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Chicken Monoclonal CTNNA1 Primary Antibody für IF, IP - ABIN967813
Baki, Marambaud, Efthimiopoulos, Georgakopoulos, Wen, Cui, Shioi, Koo, Ozawa, Friedrich, Robakis: Presenilin-1 binds cytoplasmic epithelial cadherin, inhibits cadherin/p120 association, and regulates stability and function of the cadherin/catenin adhesion complex. in Proceedings of the National Academy of Sciences of the United States of America 2001
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Chicken Monoclonal CTNNA1 Primary Antibody für IF, IP - ABIN967812
Hirano, Kimoto, Shimoyama, Hirohashi, Takeichi: Identification of a neural alpha-catenin as a key regulator of cadherin function and multicellular organization. in Cell 1992
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Polyclonal CTNNA1 Primary Antibody für WB - ABIN4948297
Yamada, Pokutta, Drees, Weis, Nelson: Deconstructing the cadherin-catenin-actin complex. in Cell 2005
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Human Polyclonal CTNNA1 Primary Antibody für WB - ABIN4948305
Drees, Pokutta, Yamada, Nelson, Weis: Alpha-catenin is a molecular switch that binds E-cadherin-beta-catenin and regulates actin-filament assembly. in Cell 2005
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Human Monoclonal CTNNA1 Primary Antibody für FACS, ICC - ABIN261465
Bajpai, Feng, Krishnamurthy, Longmore, Wirtz: Loss of alpha-catenin decreases the strength of single E-cadherin bonds between human cancer cells. in The Journal of biological chemistry 2009
Human Polyclonal CTNNA1 Primary Antibody für IHC (p), IHC - ABIN251400
Lynch, Grady, Suriano, Huntsman: Gastric cancer: new genetic developments. in Journal of surgical oncology 2005
Human Monoclonal CTNNA1 Primary Antibody für FACS, IF - ABIN2191997
Nieman, Kim, Johnson, Wheelock: Mechanism of extracellular domain-deleted dominant negative cadherins. in Journal of cell science 1999
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pseudogene CTNNAP1 is a potential tumor suppressor participating in CRC (zeige CALR Antikörper) pathogenesis by competing with the parent gene CTNNA1 for microRNA-141.
Hypermethylation of the CTNNA1 promoter was associated with unfavorable karyotype, and possessed the higher frequency of coexisting with ASXL1 (zeige ASXL1 Antikörper) and RUNX1 (zeige RUNX1 Antikörper) mutations.
The results of this study demonstrate that causative variants identified in the CTNNA1 and CYP4V2 (zeige CYP4V2 Antikörper) genes are also associated with Leber Congenital Amaurosis.
alpha- and beta-catenins may be important in the early stages of phyllodes tumours development, while E-cadherin (zeige CDH1 Antikörper) may be required for malignant development
This work identified alpha-catenin as another molecule in addition to E- and P-cadherin that were targeted to inactivate homotypic cell-in-cell structures formation in human tumor cells.
Progressive loss of e-cadherin (zeige CDH1 Antikörper)/alpha-catenin expression is associated with an aggressive phenotype (low differentiation, increased metastatic activity/advanced stage) in thyroid carcinomas.
study identifies CTNNA1 gene variants as a cause of macular dystrophy, indicates that CTNNA1 is involved in maintaining RPE (zeige RPE Antikörper) integrity
The results demonstrate a Fas (zeige FAS Antikörper)-mediated apoptotic signaling pathway that is enhanced by the age-dependent loss of alpha(E)-catenin in renal tubule epithelial cells.
Actin-dependent CTNNA1 clustering is a unique molecular mechanism mediating both integrity and reassembly of the cell-cell adhesive interface formed through weak cis (zeige CISH Antikörper)- and trans-intercadherin interactions.
alpha-catenin is a reversible, stretch-activatable sensor that mechanically links cadherin complexes and actin and is an indispensable player in cadherin-specific mechanotransduction at intercellular junctions.
