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MAD2B

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https://www.readbyqxmd.com/read/28916740/mad2b-acts-as-a-negative-regulatory-partner-of-tcf4-on-proliferation-in-human-dermal-papilla-cells
#1
Nanlan Yu, Zhiqiang Song, Kezhou Zhang, Xichuan Yang
Dermal papilla cells (DPCs) are important components of hair follicles and play a critical role in hair follicle development. However, the mechanisms by which DPCs induce hair follicle development remain unclear. In the present study, we identified the mitotic arrest deficient protein MAD2B as a modifier of DPCs. Overexpression of MAD2B inhibited DPC aggregative growth and proliferation induced by the Wnt signaling activator T cell factor 4 (TCF4), and decreased TCF4-induced expression and the release of hair growth-related cytokines, including hepatocyte growth factor, insulin-like growth factor-1, and vascular endothelial growth factor in DPCs...
September 15, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28899455/mitotic-arrest-deficient-protein-2b-overexpressed-in-lung-cancer-promotes-proliferation-emt-and-metastasis
#2
Hua Zhang, Xiuquan He, Wenfei Yu, Bingqing Yue, Ziting Yu, Ying Qin
As the non-catalytic subunit of mammalian DNA polymerase, mitotic arrest-deficient protein 2B (MAD2B) has been reportedto play a role in cell-cycle regulation, DNA damage tolerance, gene expression and carcinogenesis. Although its expression is known to be associated with poor prognosis in several types of human cancers, the significance of MAD2B expression in lung malignancies is still unclear. Our study showed that MAD2B expression significantly increased in lung cancer, especially in the metastatic tissues...
September 11, 2017: Oncology Research
https://www.readbyqxmd.com/read/28887307/dynamic-feature-of-mitotic-arrest-deficient-2-like-protein-2-mad2l2-and-structural-basis-for-its-interaction-with-chromosome-alignment-maintaining-phosphoprotein-camp
#3
Kodai Hara, Shota Taharazako, Masanori Ikeda, Hiroki Fujita, Yoshiko Mikami, Sotaro Kikuchi, Asami Hishiki, Hideshi Yokoyama, Yoshinobu Ishikawa, Shin-Ichiro Kanno, Kozo Tanaka, Hiroshi Hashimoto
Mitotic arrest deficient 2-like protein 2 (MAD2L2), also termed MAD2B or REV7, is involved in multiple cellular functions including translesion DNA synthesis (TLS), signal transduction, transcription, and mitotic events. MAD2L2 interacts with chromosome alignment-maintaining phosphoprotein (CAMP), a kinetochore-microtubule attachment protein in mitotic cells, presumably through a novel "WK" motif in CAMP. Structures of MAD2L2 in complex with binding regions of the TLS proteins REV3 and REV1 have revealed that MAD2L2 has two faces for protein-protein interactions that are regulated by its C-terminal region; however, the mechanisms underlying the MAD2L2-CAMP interaction and the mitotic role of MAD2L2 remain unknown...
October 27, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28440919/rev7-the-regulatory-subunit-of-pol%C3%AE-undergoes-uv-induced-and-cul4-dependent-degradation
#4
Audesh Bhat, Zhoushuai Qin, Guifen Wang, Wangyang Chen, Wei Xiao
In eukaryotic cells, Rev7 interacts with Rev3 and functions as a regulatory subunit of Polζ, a translesion DNA synthesis (TLS) polymerase. In addition to its role in TLS, mammalian Rev7, also known as Mad2B/Mad2L2, participates in multiple cellular activities including cell cycle progression and double-strand break repair through its interaction with several proteins. Here we show that in mammalian cells, Rev7 undergoes ubiquitin/proteasome-mediated degradation upon UV irradiation in a time-dependent manner...
June 2017: FEBS Journal
https://www.readbyqxmd.com/read/27957796/involvement-of-ampk-in-regulating-the-degradation-of-mad2b-under-high-glucose-in-neuronal-cells
#5
Xianfang Meng, Guangpin Chu, Chen Ye, Hui Tang, Ping Qiu, Yue Hu, Man Li, Chun Zhang
Although our recent study has demonstrated that mitotic spindle assembly checkpoint protein (MAD2B) mediates high glucose-induced neuronal apoptosis, the mechanisms for MAD2B degradation under hyperglycaemia have not yet been elucidated. In this study, we first found that the activation of adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) was decreased in neurons, accompanied with the increased expression of MAD2B. Mechanistically, we demonstrated that activation of AMPK with its activators such as AICAR and metformin decreased the expression of MAD2B, indicating a role of AMPK in regulating the expression of MAD2B...
