SMARCA1 Rabbit Pab

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Leader in Biomolecular Solutions for Life Science SMARCA1 Rabbit pAb Catalog No.: A10248 Basic Information Background Catalog No. This gene encodes a member of the SWI/SNF family of proteins. The encoded protein is A10248 an ATPase which is expressed in diverse tissues and contributes to the chromatin remodeling complex that is involved in transcription. The protein may also play a role in Observed MW DNA damage, growth inhibition and apoptosis of cancer cells. Alternative splicing 140kDa results in multiple transcript variants. Calculated MW 121kDa/122kDa Category Primary antibody Applications WB, IHC Cross-Reactivity Human, Mouse, Rat Recommended Dilutions Immunogen Information WB 1:1000 - 1:2000 Gene ID Swiss Prot 6594 P28370 IHC 1:50 - 1:200 Immunogen Recombinant fusion protein containing a sequence corresponding to amino acids 1-200 of human SMARCA1 (NP_003060.2). Synonyms SMARCA1;ISWI;NURF140;SNF2L;SNF2L1;SNF2LB;SNF2LT;SWI;SWI2;hSNF2L Contact Product Information 400-999-6126 Source Isotype Purification Rabbit IgG Affinity purification [email protected] www.abclonal.com.cn 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 SMARCA1 antibody (A10248) 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 Basic Kit (RM00020). Exposure time: 15s. Immunohistochemistry of paraffin- Immunohistochemistry of paraffin- embedded human lung cancer using embedded human esophageal cancer SMARCA1 Rabbit pAb (A10248) at dilution using SMARCA1 Rabbit pAb (A10248) at of 1:100 (40x lens). dilution of 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..

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SMARCA1 Antibody A
Revision 1 C 0 2 - t SMARCA1 Antibody a e r o t S Orders: 877-616-CELL (2355) [email protected] Support: 877-678-TECH (8324) 0 5 Web: [email protected] 4 www.cellsignal.com 9 # 3 Trask Lane Danvers Massachusetts 01923 USA For Research Use Only. Not For Use In Diagnostic Procedures. Applications: Reactivity: Sensitivity: MW (kDa): Source: UniProt ID: Entrez-Gene Id: WB, IP H Endogenous 130 Rabbit P28370 6594 Product Usage Information 5. Ho, L. and Crabtree, G.R. (2010) Nature 463, 474-84. 6. Landry, J.W. et al. (2011) Genes Dev 25, 275-86. Application Dilution 7. Landry, J. et al. (2008) PLoS Genet 4, e1000241. Western Blotting 1:1000 Immunoprecipitation 1:50 Storage Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody. Specificity / Sensitivity SMARCA1 Antibody recognizes endogenous levels of total SMARCA1 protein. Species Reactivity: Human Source / Purification Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human SMARCA1 protein. Antibodies are purified by protein A and peptide affinity chromatography. Background SMARCA1 (SNF2L) is one of the two orthologs of the ISWI (imitation switch) ATPases encoded by the mammalian genome (1). The ISWI chromatin remodeling complexes were first identified in Drosophila and have been shown to remodel and alter nucleosome spacing in vitro (2). SMARCA1 is the catalytic subunit of the nucleosome remodeling factor (NURF) and CECR2-containing remodeling factor (CERF) complexes (3-5).
