SMARCC2 Rabbit Pab

Total Page:16

File Type:pdf, Size:1020Kb

SMARCC2 Rabbit Pab Leader in Biomolecular Solutions for Life Science SMARCC2 Rabbit pAb Catalog No.: A1967 Basic Information Background Catalog No. The protein encoded by this gene is a member of the SWI/SNF family of proteins, whose A1967 members display helicase and ATPase activities and which are thought to regulate transcription of certain genes by altering the chromatin structure around those genes. Observed MW The encoded protein is part of the large ATP-dependent chromatin remodeling complex 171kDa SNF/SWI and contains a predicted leucine zipper motif typical of many transcription factors. Alternatively spliced transcript variants encoding different isoforms have been Calculated MW found for this gene. 124kDa/126kDa/132kDa Category Primary antibody Applications WB,IHC Cross-Reactivity Human, Mouse, Rat Recommended Dilutions Immunogen Information WB 1:200 - 1:2000 Gene ID Swiss Prot 6601 Q8TAQ2 IHC 1:50 - 1:200 Immunogen A synthetic peptide corresponding to a sequence within amino acids 150-250 of human SMARCC2 (NP_620706.1). Synonyms SMARCC2;BAF170;CRACC2;Rsc8 Contact Product Information www.abclonal.com Source Isotype Purification Rabbit IgG Affinity purification Storage Store at -20℃. Avoid freeze / thaw cycles. Buffer: PBS with 0.02% sodium azide,50% glycerol,pH7.3. Validation Data Western blot analysis of extracts of various cell lines, using SMARCC2 antibody (A1967) at 1:1000 dilution._Secondary antibody: HRP Goat Anti-Rabbit IgG (H+L) (AS014) at 1:10000 dilution._Lysates/proteins: 25ug per lane._Blocking buffer: 3% nonfat dry milk in TBST._Detection: ECL Enhanced Kit (RM00021)._Exposure time: 60s. Immunohistochemistry of paraffin- Immunohistochemistry of paraffin- embedded rat kidney using SMARCC2 embedded human prostate cancer using antibody (A1967) at dilution of 1:100 (40x SMARCC2 antibody (A1967) at dilution of lens). 1:100 (40x lens). Antibody | Protein | ELISA Kits | Enzyme | NGS | Service For research use only. Not for therapeutic or diagnostic purposes. Please visit http://abclonal.com for a complete listing of recommended products..
Recommended publications
  • Statistical Analysis of the Genomic Distribution and Correlation of Regulatory Elements in the ENCODE Regions
    Downloaded from genome.cshlp.org on October 6, 2021 - Published by Cold Spring Harbor Laboratory Press Letter Statistical analysis of the genomic distribution and correlation of regulatory elements in the ENCODE regions Zhengdong D. Zhang,1 Alberto Paccanaro,2 Yutao Fu,3 Sherman Weissman,5 Zhiping Weng,3,4 Joseph Chang,6 Michael Snyder,7 and Mark B. Gerstein1,8,9 1Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, Connecticut 06520, USA; 2Department of Computer Science Royal Holloway, University of London, Egham Hill, TW20 0EX, United Kingdom; 3Bioinformatics Program, Boston University, Boston, Massachusetts 02215, USA; 4Biomedical Engineering Department, Boston University, Boston, Massachusetts 02215, USA; 5Department of Genetics, Yale University, New Haven, Connecticut 06510, USA; 6Department of Statistics, Yale University, New Haven, Connecticut 06520, USA; 7Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, Connecticut 06520, USA; 8Program in Computational Biology and Bioinformatics Yale University, New Haven, Connecticut 06520, USA The comprehensive inventory of functional elements in 44 human genomic regions carried out by the ENCODE Project Consortium enables for the first time a global analysis of the genomic distribution of transcriptional regulatory elements. In this study we developed an intuitive and yet powerful approach to analyze the distribution of regulatory elements found in many different ChIP–chip experiments on a 10∼100-kb scale. First, we focus on the overall chromosomal distribution of regulatory elements in the ENCODE regions and show that it is highly nonuniform. We demonstrate, in fact, that regulatory elements are associated with the location of known genes. Further examination on a local, single-gene scale shows an enrichment of regulatory elements near both transcription start and end sites.
