Product Datasheet MBNL3 Antibody Orb751129

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Product Datasheet MBNL3 Antibody Orb751129

Biorbyt Ltd. Biorbyt LLC. 5 Orwell Furlong, Cowley Road, Cambridge 1100 Corporate Square Drive, Helix Center, Suite 221 CB4 0WY, United Kingdom St Louis, MO 63132, United States Email: [email protected] Email: [email protected] Phone: +44 (0)1223 859 353 | Fax: +44 (0)1223 280 240 Phone: +1 (415) 906 5211 | Fax: +1 (415) 651 8558 Product Datasheet MBNL3 antibody orb751129 Description Mouse monoclonal antibody to MBNL3 Species/Host Mouse Reactivity Human Conjugation Unconjugated Custom conjugations Unconjugated, Biotin, FITC, HRP, CF647, CF488A, CF594, CF405M Immunogen Recombinant full-length human MBNL3 protein Target Pre-mRNA splicing is a critical step in the posttranscriptional regulation of gene expression. Several protein complexes are involved in proper mRNA splicing and transport. The muscleblind proteins, MBNL1, MBNL2 and MBNL3, promote inclusion or exclusion of specific exons on different pre-mRNAs by antagonizing the activity of CUG-BP and ETR-3-like factors bound to distinct intronic sites. MBNL1 and 2, which associate with expanded CUG repeats in vitro, localize to the nuclear foci in both DM1 and DM2 (myotonic dystrophy types 1 and 2), suggesting that the nuclear accumulation of mutant RNA is pathogenic in DM1, therefore implicating MBNL1 and 2 in the pathogenesis of both disorders. MBNL3, a 354 amino acid protein, inhibits expression of muscle differentiation, opposite to the function of MBNL1, which functions as a promoter of muscle differentiation. MBNL3 shows strong expression in placenta. Form/Appearance Prepared in 10mM PBS with 0.05% BSA & 0.05% azide. Also available WITHOUT BSA & azide at 1.0mg/ml. Concentration 200 μg/ml Storage Antibody with azide - store at 2 to 8°C. Antibody without azide - store at -20 to -80°C. Antibody is stable for 24 months Note For research use only. Isotype IgG2b Clonality Monoclonal Purity Purified from Bioreactor Concentrate by Protein A/G. MW 39 kDa Clone ID PCRP-MBNL3-1D11 Uniprot ID Q9NUK0 Entrez 55796 Expiration Date 12 months from date of receipt..

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View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Current Biology 19, 1478–1484, September 15, 2009 ª2009 Elsevier Ltd All rights reserved DOI 10.1016/j.cub.2009.07.041 Report Key Features of the X Inactivation Process Are Conserved between Marsupials and Eutherians Shantha K. Mahadevaiah,1 Helene Royo,1 in situ hybridization (RNA FISH) [1] and semiquantitative John L. VandeBerg,2 John R. McCarrey,3 Sarah Mackay,4 reverse transcriptase-polymerase chain reaction (RT-PCR) and James M.A. Turner1,* [2] have concluded that the X chromosome of the marsupial 1MRC National Institute for Medical Research, Mill Hill, Monodelphis domestica (opossum) remains inactive during London NW7 1AA, UK spermiogenesis. However, Cot-1 RNA FISH has since been 2Department of Genetics, Southwest Foundation for shown to primarily detect silencing of repeat rather than Biomedical Research, San Antonio, TX 78227, USA coding X-linked sequences [16, 17], and RT-PCR cannot 3Department of Biology, University of Texas at San Antonio, discriminate between steady-state RNA levels and ongoing San Antonio, TX 78249, USA transcription. We therefore sought to reexamine male germline 4Division of Integrated Biology, Faculty of Biomedical & Life X silencing and its relationship to female XCI with a gene- Sciences, University of Glasgow, Glasgow G12 8QQ, speciﬁc RNA FISH approach. Scotland, UK For our analysis of XCI in the male germline, we selected ten genes distributed across the opossum X chromosome (Fig- ure 1A). We wished to compare X gene silencing in opossum Summary with that in mouse, in which MSCI and its maintenance have been well characterized [18, 19].