June 2017: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/27889750/metformin-protects-neurons-against-oxygen-glucose-deprivation-reoxygenation-induced-injury-by-down-regulating-mad2b
#6
Xianfang Meng, Guangpin Chu, Zhihua Yang, Ping Qiu, Yue Hu, Xiaohe Chen, Wenpeng Peng, Chen Ye, Fang-Fang He, Chun Zhang
BACKGROUND/AIMS: Metformin, the common medication for type II diabetes, has protective effects on cerebral ischemia. However, the molecular mechanisms are far from clear. Mitotic arrest deficient 2-like protein 2 (MAD2B), an inhibitor of the anaphase-promoting complex (APC), is widely expressed in hippocampal and cortical neurons and plays an important role in mediating high glucose-induced neurotoxicity. The present study investigated whether metformin modifies the expression of MAD2B and to exert its neuroprotective effects in primary cultured cortical neurons during oxygen-glucose deprivation/reoxygenation (OGD/R), a widely used in vitro model of ischemia/reperfusion...
2016: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/27488450/mad2b-promotes-tubular-epithelial-to-mesenchymal-transition-and-renal-tubulointerstitial-fibrosis-via-skp2
#7
Hui Tang, Di Fan, Chun-Tao Lei, Chen Ye, Pan Gao, Shan Chen, Xian-Fang Meng, Hua Su, Chun Zhang
The mitotic arrest deficient protein MAD2B is a well-defined anaphase-promoting complex/cyclosome (APC/C) inhibitor and a small subunit of DNA polymerase zeta. It is critical for mitotic control and DNA repair. However, the pathological role of MAD2B in kidney diseases has not been fully elucidated. In the present study, we aim to explore the role of MAD2B in the pathogenesis of renal tubulointerstitial fibrosis (TIF) and the underlying mechanism. By immunofluorescence and immunohistochemistry, we found an obvious MAD2B enhancement in tubular area of TIF patients and unilateral ureteral obstruction (UUO) mice...
November 2016: Journal of Molecular Medicine: Official Organ of the "Gesellschaft Deutscher Naturforscher und Ärzte"
https://www.readbyqxmd.com/read/27122545/mad2b-mediated-snon-downregulation-is-implicated-in-fibroblast-activation-and-tubulointerstitial-fibrosis
#8
Hui Tang, Hua Su, Di Fan, Chen Ye, Chun-Tao Lei, Hua-Jun Jiang, Pan Gao, Fang-Fang He, Chun Zhang
MAD2B, an anaphase-promoting complex/cyclosome (APC/C) inhibitor and a small subunit of DNA polymerase ζ, is indispensible for mitotic checkpoint control and DNA repair. Previously, we established that MAD2B is expressed in glomerular and tubulointerstitial compartments and participates in high glucose-induced podocyte injury. However, its role in other renal diseases remains elusive. In the present study, we aim to illustrate the potential role of MAD2B in the pathogenesis of renal fibrosis. By immunofluorescence and Western blotting, we found MAD2B expression is obviously increased in tubulointerstitial fibrosis (TIF) patients and unilateral ureteral obstruction (UUO) mice...
July 1, 2016: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/26697843/rev7-mad2b-plays-a-critical-role-in-the-assembly-of-a-functional-mitotic-spindle
#9
Audesh Bhat, Zhaojia Wu, Veronica M Maher, J Justin McCormick, Wei Xiao
The spindle assembly checkpoint (SAC) acts as a guardian against cellular threats that may lead to chromosomal missegregation and aneuploidy. Mad2, an anaphase-promoting complex/cyclosome-Cdc20 (APC/C(Cdc20)) inhibitor, has an additional homolog in mammals known as Mad2B, Mad2L2 or Rev7. Apart from its role in Polζ-mediated translesion DNA synthesis and double-strand break repair, Rev7 is also believed to inhibit APC/C by negatively regulating Cdh1. Here we report yet another function of Rev7 in cultured human cells...
2015: Cell Cycle
https://www.readbyqxmd.com/read/25928475/destabilization-of-pluripotency-in-the-absence-of-mad2l2
#10
Mehdi Pirouz, Ali Rahjouei, Farnaz Shamsi, Kolja Neil Eckermann, Gabriela Salinas-Riester, Claudia Pommerenke, Michael Kessel
The induction and maintenance of pluripotency requires the expression of several core factors at appropriate levels (Oct4, Sox2, Klf4, Prdm14). A subset of these proteins (Oct4, Sox2, Prdm14) also plays crucial roles for the establishment of primordial germ cells (PGCs). Here we demonstrate that the Mad2l2 (MAD2B, Rev7) gene product is not only required by PGCs, but also by pluripotent embryonic stem cells (ESCs), depending on the growth conditions. Mad2l2(-/-) ESCs were unstable in LIF/serum medium, and differentiated into primitive endoderm...