    [Show full text]
  • Sox2-RNA Mechanisms of Chromosome Topological Control in Developing Forebrain
    bioRxiv preprint doi: https://doi.org/10.1101/2020.09.22.307215; this version posted September 22, 2020. 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. Title: Sox2-RNA mechanisms of chromosome topological control in developing forebrain Ivelisse Cajigas1, Abhijit Chakraborty2, Madison Lynam1, Kelsey R Swyter1, Monique Bastidas1, Linden Collens1, Hao Luo1, Ferhat Ay2,3, Jhumku D. Kohtz1,4 1Department of Pediatrics, Northwestern University, Feinberg School of Medicine, Department of Human Molecular Genetics, Stanley Manne Children's Research Institute 2430 N Halsted, Chicago, IL 60614 2Centers for Autoimmunity and Cancer Immunotherapy, La Jolla Institute for Immunology, 9420 Athena Circle, La Jolla, CA, 92037, USA 3School of Medicine, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA 4To whom correspondence should be addressed: [email protected] 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.09.22.307215; this version posted September 22, 2020. 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. Summary Precise regulation of gene expression networks requires the selective targeting of DNA enhancers. The Evf2 long non-coding RNA regulates Dlx5/6 ultraconserved enhancer(UCE) interactions with long-range target genes, controlling gene expression over a 27Mb region in mouse developing forebrain. Here, we show that Evf2 long range gene repression occurs through multi-step mechanisms involving the transcription factor Sox2, a component of the Evf2 ribonucleoprotein complex (RNP).
    [Show full text]
  • Epidyne®-FRET for Nucleosome Remodeling Assays
    Nucleosome Remodeling Assay by EpiDyne®-FRET EpiDyne®-FRET allows unprecedented access to disease-relevant ATP-dependent chromatin remodeling complexes FIGURE 3 SMARCA 2 SMARCA 4 EpiDyne®-FRET nucleosomes (20 nM) were incubated with Figure 3A Figure 3B chromatin remodeling enzyme (Panel 3A, SMARCA2; panel 3B, SMARCA4) at the indicated concentration in 4.0 3.5 the presence of ATP (2 mM). 3.5 Upon ATP addition, reactions 3.0 were immediately read in 3.0 an Envision Multi-label plate 2.5 reader. Data are presented as 2.5 the mean of the Cy3-Cy5 ratio 2.0 (N=2). 2.0 1.5 Cy3/Cy5 Ratio Cy3/Cy5 1.5 Ratio Cy3/Cy5 1.0 1.0 0 1 2 3 4 5 6 7 8 9 10 0 10 20 30 40 Time, Min Time, Min nM Enzyme nM Enzyme 28 14 7 3.5 0.0 12.50 6.25 3.13 1.56 0 ORDERING INFO Chromatin Remodeling Substrate, Fluorescent Readout Enzymes EpiDyne®-FRET Nucleosome Remodeling Assay Substrate SMARCA2 Chromatin Remodeling Enzyme Catalog No. 16-4201 (Human BRM) Pack Size: 50 μg Catalog No. 15-1015 Pack Size: 100 remodeling rxns Chromatin Remodeling Substrates, Non-Fluorescent Readout SMARCA4 Chromatin Remodeling Enzyme (Human BRG1) ST601-GATC1 ST601-GATC1, 50-N-66, Biotinylated Catalog No. 15-1014 Cat. No. 16-4101 Cat. No.: 16-4114 Pack Size: 100 remodeling rxns Pack Size: 50 μg Pack Size: 50 μg ACF Chromatin Remodeling Enzyme Complex ST601-GATC1, Biotinylated ST601-GATC1,2, 50-N-66, Biotinylated Catalog No. 15-1013 Cat.