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Monoclonal Antibody to SMARCA1
AM50455PU-N OriGene Technologies Inc. OriGene EU Acris Antibodies GmbH 9620 Medical Center Drive, Ste 200 Schillerstr. 5 Rockville, MD 20850 32052 Herford UNITED STATES GERMANY Phone: +1-888-267-4436 Phone: +49-5221-34606-0 Fax: +1-301-340-8606 Fax: +49-5221-34606-11 [email protected] [email protected] Monoclonal Antibody to SMARCA1 - Purified Alternate names: ATP-dependent helicase SMARCA1, Nucleosome-remodeling factor subunit SNF2L, Probable global transcription activator SNF2L1, SNF2L, SNF2L1, SWI/SNF-related matrix- associated actin-dependent regulator of chromatin subfamily A member 1 Catalog No.: AM50455PU-N Quantity: 0.1 mg Concentration: lot-specific Background: Nucleosome-remodeling factor subunit SNF2L, also known as SWI/SNF-related matrix- associated actin-dependent regulator of chromatin subfamily A member 1 (SMARCA1), is the energy-transducing component of NURF (nucleosome-remodeling factor) and CERF (CECR2-containing-remodeling factor) complexes. These complexes facilitate the disruption of chromatin structure in an ATP-dependent manner. SNF2L potentiates neurite outgrowth, and may be involved in brain development by regulating En-1 and En-2 expression as well as in the development of luteal cells. Uniprot ID: P28370 NCBI: NP_003060.2 GeneID: 6594 Host / Isotype: Rat / IgG2b Clone: SNF 2C4 Immunogen: GST-tagged recombinant protein corresponding to human SNF2L. Format: State: Liquid purified Ig fraction Purification: Protein G Chromatography Buffer System: 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide. Applications: Immunohistochemistry: A representative lot was used by an an independent laboratory to detect SNF2L in certain, normal human organ tissues. (Eckey, M., et al.
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SMARCA1 (D4Q7V) Rabbit
SMARCA1 (D4Q7V) Rabbit mAb Store at -20°C 3 n 100 µl Orders n 877-616-CELL (2355) (10 western blots) [email protected] Support n 877-678-TECH (8324) [email protected] Web n www.cellsignal.com New 03/13 #12483 For Research Use Only. Not For Use In Diagnostic Procedures. Entrez-Gene ID #6594 Swiss-Prot Acc. #P28370 Storage: Supplied in 10 mM sodium HEPES (pH 7.5), 150 Applications Species Cross-Reactivity* Molecular Wt. Isotype mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% W, IP H, Mk 130 kDa Rabbit IgG** sodium azide. Store at –20°C. Do not aliquot the antibody. Endogenous *Species cross-reactivity is determined by western blot. Background: SMARCA1 (SNF2L) is one of the two ortho- ** Anti-rabbit secondary antibodies must be used to logs of the ISWI (imitation switch) ATPases encoded by the detect this antibody. kDa LN18 SW620 HeLa HT-29 Saos-2 OVCAR8COS-7 mammalian genome (1). The ISWI chromatin remodeling Recommended Antibody Dilutions: complexes were first identified in Drosophila and have been 200 140 Western blotting 1:1000 shown to remodel and alter nucleosome spacing in vitro (2). SMARCA1 100 Immunoprecipitation 1:100 SMARCA1 is the catalytic subunit of the nucleosome re- 80 modeling factor (NURF) and CECR2-containing remodeling For product specific protocols please see the web page 60 factor (CERF) complexes (3-5). The NURF complex plays an 50 for this product at www.cellsignal.com. important role in neuronal physiology by promoting neurite 40 Please visit www.cellsignal.com for a complete listing outgrowth and regulation of Engrailed homeotic genes that 30 of recommended complementary products.
