CCM2 anticorps

N° du produit ABIN1589848

Détail du produit anti-CCM2 anticorps

Antigène: CCM2 (Cerebral Cavernous Malformation 2 (CCM2))

Reactivité: Humain

Hôte: Lapin

Clonalité: Polyclonal

Conjugué: Cet anticorp CCM2 est non-conjugé

Application: Western Blotting (WB), Immunofluorescence (IF)

Fonction: CCM-2 antibody

Specificité: Recombinant human CCM2

Attributs du produit: Chromosomal location: 7p13

Purification: Protein A purified

Immunogène: Recombinant human CCM2 (ABIN1589765)

Isotype: IgG

Information d'application

Indications d'application: Western Blot: Use 1-5 μg/mL

Restrictions: For Research Use only

Stockage

Format: Lyophilized

Reconstitution: Centrifuge vial prior to opening. Reconstitute in sterile water to a concentration of 0.1-1.0 mg/mL.

Buffer: 0.5X PBS, pH 7.2

Conseil sur la manipulation: Centrifuge vial prior to opening. Avoid repeated freeze-thaw cycles.

Stock: 4 °C,-20 °C

Stockage commentaire: The lyophilized antibody is stable for at least 2 years at -20°C. After sterile reconstitution the antibody is stable at 2-8°C for up to 6 months. Frozen aliquots are stable for at least 6 months when stored at -20°C. Addition of a carrier protein or 50% glycerol is recommended for frozen aliquots.

Date de péremption: 24 months

Détails sur CCM2

Antigène: CCM2 (Cerebral Cavernous Malformation 2 (CCM2))

Autre désignation: CCM-2 (CCM2 Produits)

Synonymes: anticorps C7orf22, anticorps OSM, anticorps malcavernin, anticorps CCM2, anticorps BC029157, anticorps TUF2, anticorps vtn, anticorps zgc:110233, anticorps CCM2 scaffolding protein, anticorps cerebral cavernous malformation 2, anticorps malcavernin, anticorps CCM2, anticorps Ccm2, anticorps LOC100304744, anticorps ccm2

Sujet: CCM-2, malcavernin, cerebral cavernous malformation 2, OSM, C7orf22, PP10187,Cerebral cavernous malformations (CCMs) are sporadically acquired or inherited vascular lesions of the central nervous system consisting of clusters of dilated thin-walled blood vessels that predispose individuals to seizures and stroke. Familial CCM is caused by mutations in KRIT1 (CCM1) or in malcavernin (CCM2). The roles of the CCM proteins in the pathogenesis of the disorder remain largely unknown. It was shown that the CCM1 gene product, KRIT1, interacts with the CCM2 gene product, malcavernin. Analogous to the established interactions of CCM1 and beta1 integrin with ICAP1, the CCM1/CCM2 association is dependent upon the phosphotyrosine binding (PTB) domain of CCM2. A familial CCM2 missense mutation abrogates the CCM1/CCM2 interaction, suggesting that loss of this interaction may be critical in CCM pathogenesis. CCM2 and ICAP1 bound to CCM1 via their respective PTB domains differentially influence the subcellular localization of CCM1. The data indicate that the genetic heterogeneity observed in familial CCM may reflect mutation of different molecular members of a coordinated signaling complex.

ID gène: 83605

NCBI Accession: NM_001029835, NP_001025006

UniProt: Q9BSQ5

Pathways: Cell-Cell Junction Organization