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==Description==
==Description==
−TORC proteins (aka CREB-regulated transcription coactivators or CRTCs) are a family of 3 highly-conserved human genes identified in high-throughput screens of cDNAs that activated the IL-8 promoter {Iourgenko, 2003 #1935} or a CRE-containing reporter construct {Conkright, 2003 #1936}. All 3 TORCs are expressed in the brain, with highest expression of TORC1 {Altarejos, 2008 #1938}. TORCs do not bind DNA directly, but are CREB co-activators that enhance CRE-regulated transcription after binding CREB and recruiting TFIID {Iourgenko, 2003 #1935}{Conkright, 2003 #1936}.
+TORC proteins (Transducer of Regulated CREB activity, aka CREB-regulated transcription coactivators or CRTCs) are a family of 3 highly-conserved human genes identified in high-throughput screens of cDNAs that activated the IL-8 promoter {Iourgenko, 2003 #1935} or a CRE-containing reporter construct {Conkright, 2003 #1936}. All 3 TORCs are expressed in the brain, with highest expression of TORC1 {Altarejos, 2008 #1938}. TORCs do not bind DNA directly, but are CREB co-activators that enhance CRE-regulated transcription after binding CREB and recruiting TFIID {Iourgenko, 2003 #1935}{Conkright, 2003 #1936}.
Phosphorylation of CREB at S133 by PKA and binding of TORC to CREB can independently {Xu, 2007 #1943} or additively {Conkright, 2003 #1936} act at the CRE to enhance expression. Thus, full activation of CREB-mediated transcription requires the nuclear translocation of both catalytic PKA and TORC. Phosphorylated TORC (pTORC) is sequestered in the cytoplasm by binding to the scaffolding protein 14-3-3. TORC dephosphorylation by Ca++-activated CaN (or by PKA-mediated inhibition of the AMPK family kinases that phosphorylate TORC) causes the release of TORC from 14-3-3 and its translocation to the nucleus {Spencer, 2010 #1946}.
Phosphorylation of CREB at S133 by PKA and binding of TORC to CREB can independently {Xu, 2007 #1943} or additively {Conkright, 2003 #1936} act at the CRE to enhance expression. Thus, full activation of CREB-mediated transcription requires the nuclear translocation of both catalytic PKA and TORC. Phosphorylated TORC (pTORC) is sequestered in the cytoplasm by binding to the scaffolding protein 14-3-3. TORC dephosphorylation by Ca++-activated CaN (or by PKA-mediated inhibition of the AMPK family kinases that phosphorylate TORC) causes the release of TORC from 14-3-3 and its translocation to the nucleus {Spencer, 2010 #1946}.
TORCs have been implicated in several CREB-regulated processes, including gluconeogenesis {Koo, 2005 #1941}, tumor induction {Conkright, 2003 #1936}{Amelio, 2009 #1942}, CRH expression {Liu, 2010 #1940}, long-term potentiation {Kovacs, 2007 #1945}, hypothalamic responses to metabolic deficits {Altarejos, 2008 #1938}, and cocaine self-administration {Hollander, 2010 #1939}.
TORCs have been implicated in several CREB-regulated processes, including gluconeogenesis {Koo, 2005 #1941}, tumor induction {Conkright, 2003 #1936}{Amelio, 2009 #1942}, CRH expression {Liu, 2010 #1940}, long-term potentiation {Kovacs, 2007 #1945}, hypothalamic responses to metabolic deficits {Altarejos, 2008 #1938}, and cocaine self-administration {Hollander, 2010 #1939}.
−==Antisera from Cell Signaling==
==Antisera from Cell Signaling==