2015: Cell Cycle
https://www.readbyqxmd.com/read/25799990/mad2l2-controls-dna-repair-at-telomeres-and-dna-breaks-by-inhibiting-5-end-resection
#11
Vera Boersma, Nathalie Moatti, Sandra Segura-Bayona, Marieke H Peuscher, Jaco van der Torre, Brigitte A Wevers, Alexandre Orthwein, Daniel Durocher, Jacqueline J L Jacobs
Appropriate repair of DNA lesions and the inhibition of DNA repair activities at telomeres are crucial to prevent genomic instability. By fuelling the generation of genetic alterations and by compromising cell viability, genomic instability is a driving force in cancer and ageing. Here we identify MAD2L2 (also known as MAD2B or REV7) through functional genetic screening as a novel factor controlling DNA repair activities at mammalian telomeres. We show that MAD2L2 accumulates at uncapped telomeres and promotes non-homologous end-joining (NHEJ)-mediated fusion of deprotected chromosome ends and genomic instability...
May 28, 2015: Nature
https://www.readbyqxmd.com/read/25651564/mad2b-contributes-to-podocyte-injury-of-diabetic-nephropathy-via-inducing-cyclin-b1-and-skp2-accumulation
#12
Hua Su, Qiang Wan, Xiu-Juan Tian, Fang-Fang He, Pan Gao, Hui Tang, Chen Ye, Di Fan, Shan Chen, Yu-Mei Wang, Xian-Fang Meng, Chun Zhang
It is well documented that mitotic arrest deficiency (MAD)2B can inhibit the anaphase-promoting complex/cyclosome (APC/C) via cadherin (Cdh)1 and, consequently, can destroy the effective mitotic spindle checkpoint control. Podocytes have been observed to rapidly detach and die when being forced to bypass cell cycle checkpoints. However, the role of MAD2B, a cell cycle regulator, in podocyte impairment of diabetic nephropathy (DN) is unclear. In the present study, we investigated the significance of MAD2B in the pathogenesis of DN in patients, an animal model, and in vitro podocyte cultures...
April 1, 2015: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/25547045/attenuation-of-glomerular-endothelial-cells-from-high-glucose-induced-injury-by-blockade-of-mad2b
#13
Yu-Mei Wang, Yu Hao, Xian-Fang Meng, Fang-Fang He, Shan Chen, Pan Gao, Hui Tang, Hua Su, Chun Zhang
BACKGROUND/AIMS: To assess the role of mitotic arrest-deficient 2-like protein 2 (MAD2B) in high glucose-induced injury in mouse glomerular endothelial cells (GEnCs). METHODS: GEnCs were cultured in vitro, and MAD2B protein levels were measured by Western blot in cells stimulated with high glucose (30 mM) for various periods of time. MAD2B and scrambled shRNA were introduced into GEnCs by liposomal transfection. Cell proliferation, apoptosis, nitric oxide (NO) production, and monolayer permeability were then measured in cells grown in the following conditions: control, high glucose treatment, MAD2B shRNA transfection with high glucose treatment, and scrambled shRNA transfection with high glucose treatment...
2015: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/24597627/suppression-of-rev7-enhances-cisplatin-sensitivity-in-ovarian-clear-cell-carcinoma-cells
#14
Kaoru Niimi, Yoshiki Murakumo, Naoki Watanabe, Takuya Kato, Shinji Mii, Atsushi Enomoto, Masato Asai, Naoya Asai, Eiko Yamamoto, Hiroaki Kajiyama, Kiyosumi Shibata, Fumitaka Kikkawa, Masahide Takahashi
Human REV7 (also known as MAD2L2 and MAD2B) is involved in DNA repair, cell cycle regulation, gene transcription, and carcinogenesis. In this study, we evaluated the expression of REV7 in epithelial ovarian cancer (EOC) and analyzed the association between its expression and chemosensitivity in ovarian clear cell carcinoma (CCC) cells. Expression of REV7 in human EOC tissues was assessed by immunohistochemical staining. Expression was detected in the majority of EOCs (92.0%) with especially high levels of expression frequently observed in CCCs (73...
May 2014: Cancer Science
https://www.readbyqxmd.com/read/24444371/protection-of-neurons-from-high-glucose-induced-injury-by-deletion-of-mad2b
#15
Xianfang Meng, Xiaolan Wang, Xiujuan Tian, Zhihua Yang, Man Li, Chun Zhang
Diabetic encephalopathy may lead to cognitive deficits in diabetic patients and diminish quality of life. It has been shown that protracted hyperglycaemia is directly associated with neuronal apoptosis, which is involved in diabetic encephalopathy. The anaphase-promoting complex (APC) is essential for the survival of post-mitotic neurons. In our previous study, we found that the mitotic arrest deficient protein MAD2B, one of APC inhibitors, was expressed in neurons in central nervous system. However, whether MAD2B is involved in hyperglycaemia-induced apoptosis and thus takes part in diabetic encephalopathy is still unknown...
