Aliases for CRTC2 Gene
External Ids for CRTC2 Gene
Previous GeneCards Identifiers for CRTC2 Gene
This gene encodes a member of the transducers of regulated cAMP response element-binding protein activity family of transcription coactivators. These proteins promote the transcription of genes targeted by the cAMP response element-binding protein, and therefore play an important role in many cellular processes. Under basal conditions the encoded protein is phosphorylated by AMP-activated protein kinase or the salt-inducible kinases and is sequestered in the cytoplasm. Upon activation by elevated cAMP or calcium, the encoded protein translocates to the nucleus and increases target gene expression. Single nucleotide polymorphisms in this gene may increase the risk of type 2 diabetes. A pseudogene of this gene is located on the long arm of chromosome 5. [provided by RefSeq, Dec 2010]
GeneCards Summary for CRTC2 Gene
CRTC2 (CREB Regulated Transcription Coactivator 2) is a Protein Coding gene. Diseases associated with CRTC2 include Human T-Cell Leukemia Virus Type 1 and T-Cell Leukemia. Among its related pathways are Glucagon signaling pathway and AMPK signaling pathway. GO annotations related to this gene include cAMP response element binding protein binding. An important paralog of this gene is CRTC1.
UniProtKB/Swiss-Prot for CRTC2 Gene
Transcriptional coactivator for CREB1 which activates transcription through both consensus and variant cAMP response element (CRE) sites. Acts as a coactivator, in the SIK/TORC signaling pathway, being active when dephosphorylated and acts independently of CREB1 Ser-133 phosphorylation. Enhances the interaction of CREB1 with TAF4. Regulates gluconeogenesis as a component of the LKB1/AMPK/TORC2 signaling pathway. Regulates the expression of specific genes such as the steroidogenic gene, StAR. Potent coactivator of PPARGC1A and inducer of mitochondrial biogenesis in muscle cells. Also coactivator for TAX activation of the human T-cell leukemia virus type 1 (HTLV-1) long terminal repeats (LTR).