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CCM2 anticorps

Cet anticorps Lapin Polyclonal détecte spécifiquement CCM2 dans WB et IF. Il présente une réactivité envers Humain.
N° du produit ABIN1589848

Aperçu rapide pour CCM2 anticorps (ABIN1589848)

Antigène

Voir toutes CCM2 Anticorps
CCM2 (Cerebral Cavernous Malformation 2 (CCM2))

Reactivité

  • 26
  • 4
  • 4
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
Humain

Hôte

  • 18
  • 7
  • 1
Lapin

Clonalité

  • 22
  • 4
Polyclonal

Conjugué

  • 19
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
Cet anticorp CCM2 est non-conjugé

Application

  • 17
  • 5
  • 5
  • 5
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
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
  • Indications d'application

    Western Blot: Use 1-5 μg/mL

    Restrictions

    For Research Use only
  • 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
  • Antigène

    CCM2 (Cerebral Cavernous Malformation 2 (CCM2))

    Autre désignation

    CCM-2

    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
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