Anti-Phospho-TORC2 Antibody (FITC)
Rabbit polyclonal antibody to Phospho-TORC2 (FITC) from FabGennix (PTORC2-FITC).
|Name:||Anti-Phospho-TORC2 Antibody (FITC)|
|Description:||Rabbit polyclonal antibody to Phospho-TORC2 (FITC)|
|Applications:||ELISA, IP, WB|
|Dilutions:||ELISA: 1:10,000; ELISA: 1:10,000; Immunoprecipitation: 1:200; Western Blot: 1:500|
|Reactivity:||Human, Mouse, Rat|
|Immunogen:||Phosphorylated synthetic peptide corresponding to unique amino acid sequence on TORC2 protein.|
|Concentration:||0.55-0.75 µg/µl in antibody stabilization buffer|
|Storage:||-20⁰C for long term storage|
|Function:||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).|
|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.|
|Sequence Similarities:||Belongs to the TORC family.|
|Post-Translational Modification:||Phosphorylation/dephosphorylation states of Ser-171 are required for regulating transduction of CREB activity. 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. 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.|
|Cellular Location:||Cytoplasm. Nucleus.
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).
Please Note: Anti-Phospho-TORC2 Antibody (FITC) is for research use only. It is not intended for diagnostic of therapeutic use.