    [Show full text]
  • Intrinsic Disorder of the BAF Complex: Roles in Chromatin Remodeling and Disease Development
    International Journal of Molecular Sciences Article Intrinsic Disorder of the BAF Complex: Roles in Chromatin Remodeling and Disease Development Nashwa El Hadidy 1 and Vladimir N. Uversky 1,2,* 1 Department of Molecular Medicine, Morsani College of Medicine, University of South Florida, 12901 Bruce B. Downs Blvd. MDC07, Tampa, FL 33612, USA; [email protected] 2 Laboratory of New Methods in Biology, Institute for Biological Instrumentation of the Russian Academy of Sciences, Federal Research Center “Pushchino Scientific Center for Biological Research of the Russian Academy of Sciences”, Pushchino, 142290 Moscow Region, Russia * Correspondence: [email protected]; Tel.: +1-813-974-5816; Fax: +1-813-974-7357 Received: 20 September 2019; Accepted: 21 October 2019; Published: 23 October 2019 Abstract: The two-meter-long DNA is compressed into chromatin in the nucleus of every cell, which serves as a significant barrier to transcription. Therefore, for processes such as replication and transcription to occur, the highly compacted chromatin must be relaxed, and the processes required for chromatin reorganization for the aim of replication or transcription are controlled by ATP-dependent nucleosome remodelers. One of the most highly studied remodelers of this kind is the BRG1- or BRM-associated factor complex (BAF complex, also known as SWItch/sucrose non-fermentable (SWI/SNF) complex), which is crucial for the regulation of gene expression and differentiation in eukaryotes. Chromatin remodeling complex BAF is characterized by a highly polymorphic structure, containing from four to 17 subunits encoded by 29 genes. The aim of this paper is to provide an overview of the role of BAF complex in chromatin remodeling and also to use literature mining and a set of computational and bioinformatics tools to analyze structural properties, intrinsic disorder predisposition, and functionalities of its subunits, along with the description of the relations of different BAF complex subunits to the pathogenesis of various human diseases.
    [Show full text]
  • Residual Complexes Containing SMARCA2 (BRM) Underlie the Oncogenic Drive of SMARCA4 (BRG1) Mutation
    Residual Complexes Containing SMARCA2 (BRM) Underlie the Oncogenic Drive of SMARCA4 (BRG1) Mutation The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Wilson, B. G., K. C. Helming, X. Wang, Y. Kim, F. Vazquez, Z. Jagani, W. C. Hahn, and C. W. M. Roberts. 2014. “Residual Complexes Containing SMARCA2 (BRM) Underlie the Oncogenic Drive of SMARCA4 (BRG1) Mutation.” Molecular and Cellular Biology 34 (6): 1136–44. doi:10.1128/MCB.01372-13. Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:41542741 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA Residual Complexes Containing SMARCA2 (BRM) Underlie the Oncogenic Drive of SMARCA4 (BRG1) Mutation Boris G. Wilson,a Katherine C. Helming,a Xiaofeng Wang,a Youngha Kim,a Francisca Vazquez,c,d Zainab Jagani,f William C. Hahn,c,d,e Charles W. M. Robertsa,b,d,e Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USAa; Division of Hematology/Oncology, Boston Children’s Hospital, Boston, Massachusetts, USAb; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USAc; Cancer Program, Broad Institute of Harvard and Massachusetts Institute of Technology, Boston, Massachusetts, USAd; Center for Cancer Genome Discovery, Dana-Farber Cancer Institute, Boston, Massachusetts, USAe; Novartis Institutes for BioMedical Research, Cambridge, Massachusetts, USAf Collectively, genes encoding subunits of the SWI/SNF (BAF) chromatin remodeling complex are mutated in 20% of all human Downloaded from cancers, with the SMARCA4 (BRG1) subunit being one of the most frequently mutated.
