anti-MAD2 Mitotic Arrest Deficient-Like 1 (Yeast) (MAD2L1) Anticorps

Human MAD2 Mitotic Arrest Deficient-Like 1 (Yeast) (MAD2L1) interaction partners

1. we took advantage of a chemical and chemical-genetic approach to specifically inhibit Aurora A kinase activity in late prometaphase. We observed that a loss of Aurora A activity directly affects SAC function, that Aurora A is essential for maintaining the checkpoint protein Mad2 on unattached kinetochores and that inhibition of Aurora A leads to loss of the SAC, even in the presence of nocodazole or Taxol.

2. Low expression of BRCA1 and its transcriptional target MAD2 expression are strongly correlated with improved survival in high-grade serous carcinoma.

3. study provides insights into how specific substrates are recruited to AAA+ ATPases (like TRIP13) through adaptor proteins and suggests a model of how translocation through the axial pore of AAA+ ATPases is coupled to protein remodelling

4. MAD2 was found both in SCLC and NSCLC. Interestingly, there was a significant difference found between SCLC and NSCLC using qt-PCR (P<0.05).

5. we demonstrate that the CDC20-MAD2 complex could also be formed independently of the SAC. Moreover, in prolonged arrest caused by nocodazole treatment, the overall levels of the CDC20-MAD2 complex are gradually, but significantly, reduced and this is associated with lower levels of cyclin B1, which brings a new insight into the mechanism of mitotic "slippage" of the arrested cells.

6. MAD2-p31(comet) axis may serve as a potential therapeutic target for glioma.

7. These results identify an unexpected dependency on TRIP13 in cells overexpressing Mad2.

8. this study shows that MAD2L1 is a prognostic biomarker for lung adenocarcinoma

9. MiR-200c-5p suppresses proliferation and metastasis of human hepatocellular carcinoma by suppressing MAD2L1 expression.

10. Low MAD2L1 expression is associated with Chromophobe Renal Cell Carcinomas.

11. TRAP1 is relevant in the control of key cell cycle regulators in tumor cells. TRAP1/TBP7 quality control of CDK1 and MAD2 contributes mechanistically to the regulation of mitotic entry and transit.

12. Thes authors show that p31(comet) binding to the TRIP13 N-terminal domain positions the disordered MAD2 N-terminus for engagement by the TRIP13 "pore loops", which then unfold MAD2 in the presence of ATP.

13. catalytic activation of the spindle assembly checkpoint depends on regulated protein-protein interactions that accelerate the spontaneous but rate-limiting conversion of MAD2 required for mitotic checkpoint complex assembly

14. in addition to its role in checkpoint signaling, MAD2 ensures chromosome stability through the regulation of AURORA B.

15. Overexpression of MAD2gamma may play a role in checkpoint disruption and is associated with resistance to cisplatin-based chemotherapy in testicular germ cell tumors.

16. Aberrant Mad2 expression was associated with cell proliferation and genetic instability, which may contribute to the carcinogenesis of PGI-DLBCL. Mad2 overexpression indicated a poor DFS.

17. interactions between Mad2 and H3K4 regulate resolution of the spindle assembly checkpoint by limiting closed Mad2 availability for Cdc20 inhibition.

18. we showed that BubR1 and Mad2 are overexpressed in oral squamous cell carcinoma cell lines and linked such overexpression to attenuated spindle assembly checkpoint activity.

19. Studied the folding/unfolding process of the open and closed conformers of human Mad2.

20. MAD1L1 Arg558His and MAD2L1 Leu84Met interaction with smoking increase the risk of colorectal cancer

Mouse (Murine) MAD2 Mitotic Arrest Deficient-Like 1 (Yeast) (MAD2L1) interaction partners

1. immunofluorescence staining for mitotic arrest deficient 2-like 1 and the protein kinase TTK, components of the spindle assembly checkpoint (SAC), suggested that this delay possibly involved SAC activation.

2. Mad2-positive tumors have a higher frequency of developing persistent subclones that avoid remission and continue to grow.

3. reduced MAD2 levels attenuate the apoptotic response to mis-segregating sex chromosomes and allow the formation of aneuploid sperm.

4. p31comet-induced cell death is mediated by interactions with Mad2

5. study shows that Mad2 is a novel substrate for CCP6 in megakaryocytes; Mad2 polyglutamylation plays a crucial role in the regulation of megakaryopoiesis

6. Exacerbating chromosome missegregation in CENP-E+/- mice by reducing levels of another mitotic checkpoint component, Mad2, results in elevated cell death and decreased tumor formation compared with reduction of either protein alone.

7. Mad2 is also repressed by p53 and its upregulation is required for chromosome instability in a p53 mutant tumor model

8. Data show that Mad2 haploinsufficiency is protective in the presence of a cycle-specific DNA synthesis agent in vivo, and Ape1/Ref-1 inhibitor in vitro.

9. Pcid2 is essential for B cell survival through the regulation of MAD2 expression during B cell differentiation

10. tumours that experience transient Mad2 overexpression and consequent chromosome instability recur at markedly elevated rates

11. a functional Mad2-dependent spindle checkpoint exists during the first meiotic division in mammalian oocytes

12. Data show that the loss of Trrap leads to chromosome missegregation, mitotic exit failure and compromised mitotic checkpoints, which are caused by defective Trrap-mediated transcription of the mitotic checkpoint proteins Mad1 and Mad2.

13. that Brca1(Delta11/Delta11) cells displayed decreased expression of a number of genes that are involved in the spindle checkpoint, including Mad2

14. Data suggest that Mad2 and BubR1 must cooperate to inhibit Cdc20 activity.

15. Our results provide further evidence for the role of MAD2 as a spindle checkpoint protein in mouse oocytes.

16. Mad2 is involved in synergistic growth of immature hematopoietic progenitor cells in response to stem cell factor plus Granulocyte-Macrophage Colony-Stimulating Factor