MAD2L2 Antibody [P22A23] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat

Lane 1: NCI-H1963, Lane 2: NCCIT

Usage Information

Dilution
WB1:1000 IP1:100

Application
WB, IP

Reactivity
Human, Mouse, Rat

Source
Rabbit Monoclonal Antibody

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
24 kDa

Datasheet & SDS

Biological Description

Specificity
MAD2L2 Antibody [P22A23] detects endogenous levels of total MAD2L2 protein.

Clone
P22A23

Synonym(s)
Mitotic spindle assembly checkpoint protein MAD2B; MAD2-like protein 2; REV7; MAD2L2

Background
Mitotic arrest deficient 2 like 2 (MAD2L2, also known as REV7) is a multifunctional HORMA‑domain protein that integrates cell‑cycle control with DNA damage response by participating in the spindle checkpoint machinery and several DNA repair pathways. It belongs to the MAD2‑like or HORMA family and adopts a closing‑clamshell architecture that enables it to act as an adaptor or scaffold, engaging partner proteins through interface‑switching modes rather than forming the core of the spindle assembly checkpoint itself. MAD2L2 functions as a core subunit of DNA polymerase ζ, where it bridges the catalytic subunit REV3 and the TLS scaffold REV1, coordinating lesion bypass during translesion synthesis and enabling replication through blocking DNA adducts. In double‑strand break repair, MAD2L2 joins REV1 and polymerase ζ at stalled forks and contributes to repair‑synthesis steps, while also participating in the shieldin complex, where it helps regulate pathway choice by limiting 5ʹ end resection and thereby favoring non‑homologous end joining over homologous recombination. MAD2L2 also contributes to mitotic regulation by restraining premature activation of the anaphase‑promoting complex/cyclosome through interactions with CDH1 and related checkpoint proteins, thereby helping to delay mitotic progression and maintain genome integrity under replication stress. MAD2L2 is frequently overexpressed compared with adjacent normal tissue, and high message or protein levels correlate with increased numbers of aberrant mitotic figures, chromosomal instability, and reduced overall survival in colorectal cancer and other solid malignancies, suggesting that elevated MAD2L2 expression reinforces error‑prone DNA repair and checkpoint adaptations that support tumor evolution.

Background

Mitotic arrest deficient 2 like 2 (MAD2L2, also known as REV7) is a multifunctional HORMA‑domain protein that integrates cell‑cycle control with DNA damage response by participating in the spindle checkpoint machinery and several DNA repair pathways. It belongs to the MAD2‑like or HORMA family and adopts a closing‑clamshell architecture that enables it to act as an adaptor or scaffold, engaging partner proteins through interface‑switching modes rather than forming the core of the spindle assembly checkpoint itself. MAD2L2 functions as a core subunit of DNA polymerase ζ, where it bridges the catalytic subunit REV3 and the TLS scaffold REV1, coordinating lesion bypass during translesion synthesis and enabling replication through blocking DNA adducts. In double‑strand break repair, MAD2L2 joins REV1 and polymerase ζ at stalled forks and contributes to repair‑synthesis steps, while also participating in the shieldin complex, where it helps regulate pathway choice by limiting 5ʹ end resection and thereby favoring non‑homologous end joining over homologous recombination. MAD2L2 also contributes to mitotic regulation by restraining premature activation of the anaphase‑promoting complex/cyclosome through interactions with CDH1 and related checkpoint proteins, thereby helping to delay mitotic progression and maintain genome integrity under replication stress. MAD2L2 is frequently overexpressed compared with adjacent normal tissue, and high message or protein levels correlate with increased numbers of aberrant mitotic figures, chromosomal instability, and reduced overall survival in colorectal cancer and other solid malignancies, suggesting that elevated MAD2L2 expression reinforces error‑prone DNA repair and checkpoint adaptations that support tumor evolution.

References
https://pubmed.ncbi.nlm.nih.gov/17044027/ https://pubmed.ncbi.nlm.nih.gov/39839778/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%