Datasheet

生物学的記述

Specificity	Mad2L1 Antibody [L3N17] detects endogenous levels of total Mad2L1 protein.
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.

Specificity

Mad2L1 Antibody [L3N17] detects endogenous levels of total Mad2L1 protein.

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.

使用情報

Application

WB, IHC

Dilution

WB

1:1000

Reactivity

Human

Source

Mouse Monoclonal Antibody

MW

24 kDa

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

プロトコール

References

https://pubmed.ncbi.nlm.nih.gov/25754611/
https://pubmed.ncbi.nlm.nih.gov/22497940/

Mad2L1 Antibody [L3N17]

生物学的記述

使用情報

References

Application Data