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    Mad2l1 MAD2 mitotic arrest deficient-like 1 [ Mus musculus (house mouse) ]

    Gene ID: 56150, updated on 27-Nov-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    MAD2-Dependent Insulin Receptor Endocytosis Regulates Metabolic Homeostasis.

    MAD2-Dependent Insulin Receptor Endocytosis Regulates Metabolic Homeostasis.
    Park J, Hall C, Hubbard B, LaMoia T, Gaspar R, Nasiri A, Li F, Zhang H, Kim J, Haeusler RA, Accili D, Shulman GI, Yu H, Choi E., Free PMC Article

    12/20/2023
    Inhibition of MAD2L1 Mediates Pulmonary Fibrosis through Impairment of Mitochondrial Function and Induction of Cell Senescence.

    Inhibition of MAD2L1 Mediates Pulmonary Fibrosis through Impairment of Mitochondrial Function and Induction of Cell Senescence.
    Wang L, Wan R, Chen X, Guo X, Li Z, Zhao W, Yan P, Yu G., Free PMC Article

    01/14/2023
    Acute systemic loss of Mad2 leads to intestinal atrophy in adult mice.

    Acute systemic loss of Mad2 leads to intestinal atrophy in adult mice.
    Schukken KM, Zhu Y, Bakker PL, Koster MH, Harkema L, Youssef SA, de Bruin A, Foijer F., Free PMC Article

    07/24/2021
    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.

    Oxidative Stress Delays Prometaphase/Metaphase of the First Cleavage in Mouse Zygotes via the MAD2L1-Mediated Spindle Assembly Checkpoint.
    Wu Q, Li Z, Huang Y, Qian D, Chen M, Xiao W, Wang B., Free PMC Article

    07/14/2018
    Mad2-positive tumors have a higher frequency of developing persistent subclones that avoid remission and continue to grow.

    Negative Selection and Chromosome Instability Induced by Mad2 Overexpression Delay Breast Cancer but Facilitate Oncogene-Independent Outgrowth.
    Rowald K, Mantovan M, Passos J, Buccitelli C, Mardin BR, Korbel JO, Jechlinger M, Sotillo R., Free PMC Article

    10/14/2017
    reduced MAD2 levels attenuate the apoptotic response to mis-segregating sex chromosomes and allow the formation of aneuploid sperm.

    Reduced MAD2 levels dampen the apoptotic response to non-exchange sex chromosomes and lead to sperm aneuploidy.
    Faisal I, Kauppi L.

    09/23/2017
    p31comet-induced cell death is mediated by interactions with Mad2

    p31comet-Induced Cell Death Is Mediated by Binding and Inactivation of Mad2.
    Shin HJ, Park ER, Yun SH, Kim SH, Jung WH, Woo SR, Joo HY, Jang SH, Chung HY, Hong SH, Cho MH, Park JJ, Yun M, Lee KH., Free PMC Article

    06/28/2016
    study shows that Mad2 is a novel substrate for CCP6 in megakaryocytes; Mad2 polyglutamylation plays a crucial role in the regulation of megakaryopoiesis

    Cytosolic carboxypeptidase CCP6 is required for megakaryopoiesis by modulating Mad2 polyglutamylation.
    Ye B, Li C, Yang Z, Wang Y, Hao J, Wang L, Li Y, Du Y, Hao L, Liu B, Wang S, Xia P, Huang G, Sun L, Tian Y, Fan Z., Free PMC Article

    04/25/2015
    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.

    Chromosome missegregation rate predicts whether aneuploidy will promote or suppress tumors.
    Silk AD, Zasadil LM, Holland AJ, Vitre B, Cleveland DW, Weaver BA., Free PMC Article

    01/11/2014
    Mad2 is also repressed by p53 and its upregulation is required for chromosome instability in a p53 mutant tumor model

    Mad2 is a critical mediator of the chromosome instability observed upon Rb and p53 pathway inhibition.
    Schvartzman JM, Duijf PH, Sotillo R, Coker C, Benezra R., Free PMC Article

    08/13/2011
    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.

    Mad2 haploinsufficiency protects hematopoietic progenitor cells subjected to cell-cycle stress in vivo and to inhibition of redox function of Ape1/Ref-1 in vitro.
    Rohrabaugh SL, Hangoc G, Kelley MR, Broxmeyer HE., Free PMC Article

    06/18/2011
    Pcid2 is essential for B cell survival through the regulation of MAD2 expression during B cell differentiation

    Critical role of Pcid2 in B cell survival through the regulation of MAD2 expression.
    Nakaya T, Kuwahara K, Ohta K, Kitabatake M, Toda T, Takeda N, Tani T, Kondo E, Sakaguchi N.

    11/13/2010
    tumours that experience transient Mad2 overexpression and consequent chromosome instability recur at markedly elevated rates

    Mad2-induced chromosome instability leads to lung tumour relapse after oncogene withdrawal.
    Sotillo R, Schvartzman JM, Socci ND, Benezra R., Free PMC Article

    05/3/2010
    Mad2 is involved in synergistic growth of immature hematopoietic progenitor cells in response to stem cell factor plus Granulocyte-Macrophage Colony-Stimulating Factor

    Mad2 is required for optimal hematopoiesis: Mad2 associates with c-Kit in MO7e cells.
    Ito S, Mantel CR, Han MK, Basu S, Fukuda S, Cooper S, Broxmeyer HE., Free PMC Article

    01/21/2010
    Our results provide further evidence for the role of MAD2 as a spindle checkpoint protein in mouse oocytes.

    RNA Interference as a tool to study the function of MAD2 in mouse oocyte meiotic maturation.
    Wang JY, Lei ZL, Nan CL, Yin S, Liu J, Hou Y, Li YL, Chen DY, Sun QY.

    01/21/2010
    a functional Mad2-dependent spindle checkpoint exists during the first meiotic division in mammalian oocytes

    Metaphase I arrest upon activation of the Mad2-dependent spindle checkpoint in mouse oocytes.
    Wassmann K, Niault T, Maro B.

    01/21/2010
    Data suggest that Mad2 and BubR1 must cooperate to inhibit Cdc20 activity.

    Spindle checkpoint function requires Mad2-dependent Cdc20 binding to the Mad3 homology domain of BubR1.
    Davenport J, Harris LD, Goorha R.

    01/21/2010
    that Brca1(Delta11/Delta11) cells displayed decreased expression of a number of genes that are involved in the spindle checkpoint, including Mad2

    A requirement for breast-cancer-associated gene 1 (BRCA1) in the spindle checkpoint.
    Wang RH, Yu H, Deng CX., Free PMC Article

    01/21/2010
    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.

    HAT cofactor Trrap regulates the mitotic checkpoint by modulation of Mad1 and Mad2 expression.
    Li H, Cuenin C, Murr R, Wang ZQ, Herceg Z., Free PMC Article

    01/21/2010
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