Mad2L1 Antibody [L3N17]

Catalog No.: F4911

    Application: Reactivity:

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    代表番号: 045-509-1970|電子メール:sales@selleck.co.jp

    使用情報

    Dilution
    1:1000
    Application
    WB, IHC
    Source
    Mouse Monoclonal Antibody
    Reactivity
    Human
    Storage Buffer
    PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3
    Storage (from the date of receipt)
    -20°C (avoid freeze-thaw cycles), 2 years
    Predicted MW Observed MW
    24 kDa 24 kDa
    *なぜ予測分子量と実際の分子量が異なるのか?
    下記の原因により、実際の分子量が予測と異なる:タンパク質の翻訳後修飾(リン酸化/糖鎖付加),スプライシングバリアント,イソフォーム,相対的な電荷,ポリマー。

    Datasheet & SDS

    生物学的記述

    Specificity
    Mad2L1 Antibody [L3N17] detects endogenous levels of total Mad2L1 protein.
    Clone
    L3N17
    Synonym(s)
    MAD2, MAD2L1, Mitotic spindle assembly checkpoint protein MAD2A, HsMAD2, Mitotic arrest deficient 2-like protein 1, MAD2-like protein 1
    Background
    Mad2L1, a pivotal component of the spindle assembly checkpoint (SAC) within the MAD/BUB protein family, safeguards genomic integrity by delaying anaphase onset until bi-orientation of all kinetochores on the mitotic spindle. The protein adopts open (O-Mad2) and closed (C-Mad2) conformations, with C-Mad2 forming a stable tetramer with Mad1 at unattached kinetochores to catalyze O-Mad2 conversion and template Cdc20 binding, generating the mitotic checkpoint complex (MCC) comprising Mad2, BubR1, Bub3, and Cdc20. MCC binding to APC/C inhibits its E3 ubiquitin ligase activity, stabilizing securin and cyclin B1 to prevent separase activation and sister chromatid separation; microtubule attachment and tension relieve SAC via Aurora B-mediated stripping of Knl1 and PP1 recruitment, disassembling MCC and licensing anaphase. Mad2 overexpression destabilizes microtubule plus ends through EB1 interaction, promoting microtubule catastrophe and merotelic attachments independent of checkpoint signaling, while nuclear Mad2 binds E2F1 to repress transcription. Ubiquitously expressed but elevated in proliferative tissues, Mad2L1 ensures faithful chromosome segregation critical for development and tissue renewal. Dysregulation drives chromosomal instability (CIN) hallmarking cancers, where overexpression correlates with aneuploidy, proliferation, poor prognosis, and chemoresistance in oral, gastric, and other carcinomas; silencing induces senescence, underscoring therapeutic potential via SAC modulation.
    References

    技術サポート

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