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Rabbit Anti-MAD2L2 Recombinant Antibody (CBFYM-0304) (CBMAB-M0369-FY)

This product is rabbit antibody that recognizes MAD2L2. The antibody CBFYM-0304 can be used for immunoassay techniques such as: WB, IP, IHC-P, FC, IF.
See all MAD2L2 antibodies

Summary

Host Animal
Rabbit
Specificity
Mouse, Rat, Human
Clone
CBFYM-0304
Antibody Isotype
IgG
Application
WB, IP, IHC-P, FC, IF

Basic Information

Specificity
Mouse, Rat, Human
Antibody Isotype
IgG
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Concentration
0.385 mg/mL
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
MITOTIC ARREST DEFICIENT 2 LIKE 2
Introduction
The protein encoded by this gene is a component of the mitotic spindle assembly checkpoint that prevents the onset of anaphase until all chromosomes are properly aligned at the metaphase plate. The encoded protein, which is similar to MAD2L1, is capable of interacting with ADAM9, ADAM15, REV1, and REV3 proteins.
Entrez Gene ID
Human10459
Mouse71890
Rat313702
UniProt ID
HumanQ9UI95
MouseQ9D752
RatD3Z8D9
Alternative Names
Mitotic Arrest Deficient 2 Like 2; MAD2 (Mitotic Arrest Deficient, Yeast, Homolog)-Like 2; Polymerase (DNA-Directed), Zeta 2, Accessory Subunit; Mitotic Arrest Deficient 2-Like Protein 2; Mitotic Arrest Deficient Homolog-Like 2; MAD2-Like Protein 2; REV7 Homolog; MAD2B
Function
Adapter protein able to interact with different proteins and involved in different biological processes (PubMed:11459825, PubMed:11459826, PubMed:17719540, PubMed:17296730, PubMed:19443654, PubMed:29656893).
Mediates the interaction between the error-prone DNA polymerase zeta catalytic subunit REV3L and the inserter polymerase REV1, thereby mediating the second polymerase switching in translesion DNA synthesis (PubMed:20164194).
Translesion DNA synthesis releases the replication blockade of replicative polymerases, stalled in presence of DNA lesions (PubMed:20164194).
Component of the shieldin complex, which plays an important role in repair of DNA double-stranded breaks (DSBs) (PubMed:29656893).
During G1 and S phase of the cell cycle, the complex functions downstream of TP53BP1 to promote non-homologous end joining (NHEJ) and suppress DNA end resection (PubMed:29656893).
Mediates various NHEJ-dependent processes including immunoglobulin class-switch recombination, and fusion of unprotected telomeres (PubMed:29656893).
May also regulate another aspect of cellular response to DNA damage through regulation of the JNK-mediated phosphorylation and activation of the transcriptional activator ELK1 (PubMed:17296730).
Inhibits the FZR1- and probably CDC20-mediated activation of the anaphase promoting complex APC thereby regulating progression through the cell cycle (PubMed:11459825, PubMed:17719540).
Regulates TCF7L2-mediated gene transcription and may play a role in epithelial-mesenchymal transdifferentiation (PubMed:19443654).
Biological Process
Actin filament organizationManual Assertion Based On ExperimentIMP:BHF-UCL
Cell divisionIEA:UniProtKB-KW
DNA damage response, signal transduction resulting in transcriptionManual Assertion Based On ExperimentIDA:UniProtKB
Double-strand break repairManual Assertion Based On ExperimentIGI:UniProtKB
Error-prone translesion synthesisManual Assertion Based On ExperimentIDA:ComplexPortal
Mitotic spindle assembly checkpoint signalingManual Assertion Based On ExperimentTAS:ProtInc
Negative regulation of canonical Wnt signaling pathwayManual Assertion Based On ExperimentIMP:BHF-UCL
Negative regulation of cell-cell adhesion mediated by cadherinManual Assertion Based On ExperimentIMP:BHF-UCL
Negative regulation of DNA-binding transcription factor activityManual Assertion Based On ExperimentIDA:BHF-UCL
Negative regulation of double-strand break repair via homologous recombinationManual Assertion Based On ExperimentIDA:UniProtKB
Negative regulation of epithelial to mesenchymal transitionManual Assertion Based On ExperimentIMP:BHF-UCL
Negative regulation of protein catabolic processManual Assertion Based On ExperimentIDA:UniProtKB
Negative regulation of transcription by competitive promoter bindingManual Assertion Based On ExperimentIMP:BHF-UCL
Negative regulation of transcription by RNA polymerase IIManual Assertion Based On ExperimentIDA:BHF-UCL
Negative regulation of transcription regulatory region DNA bindingManual Assertion Based On ExperimentIMP:BHF-UCL
Negative regulation of ubiquitin protein ligase activityManual Assertion Based On ExperimentIDA:UniProtKB
Positive regulation of double-strand break repair via nonhomologous end joiningManual Assertion Based On ExperimentIDA:UniProtKB
Positive regulation of isotype switchingManual Assertion Based On ExperimentIDA:UniProtKB
Positive regulation of peptidyl-serine phosphorylationManual Assertion Based On ExperimentIDA:UniProtKB
Positive regulation of transcription, DNA-templatedManual Assertion Based On ExperimentIMP:UniProtKB
Regulation of cell growthManual Assertion Based On ExperimentIGI:UniProtKB
Somatic diversification of immunoglobulins involved in immune response1 PublicationIC:ComplexPortal
Telomere maintenance in response to DNA damage1 PublicationIC:ComplexPortal
Cellular Location
Nucleus
Cytoplasm, cytoskeleton, spindle
Cytoplasm
Chromosome
Recruited to sites of chromosomal double-stranded breaks during G1 and S phase of the cell cycle.
Involvement in disease
Fanconi anemia, complementation group V (FANCV):
A disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair.

