Maintenance of Mammary Epithelial Phenotype by Transcription Factor Runx1 Through Mitotic Gene Bookmarking Joshua Rose University of Vermont
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RUNX1 Control of Mammary Epithelial and Breast Cancer Cell Phenotypes
University of Massachusetts Medical School eScholarship@UMMS GSBS Dissertations and Theses Graduate School of Biomedical Sciences 2017-12-12 RUNX1 Control of Mammary Epithelial and Breast Cancer Cell Phenotypes Deli Hong University of Massachusetts Medical School Let us know how access to this document benefits ou.y Follow this and additional works at: https://escholarship.umassmed.edu/gsbs_diss Part of the Cancer Biology Commons, and the Cell Biology Commons Repository Citation Hong D. (2017). RUNX1 Control of Mammary Epithelial and Breast Cancer Cell Phenotypes. GSBS Dissertations and Theses. https://doi.org/10.13028/M21Q2F. Retrieved from https://escholarship.umassmed.edu/gsbs_diss/949 This material is brought to you by eScholarship@UMMS. It has been accepted for inclusion in GSBS Dissertations and Theses by an authorized administrator of eScholarship@UMMS. For more information, please contact [email protected]. RUNX1 CONTROL OF MAMMARY EPITHELIAL AND BREAST CANCER CELL PHENOTYPES A Dissertation Presented By Deli Hong Submitted to the Faculty of the University of Massachusetts Graduate School of Biomedical Sciences, Worcester in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY December 12, 2017 Program of Cell Biology RUNX1 CONTROL OF MAMMARY EPITHELIAL AND BREAST CANCER CELL PHENOTYPES A Dissertation Presented By Deli Hong This work was undertaken in the Graduate School of Biomedical Sciences Program of Cell Biology The signature of the Thesis Advisor signifies validation of Dissertation content Gary S. Stein, Ph. D., Thesis Advisor The signatures of the Dissertation Defense Committee signify completion and approval as to style and content of the Dissertation Leslie Shaw, Ph. -
Functions of the Mineralocorticoid Receptor in the Hippocampus By
Functions of the Mineralocorticoid Receptor in the Hippocampus by Aaron M. Rozeboom A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy (Cellular and Molecular Biology) in The University of Michigan 2008 Doctoral Committee: Professor Audrey F. Seasholtz, Chair Professor Elizabeth A. Young Professor Ronald Jay Koenig Associate Professor Gary D. Hammer Assistant Professor Jorge A. Iniguez-Lluhi Acknowledgements There are more people than I can possibly name here that I need to thank who have helped me throughout the process of writing this thesis. The first and foremost person on this list is my mentor, Audrey Seasholtz. Between working in her laboratory as a research assistant and continuing my training as a graduate student, I spent 9 years in Audrey’s laboratory and it would be no exaggeration to say that almost everything I have learned regarding scientific research has come from her. Audrey’s boundless enthusiasm, great patience, and eager desire to teach students has made my time in her laboratory a richly rewarding experience. I cannot speak of Audrey’s laboratory without also including all the past and present members, many of whom were/are not just lab-mates but also good friends. I also need to thank all the members of my committee, an amazing group of people whose scientific prowess combined with their open-mindedness allowed me to explore a wide variety of interests while maintaining intense scientific rigor. Outside of Audrey’s laboratory, there have been many people in Ann Arbor without whom I would most assuredly have gone crazy. -
ESRRB Regulates Glucocorticoid Gene Expression in Mice and Patients with Acute Lymphoblastic Leukemia
University of Massachusetts Medical School eScholarship@UMMS Open Access Articles Open Access Publications by UMMS Authors 2020-07-13 ESRRB regulates glucocorticoid gene expression in mice and patients with acute lymphoblastic leukemia Kayleigh M. Gallagher University of Massachusetts Medical School Et al. Let us know how access to this document benefits ou.y Follow this and additional works at: https://escholarship.umassmed.edu/oapubs Part of the Cancer Biology Commons, and the Neoplasms Commons Repository Citation Gallagher KM, Roderick JE, Tan SH, Tan TK, Murphy L, Yu J, Li R, O'Connor K, Zhu LJ, Green MR, Sanda T, Kelliher MA. (2020). ESRRB regulates glucocorticoid gene expression in mice and patients with acute lymphoblastic leukemia. Open Access Articles. https://doi.org/10.1182/bloodadvances.2020001555. Retrieved from https://escholarship.umassmed.edu/oapubs/4285 This material is brought to you by eScholarship@UMMS. It has been accepted for inclusion in Open Access Articles by an authorized administrator of eScholarship@UMMS. For more information, please contact [email protected]. REGULAR ARTICLE ESRRB regulates glucocorticoid gene expression in mice and patients with acute lymphoblastic leukemia Downloaded from https://ashpublications.org/bloodadvances/article-pdf/4/13/3154/1748491/advancesadv2020001555.pdf by UNIV OF MASSACHUSETTS user on 10 August 2020 Kayleigh M. Gallagher,1 Justine E. Roderick,1 Shi Hao Tan,2 Tze King Tan,2 Leonard Murphy,1 Jun Yu,1 Rui Li,1 Kevin W. O’Connor,1 Julie Zhu,1 Michael R. Green,1 Takaomi Sanda,2 and Michelle A. Kelliher1 1Department of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA; and 2Cancer Science Institute of Singapore, Center of Translational Medicine, Singapore Synthetic glucocorticoids (GCs), such as dexamethasone and prednisone, remain key Key Points components of therapy for patients with lymphoid malignancies. -
