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CCM2 Antikörper (N-Term)

Dieses Anti-CCM2-Antikörper ist ein Kaninchen Polyklonal-Antikörper zur Detektion von CCM2 in WB und IF. Geeignet für Human.
Produktnummer ABIN616006

Kurzübersicht für CCM2 Antikörper (N-Term) (ABIN616006)

Target

Alle CCM2 Antikörper anzeigen
CCM2 (Cerebral Cavernous Malformation 2 (CCM2))

Reaktivität

  • 25
  • 3
  • 3
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
Human

Wirt

  • 17
  • 7
  • 1
Kaninchen

Klonalität

  • 21
  • 4
Polyklonal

Konjugat

  • 18
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
Dieser CCM2 Antikörper ist unkonjugiert

Applikation

  • 16
  • 5
  • 5
  • 4
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
Western Blotting (WB), Immunofluorescence (IF)
  • Bindungsspezifität

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

    Spezifität

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

    Kreuzreaktivität (Details)

    Species reactivity (tested):Human.

    Aufreinigung

    Protein A Chromatography

    Immunogen

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

    Optimal working dilution should be determined by the investigator.

    Beschränkungen

    Nur für Forschungszwecke einsetzbar
  • Rekonstitution

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

    Buffer

    5 mM PBS pH 7.2 without preservatives

    Konservierungsmittel

    Without preservative

    Handhabung

    Avoid repeated freezing and thawing.

    Lagerung

    4 °C/-20 °C

    Informationen zur Lagerung

    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.
  • Target

    CCM2 (Cerebral Cavernous Malformation 2 (CCM2))

    Andere Bezeichnung

    Malcavernin

    Hintergrund

    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

    Gen-ID

    83605

    NCBI Accession

    NP_001025006

    UniProt

    Q9BSQ5

    Pathways

    Cell-Cell Junction Organization
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