MAD2L2 Recombinant Monoclonal Antibody

Code CSB-RA782379A0HU
Size US$210
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  • Western Blot
    Positive WB detected in: 293 whole cell lysate
    All lanes: Mad2L2 antibody at 1:2000
    Secondary
    Goat polyclonal to rabbit IgG at 1/50000 dilution
    Predicted band size: 25 kDa
    Observed band size: 25 kDa
  • IHC image of CSB-RA782379A0HU diluted at 1:100 and staining in paraffin-embedded human brain tissue performed on a Leica BondTM system. After dewaxing and hydration, antigen retrieval was mediated by high pressure in a citrate buffer (pH 6.0). Section was blocked with 10% normal goat serum 30min at RT. Then primary antibody (1% BSA) was incubated at 4℃ overnight. The primary is detected by a Goat anti-rabbit IgG polymer labeled by HRP and visualized using 0.05% DAB.
  • Immunofluorescence staining of Hela Cells with CSB-RA782379A0HU at 1:50, counter-stained with DAPI. The cells were fixed in 4% formaldehyde, permeated by 0.2% TritonX-100, and blocked in 10% normal Goat Serum. The cells were then incubated with the antibody overnight at 4℃. Nuclear DNA was labeled in blue with DAPI. The secondary antibody was FITC-conjugated AffiniPure Goat Anti-Rabbit IgG (H+L).
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Product Details

Uniprot No.
Target Names
MAD2L2
Alternative Names
Mitotic spindle assembly checkpoint protein MAD2B (Mitotic arrest deficient 2-like protein 2) (MAD2-like protein 2) (REV7 homolog) (hREV7), MAD2L2, MAD2B REV7
Species Reactivity
Human
Immunogen
A synthesized peptide derived from human Mad2L2
Immunogen Species
Homo sapiens (Human)
Conjugate
Non-conjugated
Clonality
Monoclonal
Isotype
Rabbit IgG
Clone No.
4D8
Purification Method
Affinity-chromatography
Concentration
It differs from different batches. Please contact us to confirm it.
Buffer
Rabbit IgG in phosphate buffered saline, pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Form
Liquid
Tested Applications
ELISA, WB, IHC, IF
Recommended Dilution
Application Recommended Dilution
WB 1:500-1:5000
IHC 1:50-1:200
IF 1:20-1:200
Troubleshooting and FAQs
Storage
Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
Lead Time
Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
Description

MAD2L2 is a chromatin-binding protein that participates in the modulation of cell cycle and DNA damage response (DDR). MAD2L2 is involved in preventing the onset of anaphase and ensuring that all chromosomes are aligned correctly at the metaphase plate. It also takes part in translesion DNA synthesis (TLS), mitotic control, signal transduction, transcription, as well as the choice of repair pathway in DNA double-strand breaks. MAD2L2 was previously described as a non-catalytic auxiliary subunit of DNA pol zeta (ϛ), and its knockdown caused hypersensitivity to DNA damage. MAD2L2 dysregulation has been found in a variety of cancers, and MAD2L2 overexpression has been detected in glioma, epithelial ovarian cancer, and breast cancer.

CUSABIO cloned MAD2L2 antibody-coding genes into plasma vectors and then transfected these vector clones into mammalian cells using a lipid-based transfection reagent. Following transient expression, the recombinant antibodies against MAD2L2 were harvested and characterized. The recombinant MAD2L2 antibody was purified by Affinity-chromatography from the culture medium. It can be used to detect MAD2L2 protein from Human in the ELISA, WB, IHC, IF.