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Contribution of Multiple Inherited Variants to Autism Spectrum Disorder (ASD) in a Family with 3 Affected Siblings
G C A T T A C G G C A T genes Article Contribution of Multiple Inherited Variants to Autism Spectrum Disorder (ASD) in a Family with 3 Affected Siblings Jasleen Dhaliwal 1 , Ying Qiao 1,2, Kristina Calli 1,2, Sally Martell 1,2, Simone Race 3,4,5, Chieko Chijiwa 1,5, Armansa Glodjo 3,5, Steven Jones 1,6 , Evica Rajcan-Separovic 2,7, Stephen W. Scherer 4 and Suzanne Lewis 1,2,5,* 1 Department of Medical Genetics, University of British Columbia (UBC), Vancouver, BC V6H 3N1, Canada; [email protected] (J.D.); [email protected] (Y.Q.); [email protected] (K.C.); [email protected] (S.M.); [email protected] (C.C.); [email protected] (S.J.) 2 BC Children’s Hospital, Vancouver, BC V5Z 4H4, Canada; [email protected] 3 Department of Pediatrics, University of British Columbia (UBC), Vancouver, BC V6T 1Z7, Canada; [email protected] (S.R.); [email protected] (A.G.) 4 The Centre for Applied Genomics and McLaughlin Centre, Hospital for Sick Children and University of Toronto, Toronto, ON M5G 0A4, Canada; [email protected] 5 BC Children’s and Women’s Health Center, Vancouver, BC V6H 3N1, Canada 6 Michael Smith Genome Sciences Centre, Vancouver, BC V5Z 4S6, Canada 7 Department of Pathology and Laboratory Medicine, University of British Columbia (UBC), Vancouver, BC V6T 1Z7, Canada * Correspondence: [email protected] Abstract: Autism Spectrum Disorder (ASD) is the most common neurodevelopmental disorder in Citation: Dhaliwal, J.; Qiao, Y.; Calli, children and shows high heritability.
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Small Cell Carcinoma of the Ovary, Hypercalcemic Type (SCCOHT) Beyond SMARCA4 Mutations: a Comprehensive Genomic Analysis
cells Article Small Cell Carcinoma of the Ovary, Hypercalcemic Type (SCCOHT) beyond SMARCA4 Mutations: A Comprehensive Genomic Analysis Aurélie Auguste 1,Félix Blanc-Durand 2 , Marc Deloger 3 , Audrey Le Formal 1, Rohan Bareja 4,5, David C. Wilkes 4 , Catherine Richon 6,Béatrice Brunn 2, Olivier Caron 6, Mojgan Devouassoux-Shisheboran 7,Sébastien Gouy 2, Philippe Morice 2, Enrica Bentivegna 2, Andrea Sboner 4,5,8, Olivier Elemento 4,8, Mark A. Rubin 9 , Patricia Pautier 2, Catherine Genestie 10, Joanna Cyrta 4,9,11 and Alexandra Leary 1,2,* 1 Medical Oncologist, Gynecology Unit, Lead Translational Research Team, INSERM U981, Gustave Roussy, 94805 Villejuif, France; [email protected] (A.A.); [email protected] (A.L.F.) 2 Gynecological Unit, Department of Medicine, Gustave Roussy, 94805 Villejuif, France; [email protected] (F.B.-D.); [email protected] (B.B.); [email protected] (S.G.); [email protected] (P.M.); [email protected] (E.B.); [email protected] (P.P.) 3 Bioinformatics Core Facility, Gustave Roussy Cancer Center, UMS CNRS 3655/INSERM 23 AMMICA, 94805 Villejuif, France; [email protected] 4 Caryl and Israel Englander Institute for Precision Medicine, Weill Cornell Medicine, New York, NY 10001, USA; [email protected] (R.B.); [email protected] (D.C.W.); [email protected] (A.S.); [email protected] (O.E.); [email protected] (J.C.) 5 Institute for Computational Biomedicine, Weill Cornell
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6476 Vol. 9, 6476–6482, December 15, 2003 Clinical Cancer Research Frequent Loss of Heterozygosity Targeting the Inactive X Chromosome in Melanoma James O. Indsto,1 Najah T. Nassif,2 INTRODUCTION Richard F. Kefford,1 and Graham J. Mann1 Chromosomal deletions and amplification events are fre- 1Westmead Institute for Cancer Research, University of Sydney at quent in advanced neoplasms and provide evidence for the Westmead Millennium Institute, Westmead, New South Wales, existence and location of putative tumor suppressor genes Australia, and 2Department of Cell and Molecular Biology, University (TSGs) and oncogenes. In melanoma, 9p and 10q deletions are of Technology, Sydney, New South Wales, Australia most frequent, and losses on 6q, 11q, 1p, 15p, 17q, and 18q are also frequently found (1, 2). However, no studies have focused on the X chromosome. In the human female, random inactiva- ABSTRACT tion of one copy of an X chromosome by hypermethylation is an After previous preliminary observations of paradoxical early event in embryogenesis, resulting in most tissues being a deletion events affecting the inactive X chromosome in mel- mosaic in terms of X inactivation status. Neoplasms, being anoma, we have surveyed the X chromosome for deletions clonal expansions of single precursor cells, usually share a using 23 polymorphic microsatellite markers in 28 inform- common X inactivation status. This can be conveniently assayed ative (female XX) metastatic melanomas. Ten tumors (36%) using the methylation-sensitive restriction enzyme HpaII, which showed at least one loss of heterozygosity (LOH) event, and has a recognition site within the highly polymorphic exon 1 in two cases an entire chromosome showed LOH at all CAG repeat (ARTR) in the androgen receptor (AR) gene.
