癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
CRTC2 Antibody
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Application 
| WB, IF, E, IHC-P |
|---|---|
| Primary Accession | Q53ET0 |
| Other Accession | NP_859066, 32171215 |
| Reactivity | Human, Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | IgG |
| Calculated MW | 73302 Da |
| Concentration (mg/ml) | 1 mg/mL |
| Conjugate | Unconjugated |
| Application Notes | CRTC2 antibody can be used for detection of CRTC2 by Western blot at 1 - 2 µg/mL. |
| Gene ID | 200186 |
|---|---|
| Other Names | CREB-regulated transcription coactivator 2, Transducer of regulated cAMP response element-binding protein 2, TORC-2, Transducer of CREB protein 2, CRTC2, TORC2 |
| Target/Specificity | CRTC2; Multiple isoforms of CRTC2 are known to exist. CRTC2 antibody is predicted to not cross-react with CRTC1. |
| Reconstitution & Storage | CRTC2 antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. |
| Precautions | CRTC2 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | CRTC2 |
|---|---|
| Synonyms | TORC2 |
| 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). |
| Cellular 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) |
| Tissue Location | 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. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
CRTC2 Antibody: CRTC2, also known as TORC2 (Transducers Of Regulated cAMP Response Element-Binding (CREB)) 2 and the related protein CRTC1 are potent CREB coactivators that are exported from the nucleus in a CRM1-dependent manner via phosphorylation-dependent interactions. Studies suggest that their phosphorylation and nuclear/cytoplasmic shuttling play an important role in the regulation of gluconeogenesis by cAMP. CRTC2 is present in both B and T-lymphocytes and abundantly expressed in the thymus. Its activity is important in regulating the expression of genes involved in cellular energy metabolism while CRTC1 is essential for energy balance and fertility.
REFERENCES
Conkright MD, Canettieri G, Screaton R, et al. TORCs: transducers of regulated CREB activity. Mol. Cell 2003; 12:413-23.
Iourgenko V, Zhang W, Mickanin C, et al. Identification of a family of cAMP response element-binding protein coactivators by genome-scale functional analysis in mammalian cells. Proc. Natl. Acad. Sci. USA 2003; 100:12147-52.
Bittinger MA, McWhinnie E, Meltzer J, et al. Activation of cAMP response element-mediated gene expression by regulated nuclear transport of TORC proteins. Curr. Biol. 2004; 14: 2156-61.
Jiang S, Inada T, Tanaka M, et al. Involvement of TORC2, a CREB co-activator, in the in vivo-specific transcriptional control of HTLV-1. Retrovirology 2009; 6:73.
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