Xu, K., Zheng, X., Shi, H., Ou, J., & Ding, H. (2024). MAD2L2, a key regulator in ovarian cancer and promoting tumor progression. Scientific Reports, 14(1), 130.

Liu, Z., Wang, S., Yu, K., Chen, K., Zhao, L., Zhang, J., ... & Zhao, P. (2023). The promoting effect and mechanism of MAD2L2 on stemness maintenance and malignant progression in glioma. Journal of Translational Medicine, 21(1), 863.

Anuchina, A. A., Zaynitdinova, M. I., Demchenko, A. G., Evtushenko, N. A., Lavrov, A. V., & Smirnikhina, S. A. (2023). Bridging Gaps in HDR Improvement: The Role of MAD2L2, SCAI, and SCR7. International Journal of Molecular Sciences, 24(7), 6704.

Paniagua, I., Tayeh, Z., Falcone, M., Hernández Pérez, S., Cerutti, A., & Jacobs, J. J. (2022). MAD2L2 promotes replication fork protection and recovery in a shieldin-independent and REV3L-dependent manner. Nature Communications, 13(1), 5167.

Pernicone, N., Elias, M., Onn, I., Tobi, D., & Listovsky, T. (2022). Disrupting the MAD2L2-rev1 complex enhances cell death upon DNA damage. Molecules, 27(3), 636.

de Krijger, I., Föhr, B., Pérez, S. H., Vincendeau, E., Serrat, J., Thouin, A. M., ... & Jacobs, J. J. (2021). MAD2L2 dimerization and TRIP13 control shieldin activity in DNA repair. Nature Communications, 12(1), 5421.

Marima, R., Hull, R., Penny, C., & Dlamini, Z. (2021). Mitotic syndicates Aurora Kinase B (AURKB) and mitotic arrest deficient 2 like 2 (MAD2L2) in cohorts of DNA damage response (DDR) and tumorigenesis. Mutation Research/Reviews in Mutation Research, 787, 108376.

Pernicone, N., Peretz, L., Grinshpon, S., & Listovsky, T. (2020). MDA-MB-157 cell line presents high levels of MAD2L2 and dysregulated mitosis. Anticancer Research, 40(10), 5471-5480.

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For research use only. Not intended for any clinical use.

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