Sequence and Chromatin Determinants of Cell-Type Specific
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Table S1. List of Proteins in the BAHD1 Interactome
Table S1. List of proteins in the BAHD1 interactome BAHD1 nuclear partners found in this work yeast two-hybrid screen Name Description Function Reference (a) Chromatin adapters HP1α (CBX5) chromobox homolog 5 (HP1 alpha) Binds histone H3 methylated on lysine 9 and chromatin-associated proteins (20-23) HP1β (CBX1) chromobox homolog 1 (HP1 beta) Binds histone H3 methylated on lysine 9 and chromatin-associated proteins HP1γ (CBX3) chromobox homolog 3 (HP1 gamma) Binds histone H3 methylated on lysine 9 and chromatin-associated proteins MBD1 methyl-CpG binding domain protein 1 Binds methylated CpG dinucleotide and chromatin-associated proteins (22, 24-26) Chromatin modification enzymes CHD1 chromodomain helicase DNA binding protein 1 ATP-dependent chromatin remodeling activity (27-28) HDAC5 histone deacetylase 5 Histone deacetylase activity (23,29,30) SETDB1 (ESET;KMT1E) SET domain, bifurcated 1 Histone-lysine N-methyltransferase activity (31-34) Transcription factors GTF3C2 general transcription factor IIIC, polypeptide 2, beta 110kDa Required for RNA polymerase III-mediated transcription HEYL (Hey3) hairy/enhancer-of-split related with YRPW motif-like DNA-binding transcription factor with basic helix-loop-helix domain (35) KLF10 (TIEG1) Kruppel-like factor 10 DNA-binding transcription factor with C2H2 zinc finger domain (36) NR2F1 (COUP-TFI) nuclear receptor subfamily 2, group F, member 1 DNA-binding transcription factor with C4 type zinc finger domain (ligand-regulated) (36) PEG3 paternally expressed 3 DNA-binding transcription factor with -
Identification of GA-Binding Protein Transcription Factor Alpha Subunit
International Journal of Molecular Sciences Article Identification of GA-Binding Protein Transcription Factor Alpha Subunit (GABPA) as a Novel Bookmarking Factor Shunya Goto 1, Masashi Takahashi 1, Narumi Yasutsune 1, Sumiki Inayama 1, Dai Kato 2, Masashi Fukuoka 3, Shu-ichiro Kashiwaba 1 and Yasufumi Murakami 1,2,* 1 Department of Biological Science and Technology, Faculty of Industrial Science and Technology, Tokyo University of Science, 6-3-1 Niijuku, Katsushika-ku, Tokyo 125-8585, Japan; [email protected] (S.G.); [email protected] (M.T.); [email protected] (N.Y.); [email protected] (S.I.); [email protected] (S.K.) 2 Order-MadeMedical Research Inc., 208Todai-Kashiwa VP, 5-4-19 Kashiwanoha, Kashiwa-shi, Chiba-ken 277-0882, Japan; [email protected] 3 Department of Molecular Pharmacology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo 187-8551, Japan; [email protected] * Correspondence: [email protected]; Tel.: +81-3-5876-1717 (ext. 1919); Fax: +81-3-5876-1470 Received: 7 February 2019; Accepted: 27 February 2019; Published: 4 March 2019 Abstract: Mitotic bookmarking constitutes a mechanism for transmitting transcriptional patterns through cell division. Bookmarking factors, comprising a subset of transcription factors (TFs), and multiple histone modifications retained in mitotic chromatin facilitate reactivation of transcription in the early G1 phase. However, the specific TFs that act as bookmarking factors remain largely unknown. Previously, we identified the “early G1 genes” and screened TFs that were predicted to bind to the upstream region of these genes, then identified GA-binding protein transcription factor alpha subunit (GABPA) and Sp1 transcription factor (SP1) as candidate bookmarking factors. -
Core Transcriptional Regulatory Circuitries in Cancer