May 2014: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/24009519/a-critical-function-of-mad2l2-in-primordial-germ-cell-development-of-mice
#16
Mehdi Pirouz, Sven Pilarski, Michael Kessel
The development of primordial germ cells (PGCs) involves several waves of epigenetic reprogramming. A major step is following specification and involves the transition from the stably suppressive histone modification H3K9me2 to the more flexible, still repressive H3K27me3, while PGCs are arrested in G2 phase of their cycle. The significance and underlying molecular mechanism of this transition were so far unknown. Here, we generated mutant mice for the Mad2l2 (Mad2B, Rev7) gene product, and found that they are infertile in both males and females...
August 2013: PLoS Genetics
https://www.readbyqxmd.com/read/23463509/the-rev7-subunit-of-dna-polymerase-%C3%AE-is-essential-for-primordial-germ-cell-maintenance-in-the-mouse
#17
Naoki Watanabe, Shinji Mii, Naoya Asai, Masato Asai, Kaoru Niimi, Kaori Ushida, Takuya Kato, Atsushi Enomoto, Hideshi Ishii, Masahide Takahashi, Yoshiki Murakumo
REV7 (also known as MAD2L2 and MAD2B) is involved in DNA repair, cell cycle regulation, gene expression, and carcinogenesis. In vitro studies show that REV7 interacts with several proteins and regulates their function. It has been reported that human REV7 is highly expressed in the adult testis by Northern blot analysis. However, the significance of REV7 in mammalian development has not been elucidated. Here, we present analyses of REV7-deficient (Rev7(-/-)) mice to clarify the significance of Rev7 in mouse development...
April 12, 2013: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/22660985/a-novel-binding-protein-of-single-minded-2-the-mitotic-arrest-deficient-protein-mad2b
#18
Xianfang Meng, Xiujuan Tian, Xiaolan Wang, Pan Gao, Chun Zhang
Single-minded 2 (Sim2) gene, located at the Down syndrome (DS) critical region, is thought to be particularly important because of its critical role in the development of the central nervous system (CNS) and its overexpression resulting in impairment of learning and memory which is similar to that in DS. However, its exact role in DS still remains elusive. Using a yeast two-hybrid interaction trap, we identified the mitotic arrest-deficient protein MAD2B as a novel Sim2 binding protein. Through confocal laser scanning microscopy, we found that Sim2 and MAD2B colocalized in rat cortex neurons...
August 2012: Neurogenetics
https://www.readbyqxmd.com/read/21514164/mitotic-arrest-deficient-protein-mad2b-is-overexpressed-in-human-glioma-with-depletion-enhancing-sensitivity-to-ionizing-radiation
#19
Jun Zhao, Shuizhong Liu, Hongwei Wang, Xiaomei Zhang, Tiejiang Kang, Zhanyi Li, Hemin Deng, Wu Yue, Shujie Cao
Mitotic arrest deficient protein MAD2B, an enzyme involved in translesion DNA synthesis, has been implicated in several cancers. However, its role in human glioma has not been defined. In the present study, we investigated the expression levels of MAD2B in human gliomas and normal brain tissues, and determined whether depletion of MAD2B enhanced the sensitivity of glioma cells to ionizing radiation. Using reverse transcription-polymerase chain reaction and immunohistochemical analysis, MAD2B was found to be overexpressed in glioma specimens compared with normal brain tissue...
June 2011: Journal of Clinical Neuroscience: Official Journal of the Neurosurgical Society of Australasia
https://www.readbyqxmd.com/read/21152103/the-mitotic-arrest-deficient-protein-mad2b-interacts-with-the-clathrin-light-chain-a-during-mitosis
#20
Klaas Medendorp, Lilian Vreede, Jan J M van Groningen, Lisette Hetterschijt, Linda Brugmans, Patrick A M Jansen, Wilhelmina H van den Hurk, Diederik R H de Bruijn, Ad Geurts van Kessel
BACKGROUND: Although the mitotic arrest deficient protein MAD2B (MAD2L2) is thought to inhibit the anaphase promoting complex (APC) by binding to CDC20 and/or CDH1 (FZR1), its exact role in cell cycle control still remains to be established. METHODOLOGY/PRINCIPAL FINDINGS: Using a yeast two-hybrid interaction trap we identified the human clathrin light chain A (CLTA) as a novel MAD2B binding protein. A direct interaction was established in mammalian cells via GST pull-down and endogenous co-immunoprecipitation during the G2/M phase of the cell cycle...
2010: PloS One
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