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CCM2 抗体

CCM2 适用: 人 WB, IF 宿主: 兔 Polyclonal unconjugated
产品编号 ABIN1589848
发货至: 中国
  • 抗原 See all CCM2 抗体
    CCM2 (Cerebral Cavernous Malformation 2 (CCM2))
    适用
    • 26
    • 4
    • 4
    • 1
    • 1
    • 1
    • 1
    • 1
    • 1
    宿主
    • 18
    • 7
    • 1
    克隆类型
    • 22
    • 4
    多克隆
    标记
    • 19
    • 1
    • 1
    • 1
    • 1
    • 1
    • 1
    • 1
    This CCM2 antibody is un-conjugated
    应用范围
    • 16
    • 5
    • 5
    • 5
    • 1
    • 1
    • 1
    • 1
    • 1
    • 1
    Western Blotting (WB), Immunofluorescence (IF)
    原理
    CCM-2 antibody
    特异性
    Recombinant human CCM2
    产品特性
    Chromosomal location: 7p13
    纯化方法
    Protein A purified
    免疫原
    Recombinant human CCM2 (ABIN1589765)
    亚型
    IgG
    Top Product
    Discover our top product CCM2 Primary Antibody
  • 应用备注
    Western Blot: Use 1-5 μg/mL
    限制
    仅限研究用
  • 状态
    Lyophilized
    溶解方式
    Centrifuge vial prior to opening. Reconstitute in sterile water to a concentration of 0.1-1.0 mg/mL.
    缓冲液
    0.5X PBS, pH 7.2
    注意事项
    Centrifuge vial prior to opening. Avoid repeated freeze-thaw cycles.
    储存条件
    4 °C,-20 °C
    储存方法
    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.
    有效期
    24 months
  • 抗原
    CCM2 (Cerebral Cavernous Malformation 2 (CCM2))
    别名
    CCM-2 (CCM2 产品)
    别名
    C7orf22 antibody, OSM antibody, malcavernin antibody, CCM2 antibody, BC029157 antibody, TUF2 antibody, vtn antibody, zgc:110233 antibody, CCM2 scaffolding protein antibody, cerebral cavernous malformation 2 antibody, malcavernin antibody, CCM2 antibody, Ccm2 antibody, LOC100304744 antibody, ccm2 antibody
    背景
    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.
    基因ID
    83605
    NCBI登录号
    NM_001029835, NP_001025006
    UniProt
    Q9BSQ5
    途径
    Cell-Cell Junction Organization
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