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The H3K9 Methylation Writer SETDB1 and Its Reader MPP8 Cooperate to Silence Satellite DNA Repeats in Mouse Embryonic Stem Cells
G C A T T A C G G C A T genes Article The H3K9 Methylation Writer SETDB1 and Its Reader MPP8 Cooperate to Silence Satellite DNA Repeats in Mouse Embryonic Stem Cells 1,2,3,4 1 1, 1 Paola Cruz-Tapias , Philippe Robin , Julien Pontis y, Laurence Del Maestro and Slimane Ait-Si-Ali 1,* 1 Epigenetics and Cell Fate (EDC), Centre National de la Recherche Scientiﬁque (CNRS), Université de Paris, Université Paris Diderot, F-75013 Paris, France; [email protected] (P.C.-T.); [email protected] (P.R.); julien.pontis@epﬂ.ch (J.P.); [email protected] (L.D.M.) 2 Faculty of Natural Sciences and Mathematics, Universidad del Rosario, Bogotá 111221, Colombia 3 School of Medicine and Health Sciences, Universidad del Rosario, Bogotá 111221, Colombia 4 Doctoral Program in Biomedical and Biological Sciences, Universidad del Rosario, Bogotá 111221, Colombia * Correspondence: [email protected]; Tel.: +33-(0)1-5727-8919 Current: Ecole Polytechnique Fédérale de Lausanne (EPFL), SV LVG Station 19, 1015 Lausanne, Switzerland. y Received: 25 August 2019; Accepted: 24 September 2019; Published: 25 September 2019 Abstract: SETDB1 (SET Domain Bifurcated histone lysine methyltransferase 1) is a key lysine methyltransferase (KMT) required in embryonic stem cells (ESCs), where it silences transposable elements and DNA repeats via histone H3 lysine 9 tri-methylation (H3K9me3), independently of DNA methylation. The H3K9 methylation reader M-Phase Phosphoprotein 8 (MPP8) is highly expressed in ESCs and germline cells. Although evidence of a cooperation between H3K9 KMTs and MPP8 in committed cells has emerged, the interplay between H3K9 methylation writers and MPP8 in ESCs remains elusive.
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Multiple Epigenetic Modifiers Induce Aggressive Viral Extinction
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Cell Stem Cell Article Multiple Epigenetic Modifiers Induce Aggressive Viral Extinction in Extraembryonic Endoderm Stem Cells Michael C. Golding,1,2,3,4 Liyue Zhang,3,5 and Mellissa R.W. Mann1,2,3,5,* 1Department of Obstetrics & Gynecology 2Department of Biochemistry University of Western Ontario, Schulich School of Medicine and Dentistry, London, Ontario N6A 4V2, Canada 3Children’s Health Research Institute, London, Ontario N6C 2V5, Canada 4Department of Veterinary Physiology, College of Veterinary Medicine, Texas A&M University, College Station, TX 77843, USA 5Lawson Health Research Institute, London, Ontario N6C 2V5, Canada *Correspondence: [email protected] DOI 10.1016/j.stem.2010.03.014 SUMMARY 5a (TRIM5a), zinc finger antiviral protein (ZAP), TRIM19/PML (promyelocytic leukemia), and the TRIM28-ZFP809 (zinc finger To prevent insertional mutagenesis arising from antiviral protein 809) complex all restrict retroviral tropism via retroviral reactivation, cells of embryonic origin direct biochemical interactions (Best et al., 1996; Kaiser et al., possess a unique capacity to silence retroviruses. 2007; Gao et al., 2002; Turelli et al., 2001; Wolf and Goff, 2009; Given the distinct modes of X chromosome inactiva- Rowe et al., 2010). tion between embryonic and extraembryonic line- Less well understood is the process of retroviral extinction, ages, we investigated paradigms of viral extinction. which is progressive silencing of proviral transcription that occurs over long-term cellular growth or differentiation (Cherry We show that trophectoderm stem cells do not et al., 2000; Laker et al., 1998).