Oncogene (2020) 39:6633–6646 https://doi.org/10.1038/s41388-020-01459-w REVIEW ARTICLE Core transcriptional regulatory circuitries in cancer 1 1,2,3 1 2 1,4,5 Ye Chen ● Liang Xu ● Ruby Yu-Tong Lin ● Markus Müschen ● H. Phillip Koeffler Received: 14 June 2020 / Revised: 30 August 2020 / Accepted: 4 September 2020 / Published online: 17 September 2020 © The Author(s) 2020. This article is published with open access Abstract Transcription factors (TFs) coordinate the on-and-off states of gene expression typically in a combinatorial fashion. Studies from embryonic stem cells and other cell types have revealed that a clique of self-regulated core TFs control cell identity and cell state. These core TFs form interconnected feed-forward transcriptional loops to establish and reinforce the cell-type- specific gene-expression program; the ensemble of core TFs and their regulatory loops constitutes core transcriptional regulatory circuitry (CRC). Here, we summarize recent progress in computational reconstitution and biologic exploration of CRCs across various human malignancies, and consolidate the strategy and methodology for CRC discovery. We also discuss the genetic basis and therapeutic vulnerability of CRC, and highlight new frontiers and future efforts for the study of CRC in cancer. Knowledge of CRC in cancer is fundamental to understanding cancer-specific transcriptional addiction, and should provide important insight to both pathobiology and therapeutics. 1234567890();,: 1234567890();,: Introduction genes. Till now, one critical goal in biology remains to understand the composition and hierarchy of transcriptional Transcriptional regulation is one of the fundamental mole- regulatory network in each specified cell type/lineage. -
Molecular and Physiological Basis for Hair Loss in Near Naked Hairless and Oak Ridge Rhino-Like Mouse Models: Tracking the Role of the Hairless Gene
University of Tennessee, Knoxville TRACE: Tennessee Research and Creative Exchange Doctoral Dissertations Graduate School 5-2006 Molecular and Physiological Basis for Hair Loss in Near Naked Hairless and Oak Ridge Rhino-like Mouse Models: Tracking the Role of the Hairless Gene Yutao Liu University of Tennessee - Knoxville Follow this and additional works at: https://trace.tennessee.edu/utk_graddiss Part of the Life Sciences Commons Recommended Citation Liu, Yutao, "Molecular and Physiological Basis for Hair Loss in Near Naked Hairless and Oak Ridge Rhino- like Mouse Models: Tracking the Role of the Hairless Gene. " PhD diss., University of Tennessee, 2006. https://trace.tennessee.edu/utk_graddiss/1824 This Dissertation is brought to you for free and open access by the Graduate School at TRACE: Tennessee Research and Creative Exchange. It has been accepted for inclusion in Doctoral Dissertations by an authorized administrator of TRACE: Tennessee Research and Creative Exchange. For more information, please contact [email protected]. To the Graduate Council: I am submitting herewith a dissertation written by Yutao Liu entitled "Molecular and Physiological Basis for Hair Loss in Near Naked Hairless and Oak Ridge Rhino-like Mouse Models: Tracking the Role of the Hairless Gene." I have examined the final electronic copy of this dissertation for form and content and recommend that it be accepted in partial fulfillment of the requirements for the degree of Doctor of Philosophy, with a major in Life Sciences. Brynn H. Voy, Major Professor We have read this dissertation and recommend its acceptance: Naima Moustaid-Moussa, Yisong Wang, Rogert Hettich Accepted for the Council: Carolyn R. -
2017.08.28 Anne Barry-Reidy Thesis Final.Pdf
REGULATION OF BOVINE β-DEFENSIN EXPRESSION THIS THESIS IS SUBMITTED TO THE UNIVERSITY OF DUBLIN FOR THE DEGREE OF DOCTOR OF PHILOSOPHY 2017 ANNE BARRY-REIDY SCHOOL OF BIOCHEMISTRY & IMMUNOLOGY TRINITY COLLEGE DUBLIN SUPERVISORS: PROF. CLIONA O’FARRELLY & DR. KIERAN MEADE TABLE OF CONTENTS DECLARATION ................................................................................................................................. vii ACKNOWLEDGEMENTS ................................................................................................................... viii ABBREVIATIONS ................................................................................................................................ix LIST OF FIGURES............................................................................................................................. xiii LIST OF TABLES .............................................................................................................................. xvii ABSTRACT ........................................................................................................................................xix Chapter 1 Introduction ........................................................................................................ 1 1.1 Antimicrobial/Host-defence peptides ..................................................................... 1 1.2 Defensins................................................................................................................. 1 1.3 β-defensins ............................................................................................................. -
Table 2. Significant
Table 2. Significant (Q < 0.05 and |d | > 0.5) transcripts from the meta-analysis Gene Chr Mb Gene Name Affy ProbeSet cDNA_IDs d HAP/LAP d HAP/LAP d d IS Average d Ztest P values Q-value Symbol ID (study #5) 1 2 STS B2m 2 122 beta-2 microglobulin 1452428_a_at AI848245 1.75334941 4 3.2 4 3.2316485 1.07398E-09 5.69E-08 Man2b1 8 84.4 mannosidase 2, alpha B1 1416340_a_at H4049B01 3.75722111 3.87309653 2.1 1.6 2.84852656 5.32443E-07 1.58E-05 1110032A03Rik 9 50.9 RIKEN cDNA 1110032A03 gene 1417211_a_at H4035E05 4 1.66015788 4 1.7 2.82772795 2.94266E-05 0.000527 NA 9 48.5 --- 1456111_at 3.43701477 1.85785922 4 2 2.8237185 9.97969E-08 3.48E-06 Scn4b 9 45.3 Sodium channel, type IV, beta 1434008_at AI844796 3.79536664 1.63774235 3.3 2.3 2.75319499 1.48057E-08 6.21E-07 polypeptide Gadd45gip1 8 84.1 RIKEN cDNA 2310040G17 gene 1417619_at 4 3.38875643 1.4 2 2.69163229 8.84279E-06 0.0001904 BC056474 15 12.1 Mus musculus cDNA clone 1424117_at H3030A06 3.95752801 2.42838452 1.9 2.2 2.62132809 1.3344E-08 5.66E-07 MGC:67360 IMAGE:6823629, complete cds NA 4 153 guanine nucleotide binding protein, 1454696_at -3.46081884 -4 -1.3 -1.6 -2.6026947 8.58458E-05 0.0012617 beta 1 Gnb1 4 153 guanine nucleotide binding protein, 1417432_a_at H3094D02 -3.13334396 -4 -1.6 -1.7 -2.5946297 1.04542E-05 0.0002202 beta 1 Gadd45gip1 8 84.1 RAD23a homolog (S. -
Genome-Wide Approach to Identify Risk Factors for Therapy-Related Myeloid Leukemia
Leukemia (2006) 20, 239–246 & 2006 Nature Publishing Group All rights reserved 0887-6924/06 $30.00 www.nature.com/leu ORIGINAL ARTICLE Genome-wide approach to identify risk factors for therapy-related myeloid leukemia A Bogni1, C Cheng2, W Liu2, W Yang1, J Pfeffer1, S Mukatira3, D French1, JR Downing4, C-H Pui4,5,6 and MV Relling1,6 1Department of Pharmaceutical Sciences, The University of Tennessee, Memphis, TN, USA; 2Department of Biostatistics, The University of Tennessee, Memphis, TN, USA; 3Hartwell Center, The University of Tennessee, Memphis, TN, USA; 4Department of Pathology, The University of Tennessee, Memphis, TN, USA; 5Department of Hematology/Oncology St Jude Children’s Research Hospital, The University of Tennessee, Memphis, TN, USA; and 6Colleges of Medicine and Pharmacy, The University of Tennessee, Memphis, TN, USA Using a target gene approach, only a few host genetic risk therapy increases, the importance of identifying host factors for factors for treatment-related myeloid leukemia (t-ML) have been secondary neoplasms increases. defined. Gene expression microarrays allow for a more 4 genome-wide approach to assess possible genetic risk factors Because DNA microarrays interrogate multiple ( 10 000) for t-ML. We assessed gene expression profiles (n ¼ 12 625 genes in one experiment, they allow for a ‘genome-wide’ probe sets) in diagnostic acute lymphoblastic leukemic cells assessment of genes that may predispose to leukemogenesis. from 228 children treated on protocols that included leukemo- DNA microarray analysis of gene expression has been used to genic agents such as etoposide, 13 of whom developed t-ML. identify distinct expression profiles that are characteristic of Expression of 68 probes, corresponding to 63 genes, was different leukemia subtypes.13,14 Studies using this method have significantly related to risk of t-ML. -
