产品详情
简单介绍:
Anti-Beta-Catenin Antibody
详情介绍:
Overview
Name: | Anti-Beta-Catenin Antibody See all Beta Catenin primary antibodies
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Description: | Rabbit monoclonal (E247) antibody to Beta-Catenin. |
Specificity: | Beta-Catenin (CTNB1); Catenin (Cadherin-associated Protein) beta 1. |
Applications: | IHC, WB |
Reactivity: | Human, Mouse |
Immunogen: | Synthetic peptide corresponding to a N-terminal aa sequence of human ?-Catenin. |
Host: | Rabbit |
Clonality: | Monoclonal |
Clone: | E247 |
Isotype: | IgG |
Conjugate: | Unconjugated |
Purity: | Tissue culture supernatant. |
Product Form: | Liquid |
Formulation: | Supplied with Phosphate Buffered Saline, Bovine Serum Albumin, Glycerol and 0.09% Sodium Azide. |
Storage: | Shipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles. |
Target
Function: | Key downstream component of the canonical Wnt signaling pathway. In the absence of Wnt, forms a complex with AXIN1, AXIN2, APC, CSNK1A1 and GSK3B that promotes phosphorylation on N-terminal Ser and Thr residues and ubiquitination of CTNNB1 via BTRC and its subsequent degradation by the proteasome. In the presence of Wnt ligand, CTNNB1 is not ubiquitinated and accumulates in the nucleus, where it acts as a coactivator for transcription factors of the TCF/LEF family, leading to activate Wnt responsive genes. Involved in the regulation of cell adhesion, as component of an E-cadherin:catenin adhesion complex. Acts as a negative regulator of centrosome cohesion. Involved in the CDK2/PTPN6/CTNNB1/CEACAM1 pathway of insulin internalization. Blocks anoikis of malignant kidney and intestinal epithelial cells and promotes their anchorage-independent growth by down-regulating DAPK2. Disrupts PML function and PML-NB formation by inhibiting RANBP2-mediated sumoylation of PML (By similarity). Promotes neurogenesis by maintaining sympathetic neuroblasts within the cell cycle (PubMed:21325504). |
Sequence Similarities: | Belongs to the beta-catenin family. |
Post-Translational Modification: | Phosphorylation by GSK3B requires prior phosphorylation of Ser-45 by another kinase. Phosphorylation proceeds then from Thr-41 to Ser-33. Phosphorylated by NEK2. EGF stimulates tyrosine phosphorylation. Phosphorylation on Tyr-654 decreases CDH1 binding and enhances TBP binding (By similarity). Phosphorylated on Ser-33 and Ser-37 by HIPK2. This phosphorylation triggers proteasomal degradation. Phosphorylation at Ser-552 by AMPK promotes stabilizion of the protein, enhancing TCF/LEF-mediated transcription. Phosphorylation on Ser-191 and Ser-246 by CDK5. Phosphorylation by CDK2 regulates insulin internalization (By similarity). Phosphorylation by PTK6 at Tyr-64, Tyr-142, Tyr-331 and/or Tyr-333 with the predominant site at Tyr-64 is not essential for inhibition of transcriptional activity (By similarity). |
Cellular Location: | Cytoplasm. Nucleus. Cytoplasm > Cytoskeleton. Cell junction > Adherens junction. Cell junction. Cell membrane. Cytoplasm > Cytoskeleton > Microtubule organizing center > Centrosome. Cytoplasm > Cytoskeleton > Spindle pole. Cell junction > Synapse. Colocalized with RAPGEF2 and TJP1 at cell-cell contacts (By similarity). Cytoplasmic when it is unstabilized (high level of phosphorylation) or bound to CDH1. Translocates to the nucleus when it is stabilized (low level of phosphorylation). Interaction with GLIS2 and MUC1 promotes nuclear translocation. Interaction with EMD inhibits nuclear localization. The majority of beta-catenin is localized to the cell membrane. In interphase, colocalizes with CROCC between CEP250 puncta at the proximal end of centrioles, and this localization is dependent on CROCC and CEP250. In mitosis, when NEK2 activity increases, it localizes to centrosomes at spindle poles independent of CROCC. Colocalizes with CDK5 in the cell-cell contacts and plasma membrane of undifferentiated and differentiated neuroblastoma cells. Interaction with FAM53B promotes translocation to the nucleus (By similarity). |
Database Links: |
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Synonyms: | |
Information: | Target information shown above is from the UniProt Consortium. |
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