso, Monterotondo, Rome, Italy.
Carsetti
Laura
L
Ruberti
Giovina
G
D020413:3' Untranslated Regions; D015703:Antigens, CD / Q000235:genetics*; D001483:Base Sequence; D060908:CTLA-4 Antigen; D002460:Cell Line; D017931:DNA Primers / Q000235:genetics; D017930:Genes, Reporter; D006801:Humans; D019169:Jurkat Cells; D049409:Luciferases, Firefly / Q000235:genetics; D010957:Plasmids / Q000235:genetics; D014176:Protein Biosynthesis; D020871:RNA Stability; D012333:RNA, Messenger / Q000235:genetics* / Q000378:metabolism*; D014162:Transfection
D020413:3' Untranslated Regions; D015703:Antigens, CD; D060908:CTLA-4 Antigen; C556706:CTLA4 protein, human; D017931:DNA Primers; D012333:RNA, Messenger; D049409:Luciferases, Firefly