    [Show full text]
  • Autism and Cancer Share Risk Genes, Pathways, and Drug Targets
    TIGS 1255 No. of Pages 8 Forum Table 1 summarizes the characteristics of unclear whether this is related to its signal- Autism and Cancer risk genes for ASD that are also risk genes ing function or a consequence of a second for cancers, extending the original finding independent PTEN activity, but this dual Share Risk Genes, that the PI3K-Akt-mTOR signaling axis function may provide the rationale for the (involving PTEN, FMR1, NF1, TSC1, and dominant role of PTEN in cancer and Pathways, and Drug TSC2) was associated with inherited risk autism. Other genes encoding common Targets for both cancer and ASD [6–9]. Recent tumor signaling pathways include MET8[1_TD$IF],[2_TD$IF] genome-wide exome-sequencing studies PTK7, and HRAS, while p53, AKT, mTOR, Jacqueline N. Crawley,1,2,* of de novo variants in ASD and cancer WNT, NOTCH, and MAPK are compo- Wolf-Dietrich Heyer,3,4 and have begun to uncover considerable addi- nents of signaling pathways regulating Janine M. LaSalle1,4,5 tional overlap. What is surprising about the the nuclear factors described above. genes in Table 1 is not necessarily the Autism is a neurodevelopmental number of risk genes found in both autism Autism is comorbid with several mono- and cancer, but the shared functions of genic neurodevelopmental disorders, disorder, diagnosed behaviorally genes in chromatin remodeling and including Fragile X (FMR1), Rett syndrome by social and communication genome maintenance, transcription fac- (MECP2), Phelan-McDermid (SHANK3), fi de cits, repetitive behaviors, tors, and signal transduction pathways 15q duplication syndrome (UBE3A), and restricted interests. Recent leading to nuclear changes [7,8].
    [Show full text]
  • Table S1. 103 Ferroptosis-Related Genes Retrieved from the Genecards
    Table S1. 103 ferroptosis-related genes retrieved from the GeneCards. Gene Symbol Description Category GPX4 Glutathione Peroxidase 4 Protein Coding AIFM2 Apoptosis Inducing Factor Mitochondria Associated 2 Protein Coding TP53 Tumor Protein P53 Protein Coding ACSL4 Acyl-CoA Synthetase Long Chain Family Member 4 Protein Coding SLC7A11 Solute Carrier Family 7 Member 11 Protein Coding VDAC2 Voltage Dependent Anion Channel 2 Protein Coding VDAC3 Voltage Dependent Anion Channel 3 Protein Coding ATG5 Autophagy Related 5 Protein Coding ATG7 Autophagy Related 7 Protein Coding NCOA4 Nuclear Receptor Coactivator 4 Protein Coding HMOX1 Heme Oxygenase 1 Protein Coding SLC3A2 Solute Carrier Family 3 Member 2 Protein Coding ALOX15 Arachidonate 15-Lipoxygenase Protein Coding BECN1 Beclin 1 Protein Coding PRKAA1 Protein Kinase AMP-Activated Catalytic Subunit Alpha 1 Protein Coding SAT1 Spermidine/Spermine N1-Acetyltransferase 1 Protein Coding NF2 Neurofibromin 2 Protein Coding YAP1 Yes1 Associated Transcriptional Regulator Protein Coding FTH1 Ferritin Heavy Chain 1 Protein Coding TF Transferrin Protein Coding TFRC Transferrin Receptor Protein Coding FTL Ferritin Light Chain Protein Coding CYBB Cytochrome B-245 Beta Chain Protein Coding GSS Glutathione Synthetase Protein Coding CP Ceruloplasmin Protein Coding PRNP Prion Protein Protein Coding SLC11A2 Solute Carrier Family 11 Member 2 Protein Coding SLC40A1 Solute Carrier Family 40 Member 1 Protein Coding STEAP3 STEAP3 Metalloreductase Protein Coding ACSL1 Acyl-CoA Synthetase Long Chain Family Member 1 Protein
    [Show full text]
  • Integrative Framework for Identification of Key Cell Identity Genes Uncovers
    Integrative framework for identification of key cell PNAS PLUS identity genes uncovers determinants of ES cell identity and homeostasis Senthilkumar Cinghua,1, Sailu Yellaboinaa,b,c,1, Johannes M. Freudenberga,b, Swati Ghosha, Xiaofeng Zhengd, Andrew J. Oldfielda, Brad L. Lackfordd, Dmitri V. Zaykinb, Guang Hud,2, and Raja Jothia,b,2 aSystems Biology Section and dStem Cell Biology Section, Laboratory of Molecular Carcinogenesis, and bBiostatistics Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709; and cCR Rao Advanced Institute of Mathematics, Statistics, and Computer Science, Hyderabad, Andhra Pradesh 500 046, India Edited by Norbert Perrimon, Harvard Medical School and Howard Hughes Medical Institute, Boston, MA, and approved March 17, 2014 (received for review October 2, 2013) Identification of genes associated with specific biological pheno- (mESCs) for genes essential for the maintenance of ESC identity types is a fundamental step toward understanding the molecular resulted in only ∼8% overlap (8, 9), although many of the unique basis underlying development and pathogenesis. Although RNAi- hits in each screen were known or later validated to be real. The based high-throughput screens are routinely used for this task, lack of concordance suggest that these screens have not reached false discovery and sensitivity remain a challenge. Here we describe saturation (14) and that additional genes of importance remain a computational framework for systematic integration of published to be discovered. gene expression data to identify genes defining a phenotype of Motivated by the need for an alternative approach for iden- interest. We applied our approach to rank-order all genes based on tification of key cell identity genes, we developed a computa- their likelihood of determining ES cell (ESC) identity.