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MBNL1 Regulates Essential Alternative RNA Splicing Patterns in MLL-Rearranged Leukemia
ARTICLE https://doi.org/10.1038/s41467-020-15733-8 OPEN MBNL1 regulates essential alternative RNA splicing patterns in MLL-rearranged leukemia Svetlana S. Itskovich1,9, Arun Gurunathan 2,9, Jason Clark 1, Matthew Burwinkel1, Mark Wunderlich3, Mikaela R. Berger4, Aishwarya Kulkarni5,6, Kashish Chetal6, Meenakshi Venkatasubramanian5,6, ✉ Nathan Salomonis 6,7, Ashish R. Kumar 1,7 & Lynn H. Lee 7,8 Despite growing awareness of the biologic features underlying MLL-rearranged leukemia, 1234567890():,; targeted therapies for this leukemia have remained elusive and clinical outcomes remain dismal. MBNL1, a protein involved in alternative splicing, is consistently overexpressed in MLL-rearranged leukemias. We found that MBNL1 loss significantly impairs propagation of murine and human MLL-rearranged leukemia in vitro and in vivo. Through transcriptomic profiling of our experimental systems, we show that in leukemic cells, MBNL1 regulates alternative splicing (predominantly intron exclusion) of several genes including those essential for MLL-rearranged leukemogenesis, such as DOT1L and SETD1A.Wefinally show that selective leukemic cell death is achievable with a small molecule inhibitor of MBNL1. These findings provide the basis for a new therapeutic target in MLL-rearranged leukemia and act as further validation of a burgeoning paradigm in targeted therapy, namely the disruption of cancer-specific splicing programs through the targeting of selectively essential RNA binding proteins. 1 Division of Bone Marrow Transplantation and Immune Deficiency, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH 45229, USA. 2 Cancer and Blood Diseases Institute, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH 45229, USA. 3 Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH 45229, USA.
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Molecular Effects of Isoflavone Supplementation Human Intervention Studies and Quantitative Models for Risk Assessment
Molecular effects of isoflavone supplementation Human intervention studies and quantitative models for risk assessment Vera van der Velpen Thesis committee Promotors Prof. Dr Pieter van ‘t Veer Professor of Nutritional Epidemiology Wageningen University Prof. Dr Evert G. Schouten Emeritus Professor of Epidemiology and Prevention Wageningen University Co-promotors Dr Anouk Geelen Assistant professor, Division of Human Nutrition Wageningen University Dr Lydia A. Afman Assistant professor, Division of Human Nutrition Wageningen University Other members Prof. Dr Jaap Keijer, Wageningen University Dr Hubert P.J.M. Noteborn, Netherlands Food en Consumer Product Safety Authority Prof. Dr Yvonne T. van der Schouw, UMC Utrecht Dr Wendy L. Hall, King’s College London This research was conducted under the auspices of the Graduate School VLAG (Advanced studies in Food Technology, Agrobiotechnology, Nutrition and Health Sciences). Molecular effects of isoflavone supplementation Human intervention studies and quantitative models for risk assessment Vera van der Velpen Thesis submitted in fulfilment of the requirements for the degree of doctor at Wageningen University by the authority of the Rector Magnificus Prof. Dr M.J. Kropff, in the presence of the Thesis Committee appointed by the Academic Board to be defended in public on Friday 20 June 2014 at 13.30 p.m. in the Aula. Vera van der Velpen Molecular effects of isoflavone supplementation: Human intervention studies and quantitative models for risk assessment 154 pages PhD thesis, Wageningen University, Wageningen, NL (2014) With references, with summaries in Dutch and English ISBN: 978-94-6173-952-0 ABSTRact Background: Risk assessment can potentially be improved by closely linked experiments in the disciplines of epidemiology and toxicology.