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X-Inactivation in Female Human Embryonic Stem Cells Is in a Nonrandom Pattern and Prone to Epigenetic Alterations
X-inactivation in female human embryonic stem cells is in a nonrandom pattern and prone to epigenetic alterations Yin Shen*, Youko Matsuno†, Shaun D. Fouse*, Nagesh Rao‡, Sierra Root§, Renhe Xu§, Matteo Pellegrini¶, Arthur D. Riggs†ʈ, and Guoping Fan*ʈ *Department of Human Genetics, Geffen School of Medicine, and Departments of ‡Pathology and Laboratory Medicine and ¶Molecular Cell and Developmental Biology, University of California, Los Angeles, CA 90095; †Division of Biology, Beckman Research Institute of the City of Hope, Duarte, CA 91010; and §Department of Genetics and Development, University of Connecticut Health Center, Farmington, CT 06032 Contributed by Arthur D. Riggs, December 21, 2007 (sent for review December 6, 2007) X chromosome inactivation (XCI) is an essential mechanism for dosage compensation of X-linked genes in female cells. We report that subcultures from lines of female human embryonic stem cells (hESCs) exhibit variation (0–100%) for XCI markers, including XIST RNA expression and enrichment of histone H3 lysine 27 trimethylation (H3K27me3) on the inactive X chromosome (Xi). Surprisingly, regard- less of the presence or absence of XCI markers in different cultures, all female hESCs we examined (H7, H9, and HSF6 cells) exhibit a monoallelic expression pattern for a majority of X-linked genes. Our results suggest that these established female hESCs have already completed XCI during the process of derivation and/or propagation, and the XCI pattern of lines we investigated is already not random. Moreover, XIST gene expression in subsets of cultured female hESCs is unstable and subject to stable epigenetic silencing by DNA meth- ylation. In the absence of XIST expression, Ϸ12% of X-linked pro- moter CpG islands become hypomethylated and a portion of X-linked alleles on the Xi are reactivated.
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Epigenetic Modulation of the Tumor Immune Microenvironment to Potentiate Immune Checkpoint Blockade Therapy Johannes Menzel and Joshua C
VIEWS IN THE SPOTLIGHT Epigenetic Modulation of the Tumor Immune Microenvironment to Potentiate Immune Checkpoint Blockade Therapy Johannes Menzel and Joshua C. Black Summary: Response rates to immune checkpoint blockade (ICB) in KRAS-mutant lung adenocarcinoma remain poor. In this issue of Cancer Discovery , Li and colleagues report an in vivo CRISPR screen of epigenetic regula- tors of the tumor immune microenvironment that uncovers Asf1a as a tumor-intrinsic suppressor of ICB through suppression of GM-CSF expression. See related article by Li et al., p. 270 (3). Lung adenocarcinoma is a leading cause of cancer-related would potentiate the effects of anti–PD-1 immunotherapy. death worldwide. Mutations in KRAS or EGFR are both Using this approach, the authors identifi ed that knockout major oncogenic drivers of lung cancer. Patients harboring (KO) of the histone H3-H4 chaperone Asf1a in the KP adeno- EGFR mutations can benefi t from EGFR tyrosine kinase carcinoma cells sensitizes the tumor to checkpoint blockade. inhibitors, but, despite the development of allele-specifi c Intriguingly, Asf1a knockout in the KP lung tumor cells KRAS G12C inhibitors, patients harboring KRAS mutations results in signifi cantly impaired tumor growth only when fail to benefi t from targeted inhibitors ( 1 ). The advance- treated with anti–PD-1. The combined Asf1a defi ciency and ment of immunotherapy is promising for treatment of anti–PD-1 treatment resulted in increased infl ammation, adenocarcinoma. Immune checkpoint blockade (ICB) thera- increased tumor-associated macrophages with M1-like polar- pies are now FDA-approved for the treatment of a broad ization, and increased T-cell infi ltration in the tumor.
