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CCM2 anticorps (N-Term)

Cet anticorps anti-CCM2 est un anticorps Lapin Polyclonal détectant CCM2 dans WB et IF. Adapté pour Humain.
N° du produit ABIN616006

Aperçu rapide pour CCM2 anticorps (N-Term) (ABIN616006)

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)
  • Épitope

    • 4
    • 2
    • 2
    • 1
    • 1
    • 1
    AA 1-444, N-Term

    Specificité

    This antibody detects recombinant Human CCM-2 in Western Blot and native CCM-2 in Immunohistochemistry.

    Réactivité croisée (Details)

    Species reactivity (tested):Human.

    Purification

    Protein A Chromatography

    Immunogène

    Highly pure (> 95%) recombinant Human CCM-2 (Cerebral cavernous malformations 2 protein, aa: Met1-Ala444) from E.coli.
  • Indications d'application

    Optimal working dilution should be determined by the investigator.

    Restrictions

    For Research Use only
  • Reconstitution

    Restore in sterile water to a concentration of 0.1-1.0 mg/mL.

    Buffer

    5 mM PBS pH 7.2 without preservatives

    Agent conservateur

    Without preservative

    Conseil sur la manipulation

    Avoid repeated freezing and thawing.

    Stock

    4 °C/-20 °C

    Stockage commentaire

    Prior to reconstitution store at 2-8 °C for one month or dessicated at -20 °C for longer. Following reconstitution store undiluted at 2-8 °C for one month or (in aliquots) at -20 °C for longer.
  • Antigène

    CCM2 (Cerebral Cavernous Malformation 2 (CCM2))

    Autre désignation

    Malcavernin

    Sujet

    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.Synonyms: C7orf22, CCM2, Cerebral cavernous malformations 2 protein, PP10187

    ID gène

    83605

    NCBI Accession

    NP_001025006

    UniProt

    Q9BSQ5

    Pathways

    Cell-Cell Junction Organization
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