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A Large-Scale Genome-Wide Association Study of Epistasis Effects of Production Traits and Daughter Pregnancy Rate in U.S
G C A T T A C G G C A T genes Article A Large-Scale Genome-Wide Association Study of Epistasis Effects of Production Traits and Daughter Pregnancy Rate in U.S. Holstein Cattle Dzianis Prakapenka 1, Zuoxiang Liang 1, Jicai Jiang 2, Li Ma 3 and Yang Da 1,* 1 Department of Animal Science, University of Minnesota, Saint Paul, MN 55108, USA; [email protected] (D.P.); [email protected] (Z.L.) 2 Department of Animal Science, North Carolina State University, Raleigh, NC 27695, USA; [email protected] 3 Department of Animal and Avian Sciences, University of Maryland, College Park, MD 20742, USA; [email protected] * Correspondence: [email protected] Abstract: Epistasis is widely considered important, but epistasis studies lag those of SNP effects. Genome-wide association study (GWAS) using 76,109 SNPs and 294,079 first-lactation Holstein cows was conducted for testing pairwise epistasis effects of five production traits and three fertility traits: milk yield (MY), fat yield (FY), protein yield (PY), fat percentage (FPC), protein percentage (PPC), and daughter pregnancy rate (DPR). Among the top 50,000 pairwise epistasis effects of each trait, the five production traits had large chromosome regions with intra-chromosome epistasis. The percentage of inter-chromosome epistasis effects was 1.9% for FPC, 1.6% for PPC, 10.6% for MY, 29.9% for FY, 39.3% for PY, and 84.2% for DPR. Of the 50,000 epistasis effects, the number of significant effects with log10(1/p) ≥ 12 was 50,000 for FPC and PPC, and 10,508, 4763, 4637 and 1 for MY, FY, PY and DPR, Citation: Prakapenka, D.; Liang, Z.; respectively, and A × A effects were the most frequent epistasis effects for all traits.
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Splice Junction Identification from RNA-Sequencing Data Shaojun Tang1,2,3,4 and Alberto Riva1,2*
Tang and Riva BMC Bioinformatics 2013, 14:116 http://www.biomedcentral.com/1471-2105/14/116 SOFTWARE Open Access PASTA: splice junction identification from RNA-Sequencing data Shaojun Tang1,2,3,4 and Alberto Riva1,2* Abstract Background: Next generation transcriptome sequencing (RNA-Seq) is emerging as a powerful experimental tool for the study of alternative splicing and its regulation, but requires ad-hoc analysis methods and tools. PASTA (Patterned Alignments for Splicing and Transcriptome Analysis) is a splice junction detection algorithm specifically designed for RNA-Seq data, relying on a highly accurate alignment strategy and on a combination of heuristic and statistical methods to identify exon-intron junctions with high accuracy. Results: Comparisons against TopHat and other splice junction prediction software on real and simulated datasets show that PASTA exhibits high specificity and sensitivity, especially at lower coverage levels. Moreover, PASTA is highly configurable and flexible, and can therefore be applied in a wide range of analysis scenarios: it is able to handle both single-end and paired-end reads, it does not rely on the presence of canonical splicing signals, and it uses organism-specific regression models to accurately identify junctions. Conclusions: PASTA is a highly efficient and sensitive tool to identify splicing junctions from RNA-Seq data. Compared to similar programs, it has the ability to identify a higher number of real splicing junctions, and provides highly annotated output files containing detailed information about their location and characteristics. Accurate junction data in turn facilitates the reconstruction of the splicing isoforms and the analysis of their expression levels, which will be performed by the remaining modules of the PASTA pipeline, still under development.
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The Influence of X Chromosome Variants on Trait Neuroticism
bioRxiv preprint doi: https://doi.org/10.1101/401166; this version posted August 27, 2018. 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. The influence of X chromosome variants on trait neuroticism Michelle Luciano 1*, Gail Davies 1, Kim M Summers 2, W David Hill 1, Caroline Hayward 3,, David C Liewald1, David J Porteous 4, Catharine R. Gale 1,5, Andrew M McIntosh 1,6, Ian J Deary 1 1 Centre for Cognitive Ageing and Cognitive Epidemiology, Department of Psychology, School of Philosophy, Psychology and Language Sciences, The University of Edinburgh, Edinburgh, UK 2 Mater Research Institute-University of Queensland, Translational Research Institute, Brisbane, Australia 3 MRC Human Genetics Unit, MRC Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK 4 Centre for Genomic and Experimental Medicine, MRC Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK 1 bioRxiv preprint doi: https://doi.org/10.1101/401166; this version posted August 27, 2018. 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. 5 MRC Lifecourse Epidemiology Unit, University of Southampton, Southampton, UK. 6 Division of Psychiatry, University of Edinburgh, Edinburgh, UK *Corresponding author: [email protected], Department of Psychology, The University of Edinburgh, 7 George Square, EH8 9JZ, Edinburgh, UK 2 bioRxiv preprint doi: https://doi.org/10.1101/401166; this version posted August 27, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder.