In this study, the authors revealed how alpha-catenin retains its activated state while avoiding unfolding under tension.
cadherin 2 (CDH2 (zeige CDH2 Antikörper)) and CDH4 (zeige CDH4 Antikörper) cooperate to regulate radial migration in mouse brain via the protein tyrosine phosphatase 1B (PTP1B (zeige PTPN1 Antikörper)) and alpha- and beta-catenins.
alphaT-catenin is a constitutively active actin-binding protein that can physically couple the cadherin.catenin complex to F-actin in the absence of tension.
Two Dtna (zeige DTNA Antikörper) interactors, alpha-catulin (zeige CTNNAL1 Antikörper) (phosphorylation independent) and Grb2 (zeige GRB2 Antikörper) (phosphorylation dependent) are localized to neuromuscular junctions in vivo, and are required for proper organization of neurotransmitter receptors on myotubes.
alphaE-catenin inhibits beta4 integrin-mediated activation of SRC (zeige SRC Antikörper) tyrosine kinase (zeige TYRO3 Antikörper)
E-cadherin (zeige CDH1 Antikörper)/alphaE-catenin chimeras used previously do not mimic alphaE-catenin in the native CCC, and imply that both CCC-bound monomer and cytosolic homodimer alphaE-catenin are required for strong cell-cell adhesion.
Loss of alpha-catenin elicits a cholestatic response and impairs liver regeneration
alphaE-catenin binding to filamentous actin favors assembly of unbranched filament bundles that are protected from severing over more dynamic, branched filament arrays.
Fusing VE-cadherin (zeige CDH5 Antikörper) to alpha-catenin presents a mutation, which leads to embryonic lethality, due to a lack of fetal liver hematopoiesis and severe lymphedema but no detectable defects in blood vessel formation and remodeling.
alphaE-catenin recruits vinculin to adherens junctions more effectively than alphaN-catenin, partly because of its higher affinity for actin filaments.
alpha-Catenin controls actomyosin dynamics by stabilising and promoting the formation of actomyosin foci, and also stabilises DE-Cadherin (Drosophila E-Cadherin (zeige CDH1 Antikörper), also known as Shotgun) at the cell membrane, suggesting that medioapical actomyosin contractility regulates junction stability.
Increased Rap1 (zeige TERF2IP Antikörper) activity restricts epithelial invagination in an alpha-catenin-dependent manner.
alpha-Cat mutant phenotype can be rescued by the expression of a DE-cadherin::alpha-Catenin fusion protein, which argues against an essential cytosolic, cadherin-independent role of Drosophila alpha-Catenin
alpha-catenin and p120(ctn (zeige CTNND1 Antikörper)) are key players in a mechanism of recruiting Rho1 to its sites of action.
Depletion of alphaE-catenin caused a defect in radial intercalation that was associated with decreased cell-cell adhesion, in a similar manner to E-cadherin (zeige CDH1 Antikörper) depletion. Depletion of alphaE-catenin also caused deep cells to have plasma membrane blebbing.
These data suggest that the interactions of beta-catenin with alpha-catenin and GSK-3beta exert opposing effects on the terminal projections of ventral optic axons.
Associates with the cytoplasmic domain of a variety of cadherins. The association of catenins to cadherins produces a complex which is linked to the actin filament network, and which seems to be of primary importance for cadherins cell-adhesion properties. Can associate with both E- and N-cadherins. Originally believed to be a stable component of E-cadherin/catenin adhesion complexes and to mediate the linkage of cadherins to the actin cytoskeleton at adherens junctions. In contrast, cortical actin was found to be much more dynamic than E-cadherin/catenin complexes and CTNNA1 was shown not to bind to F-actin when assembled in the complex suggesting a different linkage between actin and adherens junctions components. The homodimeric form may regulate actin filament assembly and inhibit actin branching by competing with the Arp2/3 complex for binding to actin filaments. May play a crucial role in cell differentiation.
, cadherin-associated protein,102kDa
, catenin alpha-1
, renal carcinoma antigen NY-REN-13
, 102 kDa cadherin-associated protein
, alpha E catenin
, cadherin associated protein
, catenin alpha 1
, catenin (cadherin associated protein), alpha 1
, catenin, alpha 1
, alpha catenin
, catenin alpha 1 subunit
, catenin (cadherin-associated protein), alpha 1, 102kDa
, catenin alpha-1-like
, catenin alpha 1 S homeolog
, LOW QUALITY PROTEIN: catenin alpha-1