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CCM2 Antikörper

Dieses Kaninchen Polyklonal-Antikörper erkennt spezifisch CCM2 in WB und IF. Er zeigt eine Reaktivität gegenüber Human.
Produktnummer ABIN1589848

Kurzübersicht für CCM2 Antikörper (ABIN1589848)

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)
  • Verwendungszweck

    CCM-2 antibody

    Spezifität

    Recombinant human CCM2

    Produktmerkmale

    Chromosomal location: 7p13

    Aufreinigung

    Protein A purified

    Immunogen

    Recombinant human CCM2 (ABIN1589765)

    Isotyp

    IgG
  • Applikationshinweise

    Western Blot: Use 1-5 μg/mL

    Beschränkungen

    Nur für Forschungszwecke einsetzbar
  • Format

    Lyophilized

    Rekonstitution

    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

    Handhabung

    Centrifuge vial prior to opening. Avoid repeated freeze-thaw cycles.

    Lagerung

    4 °C,-20 °C

    Informationen zur Lagerung

    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.

    Haltbarkeit

    24 months
  • Target

    CCM2 (Cerebral Cavernous Malformation 2 (CCM2))

    Andere Bezeichnung

    CCM-2

    Hintergrund

    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.

    Gen-ID

    83605

    NCBI Accession

    NM_001029835, NP_001025006

    UniProt

    Q9BSQ5

    Pathways

    Cell-Cell Junction Organization
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