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Content Based Search in Gene Expression Databases and a Meta-Analysis of Host Responses to Infection
Content Based Search in Gene Expression Databases and a Meta-analysis of Host Responses to Infection A Thesis Submitted to the Faculty of Drexel University by Francis X. Bell in partial fulﬁllment of the requirements for the degree of Doctor of Philosophy November 2015 c Copyright 2015 Francis X. Bell. All Rights Reserved. ii Acknowledgments I would like to acknowledge and thank my advisor, Dr. Ahmet Sacan. Without his advice, support, and patience I would not have been able to accomplish all that I have. I would also like to thank my committee members and the Biomed Faculty that have guided me. I would like to give a special thanks for the members of the bioinformatics lab, in particular the members of the Sacan lab: Rehman Qureshi, Daisy Heng Yang, April Chunyu Zhao, and Yiqian Zhou. Thank you for creating a pleasant and friendly environment in the lab. I give the members of my family my sincerest gratitude for all that they have done for me. I cannot begin to repay my parents for their sacriﬁces. I am eternally grateful for everything they have done. The support of my sisters and their encouragement gave me the strength to persevere to the end. iii Table of Contents LIST OF TABLES.......................................................................... vii LIST OF FIGURES ........................................................................ xiv ABSTRACT ................................................................................ xvii 1. A BRIEF INTRODUCTION TO GENE EXPRESSION............................. 1 1.1 Central Dogma of Molecular Biology........................................... 1 1.1.1 Basic Transfers .......................................................... 1 1.1.2 Uncommon Transfers ................................................... 3 1.2 Gene Expression ................................................................. 4 1.2.1 Estimating Gene Expression ............................................ 4 1.2.2 DNA Microarrays ......................................................
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393LN V 393P 344SQ V 393P Probe Set Entrez Gene
393LN v 393P 344SQ v 393P Entrez fold fold probe set Gene Gene Symbol Gene cluster Gene Title p-value change p-value change chemokine (C-C motif) ligand 21b /// chemokine (C-C motif) ligand 21a /// chemokine (C-C motif) ligand 21c 1419426_s_at 18829 /// Ccl21b /// Ccl2 1 - up 393 LN only (leucine) 0.0047 9.199837 0.45212 6.847887 nuclear factor of activated T-cells, cytoplasmic, calcineurin- 1447085_s_at 18018 Nfatc1 1 - up 393 LN only dependent 1 0.009048 12.065 0.13718 4.81 RIKEN cDNA 1453647_at 78668 9530059J11Rik1 - up 393 LN only 9530059J11 gene 0.002208 5.482897 0.27642 3.45171 transient receptor potential cation channel, subfamily 1457164_at 277328 Trpa1 1 - up 393 LN only A, member 1 0.000111 9.180344 0.01771 3.048114 regulating synaptic membrane 1422809_at 116838 Rims2 1 - up 393 LN only exocytosis 2 0.001891 8.560424 0.13159 2.980501 glial cell line derived neurotrophic factor family receptor alpha 1433716_x_at 14586 Gfra2 1 - up 393 LN only 2 0.006868 30.88736 0.01066 2.811211 1446936_at --- --- 1 - up 393 LN only --- 0.007695 6.373955 0.11733 2.480287 zinc finger protein 1438742_at 320683 Zfp629 1 - up 393 LN only 629 0.002644 5.231855 0.38124 2.377016 phospholipase A2, 1426019_at 18786 Plaa 1 - up 393 LN only activating protein 0.008657 6.2364 0.12336 2.262117 1445314_at 14009 Etv1 1 - up 393 LN only ets variant gene 1 0.007224 3.643646 0.36434 2.01989 ciliary rootlet coiled- 1427338_at 230872 Crocc 1 - up 393 LN only coil, rootletin 0.002482 7.783242 0.49977 1.794171 expressed sequence 1436585_at 99463 BB182297 1 - up 393
