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ELISA 1:10000, WB 1:500-1:2000, IHC 1:200-1:1000, IF/ICC 1:200-1:1000, FCM 1:200-1:400
*The optimal dilutions should be determined by the end user.

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Monoclonal [AFB1832]
CRTC2 antibody detects endogenous levels of total CRTC2.
Cite Format: Affinity Biosciences Cat# BF0596, RRID:AB_2833856.
Mouse IgG1 in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.


CREB regulated transcription coactivator 2; CREB-regulated transcription coactivator 2; CRTC2; CRTC2_HUMAN; RP11-422P24.6; TORC-2; torc2; Transducer of CREB protein 2; Transducer of regulated cAMP response element-binding protein; Transducer of regulated cAMP response element-binding protein (CREB) 2; Transducer of regulated cAMP response element-binding protein 2; Transducer of regulated CREB protein 2;



Purified recombinant fragment of human CRTC2 expressed in E. Coli.


Most abundantly expressed in the thymus. Present in both B and T-lymphocytes. Highly expressed in HEK293T cells and in insulinomas. High levels also in spleen, ovary, muscle and lung, with highest levels in muscle. Lower levels found in brain, colon, heart, kidney, prostate, small intestine and stomach. Weak expression in liver and pancreas.

the transducer of regulated CREB protein 2 (TORC2) is a cAMP responsive coactivator that, in concert with LKB1 and AMPK, controls glucose homeostasis in the liver. Under fasting conditions, cytoplasmic TORC2 is transported to the nucleus where it binds to CREB and stimulates gluconeogenisis. Re-feeding and the ensuing insulin response inhibits gluconeogenic gene expression by promoting the phosphorylation, cytoplasmic export and degradation of TORC2. TORC2 is phosphorylated by the kinase QIK which in turn is activated by phosphorylation at Ser358 by insulin-activated Akt2. Phosphorylated TORC2 is subsequently ubiquitinylated at Lys 628 and degraded by the 26S proteasome. TORC2 protein levels and activity are increased in diabetes owing to a block in TORC2 phosphorylation, implicating this pathway in the pathogenesis of diabetes. The CREB/TORC2 regulatory axis controls the normal pattern of germinal center (GC) B cell gene activation/repression that promotes B cell development and circumvents GC lymphomagenesis.

PTMs - Q53ET0 As Substrate

Site PTM Type Enzyme
A2 Acetylation
T3 Phosphorylation
S4 Phosphorylation
S17 Phosphorylation
K25 Acetylation
K25 Sumoylation
K25 Ubiquitination
K30 Ubiquitination
S64 Phosphorylation
S65 Phosphorylation
Y67 Phosphorylation
S70 Phosphorylation P57059 (SIK1) , Q9Y2K2 (SIK3)
S79 Phosphorylation
S86 Phosphorylation
S90 Phosphorylation
S94 Phosphorylation
R106 Methylation
S116 Phosphorylation
S127 Phosphorylation
S128 Phosphorylation
Y130 Phosphorylation
S131 Phosphorylation
Y134 Phosphorylation
S136 Phosphorylation
K156 Sumoylation
K156 Ubiquitination
R161 Methylation
S164 Phosphorylation
T169 Phosphorylation
S170 Phosphorylation Q13131 (PRKAA1)
S171 Phosphorylation Q9H0K1 (SIK2) , Q9Y2K2 (SIK3) , P54646 (PRKAA2) , P57059 (SIK1) , Q7KZI7 (MARK2)
S173 Phosphorylation
T177 Phosphorylation
S183 Phosphorylation
T187 Phosphorylation
T192 Phosphorylation
R201 Methylation
K224 Sumoylation
K224 Ubiquitination
K228 Acetylation
K228 Sumoylation
K228 Ubiquitination
K233 Ubiquitination
S274 Phosphorylation Q7KZI7 (MARK2) , P57059 (SIK1)
S306 Phosphorylation P57059 (SIK1)
S336 Phosphorylation
S342 Phosphorylation
S348 Phosphorylation Q9Y2K2 (SIK3) , P57059 (SIK1)
S366 Phosphorylation
S368 Phosphorylation
S375 Phosphorylation
S386 Phosphorylation
S391 Phosphorylation
S393 Phosphorylation
S398 Phosphorylation
S399 Phosphorylation
S419 Phosphorylation
S424 Phosphorylation
S433 Phosphorylation P24941 (CDK2)
S436 Phosphorylation
S447 Phosphorylation
K453 Sumoylation
S456 Phosphorylation
T458 Phosphorylation
S460 Phosphorylation
T462 Phosphorylation
Y486 Phosphorylation
Y488 Phosphorylation
S489 Phosphorylation
S490 Phosphorylation
S492 Phosphorylation
T497 Phosphorylation
T501 Phosphorylation
S504 Phosphorylation
C515 S-Nitrosylation
S519 Phosphorylation
S613 Phosphorylation
T620 Phosphorylation
S623 Phosphorylation
S624 Phosphorylation
S628 Phosphorylation