    [Show full text]
  • A Molecular Model for Neurodevelopmental Disorders
    OPEN Citation: Transl Psychiatry (2015) 5, e565; doi:10.1038/tp.2015.56 www.nature.com/tp ORIGINAL ARTICLE A molecular model for neurodevelopmental disorders CO Gigek1,2, ES Chen1,2,VKOta1, G Maussion, H Peng, K Vaillancourt, AB Diallo, JP Lopez, L Crapper, C Vasuta, GG Chen and C Ernst Genes implicated in neurodevelopmental disorders (NDDs) important in cognition and behavior may have convergent function and several cellular pathways have been implicated, including protein translational control, chromatin modification, and synapse assembly and maintenance. Here, we test the convergent effects of methyl-CpG binding domain 5 (MBD5) and special AT-rich binding protein 2 (SATB2) reduced dosage in human neural stem cells (NSCs), two genes implicated in 2q23.1 and 2q33.1 deletion syndromes, respectively, to develop a generalized model for NDDs. We used short hairpin RNA stably incorporated into healthy neural stem cells to supress MBD5 and SATB2 expression, and massively parallel RNA sequencing, DNA methylation sequencing and microRNA arrays to test the hypothesis that a primary etiology of NDDs is the disruption of the balance of NSC proliferation and differentiation. We show that reduced dosage of either gene leads to significant overlap of gene-expression patterns, microRNA patterns and DNA methylation states with control NSCs in a differentiating state, suggesting that a unifying feature of 2q23.1 and 2q33.1 deletion syndrome may be a lack of regulation between proliferation and differentiation in NSCs, as we observed previously for TCF4 and EHMT1 suppression following a similar experimental paradigm. We propose a model of NDDs whereby the balance of NSC proliferation and differentiation is affected, but where the molecules that drive this effect are largely specific to disease-causing genetic variation.
    [Show full text]
  • Genome-Wide Association Study Reveals First Locus for Anorexia Nervosa and Metabolic Correlations
    bioRxiv preprint doi: https://doi.org/10.1101/088815; this version posted November 25, 2016. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Genome-Wide Association Study Reveals First Locus for Anorexia Nervosa and Metabolic Correlations Authors Duncan, E.L.* ... 210 additional authors Thornton, L.M. Hinney, A. Daly, M.J. Sullivan, P.F. Zeggini, E. Breen, G. Bulik, C.M.* * Corresponding authors Abstract Anorexia nervosa (AN) is a serious eating disorder characterized by restriction of energy intake relative to requirements, resulting in abnormally low body weight. It has a lifetime prevalence of approximately 1%, disproportionately affects females1,2, and has no well replicated evidence of effective pharmacological or psychological treatments despite high morbidity and mortality2. Twin studies support a genetic basis for the observed aggregation of AN in families3, with heritability estimates of 48%-74%4. Although initial genome-wide association studies (GWASs) were underpowered5,6, evidence suggested that signals for AN would be detected with increased power5. We present a GWAS of 3,495 AN cases and 10,982 controls with one genome-wide significant locus (index variant rs4622308, p=4.3x10-9) in a region (chr12:56,372,585- % 56,482,185) which includes six genes. The SNP-chip heritability (h"#$) of AN from these data is 0.20 (SE=0.02), suggesting that a substantial fraction of the twin-based heritability stems from common genetic variation.