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The Influence of X Chromosome Variants on Trait Neuroticism
bioRxiv preprint doi: https://doi.org/10.1101/401166; this version posted August 27, 2018. 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. The influence of X chromosome variants on trait neuroticism Michelle Luciano 1*, Gail Davies 1, Kim M Summers 2, W David Hill 1, Caroline Hayward 3,, David C Liewald1, David J Porteous 4, Catharine R. Gale 1,5, Andrew M McIntosh 1,6, Ian J Deary 1 1 Centre for Cognitive Ageing and Cognitive Epidemiology, Department of Psychology, School of Philosophy, Psychology and Language Sciences, The University of Edinburgh, Edinburgh, UK 2 Mater Research Institute-University of Queensland, Translational Research Institute, Brisbane, Australia 3 MRC Human Genetics Unit, MRC Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK 4 Centre for Genomic and Experimental Medicine, MRC Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK 1 bioRxiv preprint doi: https://doi.org/10.1101/401166; this version posted August 27, 2018. 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. 5 MRC Lifecourse Epidemiology Unit, University of Southampton, Southampton, UK. 6 Division of Psychiatry, University of Edinburgh, Edinburgh, UK *Corresponding author: [email protected], Department of Psychology, The University of Edinburgh, 7 George Square, EH8 9JZ, Edinburgh, UK 2 bioRxiv preprint doi: https://doi.org/10.1101/401166; this version posted August 27, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder.
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X Chromosome Dosage Compensation and Gene Expression in the Sheep Kaleigh Flock [email protected]
University of Connecticut OpenCommons@UConn Master's Theses University of Connecticut Graduate School 8-29-2017 X Chromosome Dosage Compensation and Gene Expression in the Sheep Kaleigh Flock [email protected] Recommended Citation Flock, Kaleigh, "X Chromosome Dosage Compensation and Gene Expression in the Sheep" (2017). Master's Theses. 1144. https://opencommons.uconn.edu/gs_theses/1144 This work is brought to you for free and open access by the University of Connecticut Graduate School at OpenCommons@UConn. It has been accepted for inclusion in Master's Theses by an authorized administrator of OpenCommons@UConn. For more information, please contact [email protected]. X Chromosome Dosage Compensation and Gene Expression in the Sheep Kaleigh Flock B.S., University of Connecticut, 2014 A Thesis Submitted in Partial Fulfillment of the Requirements for the Degree of Masters of Science at the University of Connecticut 2017 i Copyright by Kaleigh Flock 2017 ii APPROVAL PAGE Masters of Science Thesis X Chromosome Dosage Compensation and Gene Expression in the Sheep Presented by Kaleigh Flock, B.S. Major Advisor___________________________________________________ Dr. Xiuchun (Cindy) Tian Associate Advisor_________________________________________________ Dr. David Magee Associate Advisor_________________________________________________ Dr. Sarah A. Reed Associate Advisor_________________________________________________ Dr. John Malone University of Connecticut 2017 iii Dedication This thesis is dedicated to my major advisor Dr. Xiuchun (Cindy) Tian, my lab mates Mingyuan Zhang and Ellie Duan, and my mother and father. This thesis would not be possible without your hard work, unwavering support, and guidance. Dr. Tian, I am so thankful for the opportunity to pursue a Master’s degree in your lab. The knowledge and technical skills that I have gained are invaluable and have opened many doors in my career as a scientist and future veterinarian.