Open Dogan Phdthesis Final.Pdf
The Pennsylvania State University The Graduate School Eberly College of Science ELUCIDATING BIOLOGICAL FUNCTION OF GENOMIC DNA WITH ROBUST SIGNALS OF BIOCHEMICAL ACTIVITY: INTEGRATIVE GENOME-WIDE STUDIES OF ENHANCERS A Dissertation in Biochemistry, Microbiology and Molecular Biology by Nergiz Dogan © 2014 Nergiz Dogan Submitted in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy August 2014 ii The dissertation of Nergiz Dogan was reviewed and approved* by the following: Ross C. Hardison T. Ming Chu Professor of Biochemistry and Molecular Biology Dissertation Advisor Chair of Committee David S. Gilmour Professor of Molecular and Cell Biology Anton Nekrutenko Professor of Biochemistry and Molecular Biology Robert F. Paulson Professor of Veterinary and Biomedical Sciences Philip Reno Assistant Professor of Antropology Scott B. Selleck Professor and Head of the Department of Biochemistry and Molecular Biology *Signatures are on file in the Graduate School iii ABSTRACT Genome-wide measurements of epigenetic features such as histone modifications, occupancy by transcription factors and coactivators provide the opportunity to understand more globally how genes are regulated. While much effort is being put into integrating the marks from various combinations of features, the contribution of each feature to accuracy of enhancer prediction is not known. We began with predictions of 4,915 candidate erythroid enhancers based on genomic occupancy by TAL1, a key hematopoietic transcription factor that is strongly associated with gene induction in erythroid cells. Seventy of these DNA segments occupied by TAL1 (TAL1 OSs) were tested by transient transfections of cultured hematopoietic cells, and 56% of these were active as enhancers. Sixty-six TAL1 OSs were evaluated in transgenic mouse embryos, and 65% of these were active enhancers in various tissues. -
SOX4-Mediated Repression of Specific Trnas Inhibits Proliferation of Human Glioblastoma Cells
SOX4-mediated repression of specific tRNAs inhibits proliferation of human glioblastoma cells Jianjing Yanga,b,c, Derek K. Smithc,d, Haoqi Nia,b,c,KeWua,b, Dongdong Huanga,b, Sishi Pana,b,c, Adwait A. Sathee, Yu Tangc,d, Meng-Lu Liuc,d, Chao Xinge,f,g, Chun-Li Zhangc,d,1, and Qichuan Zhugea,b,1 aDepartment of Neurosurgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China 325000; bZhejiang Provincial Key Laboratory of Aging and Neurological Disorder Research, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China 325000; cDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390; dHamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390; eMcDermott Center of Human Growth and Development, University of Texas Southwestern Medical Center, Dallas, TX 75390; fDepartment of Bioinformatics, University of Texas Southwestern Medical Center, Dallas, TX 75390; and gDepartment of Population and Data Sciences, University of Texas Southwestern Medical Center, Dallas, TX 75390 Edited by S. Altman, Yale University, New Haven, CT, and approved February 5, 2020 (received for review November 15, 2019) Transfer RNAs (tRNAs) are products of RNA polymerase III (Pol III) indicates that tRNA expression may also be under cell state- and essential for mRNA translation and ultimately cell growth and dependent regulations (12–16). proliferation. Whether and how individual tRNA genes are specif- In this study, we performed a systematic analysis on how ically regulated is not clear. Here, we report that SOX4, a well- NGN2/SOX4-mediated cell-fate reprogramming leads to cell known Pol II-dependent transcription factor that is critical for neuro- cycle exit of human glioblastoma cells. -
