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抗Human CRTC2 抗体:
抗Mouse (Murine) CRTC2 抗体:
抗Rat (Rattus) CRTC2 抗体:
Human Monoclonal CRTC2 Primary Antibody for ICC, FACS - ABIN969067
Ewing, Chu, Elisma, Li, Taylor, Climie, McBroom-Cerajewski, Robinson, OConnor, Li, Taylor, Dharsee, Ho, Heilbut, Moore, Zhang, Ornatsky, Bukhman, Ethier, Sheng, Vasilescu, Abu-Farha, Lambert, Duewel et al.: Large-scale mapping of human protein-protein interactions by mass spectrometry. ... in Molecular systems biology 2007
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Human Polyclonal CRTC2 Primary Antibody for ICC, IF - ABIN256688
Jeanneteau, Lambert, Ismaili, Bath, Lee, Garabedian, Chao: BDNF and glucocorticoids regulate corticotrophin-releasing hormone (CRH) homeostasis in the hypothalamus. in Proceedings of the National Academy of Sciences of the United States of America 2012
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Human Polyclonal CRTC2 Primary Antibody for IF (p), IHC (p) - ABIN745988
Tian, Zhao, Sun, Zhi, Cheng, Zhou, Hu: CRTC2 enhances HBV transcription and replication by inducing PGC1? expression. in Virology journal 2014
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Human Polyclonal CRTC2 Primary Antibody for ICC, IF - ABIN151246
Liu, Coello, Grinevich, Aguilera: Involvement of transducer of regulated cAMP response element-binding protein activity on corticotropin releasing hormone transcription. in Endocrinology 2010
Study suggests that Creb/Crtc2 negatively regulates the Sirt1/Pparalpha/Fgf21 axis via the induction of miR-34a under diet-induced obesity and insulin-resistant conditions.
Thyroid stimulating hormone activates CRTC2 via the TSHR/cAMP/PKA pathway.
CRTC2 polymorphism as a risk factor for the incidence of metabolic syndrome in transplant recipients after solid organ transplantation.
CRTC2 strongly enhances GR-induced transcriptional activity of glucocorticoid-responsive genes.
Our results establish a role for CRTC2 as a lymphoma tumor suppressor gene
the high expression of CRTC2 and PROM1 may play an important role in the occurrence and hereditary, and also advance the potential pathways that integrate genetic variants in the development of NSCLC.
The data from the current study demonstrated novel PROM1 and CRTC2 mutations, which could promote lung cancer development.
These results clearly indicate that non-phosphorylated CRTC2 strongly enhances hepatitis b virus biosynthesis through inducing PGC1alpha expression.
Phosphorylation of CRTC2 at its AMPK target site, Ser 171, dictated its subcellular localization, and the activation of aromatase PII in preadipocytes.
CRTC2 enhances CREB phosphorylation through an association with the protein arginine methyltransferase 5 (PRMT5).
Mechanism of CREB recognition and coactivation by the CREB-regulated transcriptional coactivator CRTC2
The lipogenic effects of GIP in the presence of insulin are therefore at least partially mediated by upregulation of adipocyte LPL gene transcription through a pathway involving PI3-K/PKB/AMPK-dependent CREB/TORC2 activation.
the association of Pin1 with CRTC2 to decrease the nuclear CBP.CRTC.CREB complex.
Tax binds the cyclin D1 promoter-proximal cyclic AMP response element (CRE) in the presence of phosphorylated CREB (pCREB) in vitro, and together the Tax-pCREB complex recruits the cellular co-activator p300 to the promoter.
Thus, both TORC1/2 and p300 families of coactivators are essential for optimal activation of HTLV-1 transcription by Tax.
These results strongly suggest that TORCs play a key role in linking these external signals to the transcriptional program of adaptive mitochondrial biogenesis by activating PGC-1alpha gene transcription.
latent cytoplasmic coactivator TORC2 mediates target gene activation in response to cAMP signaling by associating with CBP/p300 and increasing its recruitment to a subset of CREB target genes
TORC2 regulates germinal center repression of the TCL1 oncoprotein to promote B cell development and inhibit transformation.
genetic variants of LKB1-AMPK-TORC2 pathway components may exert a weak influence on the occurrence of type 2 diabetes in Japanese
identify Ser-275 of TORC2 as a 14-3-3 binding site that is phosphorylated under low glucose conditions and which becomes dephosphorylated by calcineurin in response to glucose influx
FSH enhances CRTC2-mediated gluconeogenesis dependent on AMPK Ser485 phosphorylation via GRK2 in the liver, suggesting an essential role of FSH in the pathogenesis of fasting hyperglycaemia
CRTC2 regulates the expression of Smurf1 in osteoblast differentiation.
data show that the CREB/CRTC2-dependent transcriptional pathway is critical for regulating glucose homeostasis by controlling production of GLP-1 from the L cells at the level of transcription, maturation, and exocytosis.
These results demonstrate how cross-coupling between the CREB/CRTC and JAK/STAT pathways contributes to bone marrow homeostasis.
the existence of an unusual functional interplay between STATs and CREB at the onset of adipogenesis through shared CRTC cofactors, is reported.
CRTC2 play a role in hepatic cholesterol synthesis through SREBP-2.
Catecholaminergic deletion of Rictor increases water, sucrose, and morphine intake but not preference in a two-bottle choice assay in stress-naive mice, and these effects are maintained after stress. Ventral Tegmental Area-specific knockout of Rictor increases water and sucrose intake after physical CSDS, but does not alter consummatory behavior in the absence of stress.
Three mouse CRTCs (Crtc1, Crtc2 and Crtc3) exhibit distinct patterns of 14-3-3 binding at three conserved sites corresponding to S70, S171, and S275 (in CRTC2).
the protein expression of adipose tissue CRTC 2 was reduced in mice with a combined application of change to general diet and exercise. In addition, while the protein expressions of lipase ATGL and HSL were reduced in the mice fed with the high fat diet continually after obesity was induced
CRTC2 promotes Th17 cell differentiation via stimulation of IL-17A and IL-17F expression by binding to CREB over both promoters. CRTC2-mutant mice have decreased Th17 cells, and they are protected from experimental autoimmune encephalitis.
chronic increases in CRTC2 activity in the liver are indeed sufficient to promote hepatic insulin resistance and to disrupt glucose homeostasis
cAMP, SIK and CRTC mediate StAR expression through activation of individual StAR gene loci.
RICTOR/mTORC2 is important for interactions between vasculature, adipocytes, and brain to tune physiological outcomes, such as blood pressure and locomotor activity.
CREB regulated transcription coactivator 2 (CRTC2) functions as a mediator of mTOR signalling to modulate COPII-dependent SREBP1 processing
Translational activation of CREB is caused by elevated phospho-elF2alpha.
CRTC2 mRNA levels down-regulation improves glucose control and other markers of metabolic function in experimental type 2 diabetes mellitus.
PRMT6 is involved in the regulation of hepatic glucose metabolism in a CRTC2-dependent manner.
Crtc2-overexpressing mice have increased myofiber cross-sectional area, greater intramuscular triglycerides and glycogen content.
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.
CREB regulated transcription coactivator 2
, CREB-regulated transcription coactivator 2
, CREB-regulated transcription coactivator 2-like
, transducer of regulated cAMP response element-binding protein (CREB) 2
, transducer of CREB protein 2
, transducer of regulated cAMP response element-binding protein 2