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Network Pharmacology-Based Approach Uncovers the Mechanism of Guanxinning Tablet for Treating Thrombus by Mapks Signal Pathway
ORIGINAL RESEARCH published: 13 May 2020 doi: 10.3389/fphar.2020.00652 Network Pharmacology-Based Approach Uncovers the Mechanism of GuanXinNing Tablet for Treating Thrombus by MAPKs Signal Pathway † † Mu-Lan Wang 1,2 , Qin-Qin Yang 1,3 , Xu-Hui Ying 2, Yuan-Yuan Li 1, Yang-Sheng Wu 1, Qi-Yang Shou 1, Quan-Xin Ma 1, Zi-Wei Zhu 2 and Min-Li Chen 1* 1 Academy of Chinese Medicine & Institute of Comparative Medicine, Zhejiang Chinese Medical University, Hangzhou, China, 2 The Department of Medicine, Chiatai Qingchunbao Pharmaceutical Co., Ltd., Hangzhou, China, 3 Department of Experimental Animals, Zhejiang Academy of Traditional Chinese Medicine, Hangzhou, China Edited by: Background: GuanXinNing tablet (GXNT), a traditional Chinese patent medicine, has Jianxun Liu, been found to have remarkable antithrombotic effects and can effectively inhibit pro- China Academy of Chinese Medical Sciences, China thrombotic factors in previous studies. However, the mechanism of its antithrombotic Reviewed by: effects remains little known. Songxiao Xu, ﬁ ﬁ Artron BioResearch Inc., Canada Methods: In this study, we rst determined and identi ed the sources of each main Yi Ding, compound in GXNT using liquid chromatography-mass spectrometry (LC-MS). Through Fourth Military Medical the approach of network pharmacology, we predicted the action targets of the active University, China Yunyao Jiang, components, mapped the target genes related to thrombus, and obtained potential Tsinghua University, China antithrombotic targets for active ingredients. We then performed gene ontology (GO) *Correspondence: enrichment analyses and KEGG signaling pathway analyses for the action targets, and Min-Li Chen – – – [email protected] constructed networks of active component target and active component target †These authors have contributed pathway for GXNT.
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Muscleblind-Like 2 Controls the Hypoxia Response of Cancer Cells
Downloaded from rnajournal.cshlp.org on September 28, 2021 - Published by Cold Spring Harbor Laboratory Press Muscleblind-like 2 controls the hypoxia response of cancer cells Sandra Fischer1, Antonella Di Liddo2, Katarzyna Taylor3, Jamina S. Gerhardus1, Krzysztof Sobczak3, Kathi Zarnack2 and Julia E. Weigand1,* 1 Department of Biology, Technical University of Darmstadt, Darmstadt, 64287, Germany 2 Buchmann Institute for Molecular Life Sciences, Goethe University Frankfurt, Frankfurt am Main, 60438, Germany 3 Department of Gene Expression, Institute of Molecular Biology and Biotechnology, Faculty of Biology, Adam Mickiewicz University, Poznan, 61-614, Poland * Correspondence should be addressed to [email protected] Running Title: MBNL2 drives hypoxia adaptation Keywords: hypoxia, cancer, MBNL2, HIF target genes, alternative splicing Abstract Hypoxia is a hallmark of solid cancers, supporting proliferation, angiogenesis and escape from apoptosis. There is still limited understanding of how cancer cells adapt to hypoxic conditions and survive. We analyzed transcriptome changes of human lung and breast cancer cells under chronic hypoxia. Hypoxia induced highly concordant changes in transcript abundance, but divergent splicing responses, underlining the cell type-specificity of alternative splicing programs. While RNA-binding proteins were predominantly reduced, hypoxia specifically induced muscleblind-like protein 2 (MBNL2). Strikingly, MBNL2 induction was critical for hypoxia adaptation by controlling the transcript abundance of hypoxia response genes, such as vascular endothelial growth factor A (VEGFA). MBNL2 depletion reduced the proliferation and migration of cancer cells, demonstrating an important role of MBNL2 as cancer driver. Hypoxia control is specific for MBNL2 and not shared by its paralog MBNL1. Thus, our study revealed MBNL2 as central mediator of cancer cell responses to hypoxia, regulating the expression and alternative splicing of hypoxia-induced genes.
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