A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated. -
Gene Expression Profile in Different Age Groups and Its Association With
cells Article Gene Expression Profile in Different Age Groups and Its Association with Cognitive Function in Healthy Malay Adults in Malaysia Nur Fathiah Abdul Sani 1 , Ahmad Imran Zaydi Amir Hamzah 1, Zulzikry Hafiz Abu Bakar 1 , Yasmin Anum Mohd Yusof 2, Suzana Makpol 1 , Wan Zurinah Wan Ngah 1 and Hanafi Ahmad Damanhuri 1,* 1 Department of Biochemistry, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Center, Jalan Yaacob Latif, Cheras, Kuala Lumpur 56000, Malaysia; [email protected] (N.F.A.S.); [email protected] (A.I.Z.A.H.); zulzikryhafi[email protected] (Z.H.A.B.); [email protected] (S.M.); [email protected] (W.Z.W.N.) 2 Faculty of Medicine and Defence Health, National Defence University of Malaysia, Kem Sungai Besi, Kuala Lumpur 57000, Malaysia; [email protected] * Correspondence: hanafi[email protected] Abstract: The mechanism of cognitive aging at the molecular level is complex and not well under- stood. Growing evidence suggests that cognitive differences might also be caused by ethnicity. Thus, this study aims to determine the gene expression changes associated with age-related cognitive decline among Malay adults in Malaysia. A cross-sectional study was conducted on 160 healthy Malay subjects, aged between 28 and 79, and recruited around Selangor and Klang Valley, Malaysia. Citation: Abdul Sani, N.F.; Amir Gene expression analysis was performed using a HumanHT-12v4.0 Expression BeadChip microarray Hamzah, A.I.Z.; Abu Bakar, Z.H.; kit. The top 20 differentially expressed genes at p < 0.05 and fold change (FC) = 1.2 showed that Mohd Yusof, Y.A.; Makpol, S.; Wan PAFAH1B3, HIST1H1E, KCNA3, TM7SF2, RGS1, and TGFBRAP1 were regulated with increased Ngah, W.Z.; Damanhuri, H.A. -
GABPA Is a Master Regulator of Luminal Identity and Restrains Aggressive Diseases in Bladder Cancer
Cell Death & Differentiation (2020) 27:1862–1877 https://doi.org/10.1038/s41418-019-0466-7 ARTICLE GABPA is a master regulator of luminal identity and restrains aggressive diseases in bladder cancer 1,2,3 3,4 5 2,5 5 3 5 5 Yanxia Guo ● Xiaotian Yuan ● Kailin Li ● Mingkai Dai ● Lu Zhang ● Yujiao Wu ● Chao Sun ● Yuan Chen ● 5 6 3 1,2 1,2 3,7 Guanghui Cheng ● Cheng Liu ● Klas Strååt ● Feng Kong ● Shengtian Zhao ● Magnus Bjorkhölm ● Dawei Xu 3,7 Received: 3 June 2019 / Revised: 20 November 2019 / Accepted: 21 November 2019 / Published online: 4 December 2019 © The Author(s) 2019. This article is published with open access Abstract TERT promoter mutations occur in the majority of glioblastoma, bladder cancer (BC), and other malignancies while the ETS family transcription factors GABPA and its partner GABPB1 activate the mutant TERT promoter and telomerase in these tumors. GABPA depletion or the disruption of the GABPA/GABPB1 complex by knocking down GABPB1 was shown to inhibit telomerase, thereby eliminating the tumorigenic potential of glioblastoma cells. GABPA/B1 is thus suggested as a cancer therapeutic target. However, it is unclear about its role in BC. Here we unexpectedly observed that GABPA ablation 1234567890();,: 1234567890();,: inhibited TERT expression, but robustly increased proliferation, stem, and invasive phenotypes and cisplatin resistance in BC cells, while its overexpression exhibited opposite effects, and inhibited in vivo metastasizing in a xenograft transplant model. Mechanistically, GABPA directly activates the transcription of FoxA1 and GATA3, key transcription factors driving luminal differentiation of urothelial cells. Consistently, TCGA/GEO dataset analyses show that GABPA expression is correlated positively with luminal while negatively with basal signatures.