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。
[KD]TORC2 Rabbit mAb
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Application 
| WB, IHC-P |
|---|---|
| Primary Accession | Q53ET0 |
| Reactivity | Rat, Human |
| Host | Rabbit |
| Clonality | Monoclonal Antibody |
| Isotype | IgG |
| Conjugate | Unconjugated |
| Purification | Affinity Purified |
| Calculated MW | 73302 Da |
| Gene ID | 200186 |
|---|---|
| Other Names | CRTC2 |
| Dilution | WB~~1:1000 IHC-P~~1:50~200 |
| Format | Liquid in 50mM Tris-Glycine(pH 7.4), 0.15M NaCl, 40%Glycerol, 0.01% sodium azide and 0.05% BSA. |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
For Research Use Only. Not For Use In Diagnostic 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. |
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Glucose homeostasis is regulated by hormones and cellular energy status. Elevations of blood glucose during feeding stimulate insulin release from pancreatic β-cells through a glucose sensing pathway. Feeding also stimulates release of gut hormones such as glucagon-like peptide-1 (GLP-1), which further induces insulin release, inhibits glucagon release and promotes β-cell viability. CREB-dependent transcription likely plays a role in both glucose sensing and GLP-1 signaling . The protein Torc2 (transducer of regulated CREB activity 2) functions as a CREB co-activator and is implicated in mediating the effects of these two pathways . In quiescent cells, Torc2 is phosphorylated at Ser171 and becomes sequestered in the cytoplasm via an interaction with 14-3-3 proteins. Glucose and gut hormones lead to the dephosphorylation of Torc2 and its dissociation from 14-3-3 proteins. Dephosphorylated Torc2 enters the nucleus to promote CREB-dependent transcription. Torc2 plays a key role in the regulation of hepatic gluconeogenic gene transcription in response to hormonal and energy signals during fasting.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 .
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