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Target Background

Function
Adapter protein able to interact with different proteins and involved in different biological processes. 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. Translesion DNA synthesis releases the replication blockade of replicative polymerases, stalled in presence of DNA lesions. Component of the shieldin complex, which plays an important role in repair of DNA double-stranded breaks (DSBs). 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. Mediates various NHEJ-dependent processes including immunoglobulin class-switch recombination, and fusion of unprotected telomeres. 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. Inhibits the FZR1- and probably CDC20-mediated activation of the anaphase promoting complex APC thereby regulating progression through the cell cycle. Regulates TCF7L2-mediated gene transcription and may play a role in epithelial-mesenchymal transdifferentiation.
Gene References into Functions
  1. results provide insights into the structure of the Rev1/Polzeta TLS assembly and highlight the function of Rev7 homo- and heterodimerization. PMID: 30111544
  2. Skp2, a confirmed APC/C-CDH1 substrate and E-cadherin destroyer, was increased in TGF-beta1-treated proximal tubular epithelial cells, which could be blocked by MAD2B depletion. PMID: 27488450
  3. structure-based interaction analyses revealed an unprecedented mechanism involving CAMP's WK motif. Surprisingly, in one of the crystal forms, the MAD2L2-CAMP complex formed a dimeric structure in which the C-terminal region of MAD2L2 was swapped and adopted an immature structure PMID: 28887307
  4. REV7 is a previously undescribed FA gene, which we term FANCV PMID: 27500492
  5. Knockdown of REV7 inhibited the migration, invasion, and epithelial-mesenchymal transition (EMT) of breast cancer cells. Meanwhile, overexpression of REV7 promoted the migration, invasion, and EMT of breast cancer cells. PMID: 27712588
  6. hMAD2 also binds to the hREV7-binding sequence in hREV3, whereas hMAD2 does not bind to a similar sequence in ADAM9 or ELK-1 and hREV7 does not bind to the hMAD2-binding sequence in hMAD1 or hCDC20. PMID: 20088965
  7. data establish MAD2L2 as a crucial contributor to the control of DNA repair activity by 53BP1 that promotes NHEJ by inhibiting 5' end resection downstream of RIF1 PMID: 25799990
  8. results reveal an unexpected crucial function of REV7 downstream of 53BP1 in coordinating pathological DSB repair pathway choices in BRCA1-deficient cells PMID: 25799992
  9. that MAD2B may play an important role in high glucose-mediated podocyte injury of diabetic nephropathy via modulation of Cdh1, cyclin B1, and Skp2 expression PMID: 25651564
  10. Rev7 is essential for mutagenesis and S phase progression in UV-irradiated fibroblasts. PMID: 18295554
  11. These findings indicate that depletion of REV7 enhances sensitivity to cisplatin treatment in ovarian clear cell carcinoma (CCC), suggesting that REV7 is a candidate molecular target in CCC management. PMID: 24597627
  12. MAD2L2 helps to ensure a robustly bistable switch between APC/C(CDC20) and APC/C(CDH1) during the metaphase-to-anaphase transition, thereby contributing to mitotic fidelity. PMID: 24100295
  13. REV7 is required for anaphase-promoting complex-dependent ubiquitination and degradation of translesion DNA polymerase REV1. PMID: 23287467
  14. MAD2B may mediate Sim2 function during development in CNS and thereby play a critical role in pathophysiological mechanisms in Down syndrome PMID: 22660985
  15. analysis of the crystal structure of the ternary complex composed of the C-terminal domain of human REV1, REV7, and a REV3 fragment PMID: 22859296
  16. the Rev1 C-terminal domain utilizes independent interaction interfaces to simultaneously bind a fragment of the 'inserter' poleta and Rev7 subunit of the 'extender' polvarsigma, thereby serving as a cassette that may accommodate several polymerases PMID: 22828282
  17. ternary complex of the C-terminal domain of human REV1 in complex with REV7 bound to a REV3 fragment has been crystallized. The crystals belonged to space group P3(1)21, with unit-cell parameters a = b = 74.7, c = 124.5 A PMID: 22869133
  18. The REV1/Polzeta complex maintains genomic stability by directly participating in DNA double-stranded break repair. PMID: 21926160
  19. Data show that MAD2B interacts with CLTA during the G2/M phase of the cell cycle and that depletion of MAD2B leads to a marked increase in the percentage of misaligned chromosomes and a redistribution of CLTA during mitosis. PMID: 21152103
  20. The hRev7 is required for TLS past BPDE-induced DNA lesions but that it is not essential for inserting nucleotides opposite such lesions suggest a role for hPolzeta in the extension step of translesion synthesis. PMID: 21143968
  21. show the first crystal structure of REV7 in complex with a fragment of REV3 polymerase (residues 1847-1898) and reveal the mechanism underlying REV7-REV3 interaction PMID: 20164194
  22. To clarify the structural basis of the interaction between REV7 and REV3, REV7 was crystallized in complex with a REV3 fragment. PMID: 20054135
  23. the small GTPase RAN is a novel MAD2B binding protein PMID: 19753112
  24. purified human REV1 and REV7 proteins form a heterodimer in solution, which is stable through intensive purification steps. PMID: 12529368
  25. Upregulated MAD2L2 expression is associated with colorectal tumors PMID: 17044027
  26. Human Rev7 (hRev7)/MAD2B/MAD2L2 is an interaction partner for Elk-1 and hRev7 acts to promote Elk-1 phosphorylation by the c-Jun N-terminal protein kinase (JNK) MAP kinases. PMID: 17296730
  27. Chromophobe renal cell carcinoma presented underexpression of MAD1, and MAD2L2. PMID: 17333263
  28. Hepatocellular carcinoma-associated gene 2 interacts with MAD2L2. PMID: 17541814
  29. Study provides the first evidence for the involvement of MAD2B in TCF4-mediated epithelial-mesenchymal transdifferentiation. PMID: 19443654

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Involvement in disease
Fanconi anemia, complementation group V (FANCV)
Subcellular Location
Nucleus. Cytoplasm, cytoskeleton, spindle. Cytoplasm. Chromosome.
Tissue Specificity
Ubiquitously expressed.
Database Links

HGNC: 6764

OMIM: 604094

KEGG: hsa:10459

STRING: 9606.ENSP00000235310

UniGene: Hs.19400

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