    [Show full text]
  • Interactome Analyses Revealed That the U1 Snrnp Machinery Overlaps
    www.nature.com/scientificreports OPEN Interactome analyses revealed that the U1 snRNP machinery overlaps extensively with the RNAP II Received: 12 April 2018 Accepted: 24 May 2018 machinery and contains multiple Published: xx xx xxxx ALS/SMA-causative proteins Binkai Chi1, Jeremy D. O’Connell1,2, Tomohiro Yamazaki1, Jaya Gangopadhyay1, Steven P. Gygi1 & Robin Reed1 Mutations in multiple RNA/DNA binding proteins cause Amyotrophic Lateral Sclerosis (ALS). Included among these are the three members of the FET family (FUS, EWSR1 and TAF15) and the structurally similar MATR3. Here, we characterized the interactomes of these four proteins, revealing that they largely have unique interactors, but share in common an association with U1 snRNP. The latter observation led us to analyze the interactome of the U1 snRNP machinery. Surprisingly, this analysis revealed the interactome contains ~220 components, and of these, >200 are shared with the RNA polymerase II (RNAP II) machinery. Among the shared components are multiple ALS and Spinal muscular Atrophy (SMA)-causative proteins and numerous discrete complexes, including the SMN complex, transcription factor complexes, and RNA processing complexes. Together, our data indicate that the RNAP II/U1 snRNP machinery functions in a wide variety of molecular pathways, and these pathways are candidates for playing roles in ALS/SMA pathogenesis. Te neurodegenerative disease Amyotrophic Lateral Sclerosis (ALS) has no known treatment, and elucidation of disease mechanisms is urgently needed. Tis problem has been especially daunting, as mutations in greater than 30 genes are ALS-causative, and these genes function in numerous cellular pathways1. Tese include mitophagy, autophagy, cytoskeletal dynamics, vesicle transport, DNA damage repair, RNA dysfunction, apoptosis, and pro- tein aggregation2–6.
    [Show full text]
  • Dynamic BAF Chromatin Remodeling Complex Subunit Inclusion Promotes Temporally Distinct Gene Expression Programs in Cardiogenesis Swetansu K
    First posted online on 27 February 2019 as 10.1242/dev.174086 Access the most recent version at http://dev.biologists.org/lookup/doi/10.1242/dev.174086 © 2019. Published by The Company of Biologists Ltd | Development (2019) 146, dev174086. doi:10.1242/dev.174086 STEM CELLS AND REGENERATION RESEARCH ARTICLE Dynamic BAF chromatin remodeling complex subunit inclusion promotes temporally distinct gene expression programs in cardiogenesis Swetansu K. Hota1,2, Jeffrey R. Johnson1,3, Erik Verschueren1,3, Reuben Thomas1, Aaron M. Blotnick1,2, Yiwen Zhu4,5, Xin Sun6, Len A. Pennacchio4,5, Nevan J. Krogan1,3 and Benoit G. Bruneau1,2,7,8,* ABSTRACT differentiation proceeds as a gradually increasing specification of cell Chromatin remodeling complexes instruct cellular differentiation fates (Moris et al., 2016). Delineating the factors that control crucial and lineage specific transcription. The BRG1/BRM-associated developmental decision points is essential to understand the control factor (BAF) complexes are important for several aspects of of gene regulation during differentiation and development. differentiation. We show that the catalytic subunit gene Brg1 has a Transcription factor (TF) activity regulates transcriptional output, specific role in cardiac precursors (CPs) to initiate cardiac gene and is intimately influenced by the underlying chromatin. expression programs and repress non-cardiac expression. Using Chromatin remodeling complexes are multi-subunit protein immunopurification with mass spectrometry, we have determined the complexes that alter histone-DNA contact in nucleosomes to dynamic composition of BAF complexes during mammalian cardiac reorganize chromatin and regulate transcription (Bartholomew, differentiation, identifying several cell-type specific subunits. We 2014; Clapier and Cairns, 2009; Zhou et al., 2016).
    [Show full text]