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MAD2L1 (Mitotic spindle assembly Checkpoint Protein MAD2A, HsMAD2, Mitotic arrest deficient 2-like Protein 1, MAD2-like Protein 1, MAD2) Catalog number 223989 Supplier United States Biological Cell cycle progression is subject to arrest at the mitotic spindle assembly checkpoint in response to incorrect spindle fiber assembly. MAD2 (for mitotic arrest-deficient) is a component of the mitotic spindle checkpoint. Cells with mutated MAD2 do not undergo mitotic arrest in response to incorrect spindle fiber assembly, which results in missegregation and eventual cell death. A breast carcinoma cell line with reduced MAD2 expression, T47D, was shown to complete mitosis in the presence of nocodazole, an inhibitor of mitotic spindle assembly. MAD2 is localized to unattached kinetochores during prometaphase and disassociates upon spindle fiber attachment, indicating that MAD2 regulates kinetochore binding to the spindle fibers. Human MAD2 has also been shown to associate with insulin receptor (IR), but not IGFIR, implicating MAD2 as a mediator for IR-specific signaling. MAD2B, a MAD2 homolog, is required for the execution of the mitotic checkpoint monitoring the kinetochore-spindle attachment process and if the process is not complete, MAD2B delays the onset of anaphase. Applications Suitable for use in Western Blot. Other applications not tested. Recommended Dilution Western Blot: 1:500-1:1000 Optimal dilutions to be determined by the researcher. Storage and Stability May be stored at 4°C for short-term only. Aliquot to avoid repeated freezing and thawing. Store at -20°C. Aliquots are stable for 12 months after receipt. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Immunogen Synthetic peptide corresponding to amino acids 134-179 of Human MAD2L1. Formulation Supplied as a liquid PBS, 0.05% sodium azide, pH 7.2. Purity Purified by immunoaffinity chromatography. Specificity Recognizes endogenous levels of MAD2L1. Species Crossreactivity: Human, mouse, rat Product Type Pab Source human Isotype IgG Grade Affinity Purified Applications WB Crossreactivity Hu Mo Rt Storage -20°C MW 24 Powered by TCPDF (www.tcpdf.org).

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Profiling of Cell Cycle Genes of Breast Cells Exposed to Etodolac
1383-1391.qxd 29/3/2010 11:48 Ì ™ÂÏ›‰·1383 ONCOLOGY REPORTS 23: 1383-1391, 2010 Profiling of cell cycle genes of breast cells exposed to etodolac D. ROY1,2*, G.A. ARASON2*, B. CHOWDHURY3,4, A. MITRA5 and G.M. CALAF6,7 1Department of Natural Sciences, Hostos College of the City University of New York, Bronx, NY; 2Graduate Biotechnology Program, Manhattan College, Riverdale, NY; 3Human Retrovirus Section, Vaccine Branch, National Cancer Institute, National Institutes of Health, Frederick, MD; 4Department of Cellular Injury, Military Casualty Research, Walter Reed Army Institute of Research, Silver Spring, MD; 5Department of Chemistry, The College of Mount Saint Vincent, Riverdale, NY; 6Center for Radiological Research, Columbia University Medical Center, New York, NY, USA; 7Instituto de Alta Investigación, Universidad de Tarapaca, Arica, Chile Received September 29, 2009; Accepted November 6, 2009 DOI: 10.3892/or_00000775 Abstract. Breast cancer represents the second leading cause Introduction of cancer-related deaths in the world. There is increasing evidence that perturbation of cell cycle regulation is an Breast cancer represents the second leading cause of cancer- important contributing factor to various cancer progression related deaths in the United States and other Western countries; stages. There are key checkpoints in the cell cycle involving accounting for about 30-40% of all newly diagnosed cancers various regulatory proteins. The relationship between these (1,2). Hereditary breast cancer accounts for just 5-10% of cell cycle regulatory proteins and cell cycle arrest by cyclo- cases. It is generally believed that a family history of breast oxygenase (COX) inhibitors during neoplastic progression cancer and hormonal imbalances also contributes to the remains largely unknown.
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The Mitotic Checkpoint Protein MAD2 Delivers Monoamine Transporters to Endocytosis
bioRxiv preprint doi: https://doi.org/10.1101/2021.06.09.447721; this version posted June 10, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 1 The mitotic checkpoint protein MAD2 delivers monoamine transporters to endocytosis. Florian Koban1*, Michael Freissmuth1 https://orcid.org/0000-0003-0912-3114, https://orcid.org/0000-0001-9398-1765 1Institute of Pharmacology and the Gaston H. Glock Research Laboratories for Exploratory Drug Development, Center of Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria. *Corresponding Author: Florian Koban, PhD Institute of Pharmacology and the Gaston H. Glock Research Laboratories for Exploratory Drug Development, Center of Physiology and Pharmacology, Medical University of Vienna. Waehringer Strasse 13A, 1090 Vienna, Austria E-mail: [email protected] Tel.: +43 1 40160 31328 Author contributions: F. K. conceptualized the study; F. K. conducted research; F. K. and M. F. analyzed data; F.K. and M.F. wrote the paper. bioRxiv preprint doi: https://doi.org/10.1101/2021.06.09.447721; this version posted June 10, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 2 ABSTRACT Monoamine transporters retrieve serotonin (SERT), dopamine (DAT) and norepinephrine (NET) from the synaptic cleft. Surface levels of transporters are also regulated by internalization. Clathrin-mediated endocytosis of cargo proteins requires adaptor protein 2 (AP2), which recruits cargo to the nascent clathrin- cage. The transporter C-terminus is required for internalization but lacks an AP2- binding site.
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Gene Section Review
Atlas of Genetics and Cytogenetics in Oncology and Haematology OPEN ACCESS JOURNAL AT INIST-CNRS Gene Section Review MAD2L1 (mitotic arrest deficient 2, yeast, human homolog like-1) Elizabeth M. Petty, Kenute Myrie Division of Medical Genetics Departments of Human Genetics and Internal Medicine University of Michigan Medical School 1150 West Medical Center Drive, 4301 MSRB III, Ann Arbor, Michigan 48109- 0638, USA (EMP, KM) Published in Atlas Database: March 2001 Online updated version : http://AtlasGeneticsOncology.org/Genes/MAD2L1ID304.html DOI: 10.4267/2042/37729 This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 2.0 France Licence. © 2001 Atlas of Genetics and Cytogenetics in Oncology and Haematology Identity Other names: HsMAD2; MAD2; MAD2A HGNC (Hugo): MAD2L1 Shadded boxes (1-5) depict the 5 exons of MAD2L1. The black Location : 4q27 triangle indicates a del A mutation that was found in the CAL51 Local order: As noted on the GM99-GB4 breast cancer cell line. Open triangkes depict the locations of Chromosome 4 map: Position: 548.24 (cR3000) Lod identified sequence variants. Figure is not drawn to scale. score: 1.16 Reference Interval: D4S2945-D4S430 Transcription (115.1-125.1 cM) It is located within the NCBI BAC MAD2L1 has 5 coding exons. No alternative splicing genomic contig: NT_006302.2 which is part of the has been described. Regulation of its transcription in homo sapiens chromosome 4 sequence segment. human cells is currently poorly understood. Note: MAD2L1 was intially (and errounously) mapped by fluorescence in situ hybridization (FISH) to 5q23- Protein q31. Subsequent comprehensive mapping studies using somatic cell hybrid analysis, radiation hybrid (RH) Description mapping, and FISH localized it to 4q27.
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Protein Interactions in the Cancer Proteome† Cite This: Mol
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