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Towards Personalized Medicine in Psychiatry: Focus on Suicide
TOWARDS PERSONALIZED MEDICINE IN PSYCHIATRY: FOCUS ON SUICIDE Daniel F. Levey Submitted to the faculty of the University Graduate School in partial fulfillment of the requirements for the degree Doctor of Philosophy in the Program of Medical Neuroscience, Indiana University April 2017 ii Accepted by the Graduate Faculty, Indiana University, in partial fulfillment of the requirements for the degree of Doctor of Philosophy. Andrew J. Saykin, Psy. D. - Chair ___________________________ Alan F. Breier, M.D. Doctoral Committee Gerry S. Oxford, Ph.D. December 13, 2016 Anantha Shekhar, M.D., Ph.D. Alexander B. Niculescu III, M.D., Ph.D. iii Dedication This work is dedicated to all those who suffer, whether their pain is physical or psychological. iv Acknowledgements The work I have done over the last several years would not have been possible without the contributions of many people. I first need to thank my terrific mentor and PI, Dr. Alexander Niculescu. He has continuously given me advice and opportunities over the years even as he has suffered through my many mistakes, and I greatly appreciate his patience. The incredible passion he brings to his work every single day has been inspirational. It has been an at times painful but often exhilarating 5 years. I need to thank Helen Le-Niculescu for being a wonderful colleague and mentor. I learned a lot about organization and presentation working alongside her, and her tireless work ethic was an excellent example for a new graduate student. I had the pleasure of working with a number of great people over the years. Mikias Ayalew showed me the ropes of the lab and began my understanding of the power of algorithms.
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Impaired SNF2L Chromatin Remodeling Prolongs Accessibility at Promoters Enriched for Fos/Jun Binding Sites and Delays Granule Neuron Differentiation
fnmol-14-680280 June 30, 2021 Time: 16:59 # 1 ORIGINAL RESEARCH published: 06 July 2021 doi: 10.3389/fnmol.2021.680280 Impaired SNF2L Chromatin Remodeling Prolongs Accessibility at Promoters Enriched for Fos/Jun Binding Sites and Delays Granule Neuron Differentiation Laura R. Goodwin1,2, Gerardo Zapata1,2, Sara Timpano1, Jacob Marenger1 and David J. Picketts1,2,3* 1 Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, ON, Canada, 2 Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada, 3 Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada Chromatin remodeling proteins utilize the energy from ATP hydrolysis to mobilize Edited by: nucleosomes often creating accessibility for transcription factors within gene regulatory Veronica Martinez Cerdeño, University of California, Davis, elements. Aberrant chromatin remodeling has diverse effects on neuroprogenitor United States homeostasis altering progenitor competence, proliferation, survival, or cell fate. Previous Reviewed by: work has shown that inactivation of the ISWI genes, Smarca5 (encoding Snf2h) and Mitsuhiro Hashimoto, Fukushima Medical University, Japan Smarca1 (encoding Snf2l) have dramatic effects on brain development. Smarca5 Koji Shibasaki, conditional knockout mice have reduced progenitor expansion and severe forebrain Nagasaki University, Japan hypoplasia, with a similar effect on the postnatal growth of the cerebellum. In contrast, *Correspondence: Smarca1 mutants exhibited enlarged forebrains
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