PTMs - Q53ET0 As Enzyme

Substrate Site Source
P31749 (AKT1) S473 Uniprot

Research Backgrounds


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).


Phosphorylation/dephosphorylation states of Ser-171 are required for regulating transduction of CREB activity. CRTCs/TORCs are inactive when phosphorylated, and active when dephosphorylated at this site. This primary site of phosphorylation, is regulated by cAMP and calcium levels and is dependent on the phosphorylation of SIKs (SIK1 and SIK2) by LKB1. Following adenylyl cyclase activation, dephosphorylated at Ser-171 by PPP3CA/calcineurin A resulting in CRTC2 dissociation from 14-3-3 proteins and PPP3CA (By similarity). Both insulin and AMPK increase this phosphorylation of CRTC2 while glucagon suppresses it. Phosphorylation at Ser-274 by MARK2 is induced under low glucose conditions and dephosphorylated in response to glucose influx. Phosphorylation at Ser-274 promotes interaction with 14-3-3 proteins and translocation to the cytoplasm.

Asymmetric dimethylation of arginine resisues by PRMT6 enhances the association of CRTC2 with CREB on the promoters of gluconeogenic genes.

Subcellular Location:

Cytoplasm. Nucleus.
Note: Translocated from the nucleus to the cytoplasm on interaction of the phosphorylated form with 14-3-3 protein (PubMed:15454081). In response to cAMP levels and glucagon, relocated to the nucleus (PubMed:15454081).

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Most abundantly expressed in the thymus. Present in both B and T-lymphocytes. Highly expressed in HEK293T cells and in insulinomas. High levels also in spleen, ovary, muscle and lung, with highest levels in muscle. Lower levels found in brain, colon, heart, kidney, prostate, small intestine and stomach. Weak expression in liver and pancreas.

Subunit Structure:

Binds, as a tetramer, through its N-terminal region, with the bZIP domain of CREB1. 'Arg-314' in the bZIP domain of CREB1 is essential for this interaction. Interaction, via its C-terminal, with TAF4, enhances recruitment of TAF4 to CREB1. Interacts with SIK2. Interacts with 14-3-3 proteins, YWHAB and YWHAG. Interacts (probably when phosphorylated at Ser-171) with YWHAE. Interacts with calmodulin-dependent catalytic subunit PPP3CA/calcineurin A. Interaction with COP1 mediates nuclear export and degradation of CRTC2 (By similarity).

(Microbial infection) Interaction with the human T-cell leukemia virus type 1 (HTLV-1) Tax protein is essential for optimal transcription activation by Tax.


Belongs to the TORC family.

Research Fields

· Environmental Information Processing > Signal transduction > PI3K-Akt signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > AMPK signaling pathway.   (View pathway)

· Human Diseases > Endocrine and metabolic diseases > Insulin resistance.

· Human Diseases > Infectious diseases: Viral > HTLV-I infection.

· Organismal Systems > Endocrine system > Glucagon signaling pathway.

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