The P63 Target HBP-1 Is Required for Keratinocyte Differentiation and Stratification
The p63 target HBP-1 is required for keratinocyte differentiation and stratification. Roberto Mantovani, Serena Borrelli, Eleonora Candi, Diletta Dolfini, Olì Maria Victoria Grober, Alessandro Weisz, Gennaro Melino, Alessandra Viganò, Bing Hu, Gian Paolo Dotto To cite this version: Roberto Mantovani, Serena Borrelli, Eleonora Candi, Diletta Dolfini, Olì Maria Victoria Grober, et al.. The p63 target HBP-1 is required for keratinocyte differentiation and stratification.. Cell Death and Differentiation, Nature Publishing Group, 2010, 10.1038/cdd.2010.59. hal-00542927 HAL Id: hal-00542927 https://hal.archives-ouvertes.fr/hal-00542927 Submitted on 4 Dec 2010 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Running title: HBP1 in skin differentiation. The p63 target HBP-1 is required for skin differentiation and stratification. Serena Borrelli1, Eleonora Candi2, Bing Hu3, Diletta Dolfini1, Maria Ravo4, Olì Maria Victoria Grober4, Alessandro Weisz4,5, GianPaolo Dotto3, Gerry Melino2,6, Maria Alessandra Viganò1 and Roberto Mantovani1*. 1) Dipartimento di Scienze Biomolecolari e Biotecnologie. Università degli Studi di Milano. Via Celoria 26, 20133 Milano, Italy. 2) Biochemistry IDI-IRCCS laboratory, c/o University of Rome "Tor Vergata", Via Montpellier 1, 00133 Roma, Italy. -
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. -
GATA3 As an Adjunct Prognostic Factor in Breast Cancer Patients with Less Aggressive Disease: a Study with a Review of the Literature
diagnostics Article GATA3 as an Adjunct Prognostic Factor in Breast Cancer Patients with Less Aggressive Disease: A Study with a Review of the Literature Patrizia Querzoli 1, Massimo Pedriali 1 , Rosa Rinaldi 2 , Paola Secchiero 3, Paolo Giorgi Rossi 4 and Elisabetta Kuhn 5,6,* 1 Section of Anatomic Pathology, Department of Morphology, Surgery and Experimental Medicine, University of Ferrara, 44124 Ferrara, Italy; [email protected] (P.Q.); [email protected] (M.P.) 2 Section of Anatomic Pathology, ASST Mantova, Ospedale Carlo Poma, 46100 Mantova, Italy; [email protected] 3 Surgery and Experimental Medicine and Interdepartmental Center of Technology of Advanced Therapies (LTTA), Department of Morphology, University of Ferrara, 44121 Ferrara, Italy; [email protected] 4 Epidemiology Unit, Azienda Unità Sanitaria Locale-IRCCS di Reggio Emilia, 42122 Reggio Emilia, Italy; [email protected] 5 Division of Pathology, Fondazione IRCCS Ca’ Granda, Ospedale Maggiore Policlinico, 20122 Milano, Italy 6 Department of Biomedical, Surgical, and Dental Sciences, University of Milan, 20122 Milano, Italy * Correspondence: [email protected]; Tel.: +39-02-5032-0564; Fax: +39-02-5503-2860 Abstract: Background: GATA binding protein 3 (GATA3) expression is positively correlated with Citation: Querzoli, P.; Pedriali, M.; estrogen receptor (ER) expression, but its prognostic value as an independent factor remains unclear. Rinaldi, R.; Secchiero, P.; Rossi, P.G.; Thus, we undertook the current study to evaluate the expression of GATA3 and its prognostic value Kuhn, E. GATA3 as an Adjunct in a large series of breast carcinomas (BCs) with long-term follow-up. Methods: A total of 702 Prognostic Factor in Breast Cancer consecutive primary invasive BCs resected between 1989 and 1993 in our institution were arranged Patients with Less Aggressive in tissue microarrays, immunostained for ER, progesterone receptor (PR), ki-67, HER2, p53, and Disease: A Study with a Review of GATA3, and scored. -
The REST/NRSF Pathway As a Central Mechanism in CNS Dysfunction
The REST/NRSF Pathway as a Central Mechanism in CNS Dysfunction Thesis submitted in accordance with the requirements of the University of Liverpool for the degree of Doctor in Philosophy by Alix Warburton April 2015 Disclaimer The data in this thesis is a result of my own work. The material collected for this thesis has not been presented, nor is currently being presented, either wholly or in part for any other degree or other qualification. All of the research, unless otherwise stated, was performed in the Department of Physiology and Department of Pharmacology, Institute of Translational Medicine, University of Liverpool. All other parties involved in the research presented here, and the nature of their contribution, are listed in the Acknowledgements section of this thesis. i Acknowledgements First and foremost, I would like to express my upmost gratitude to my primary and secondary supervisors Professor John Quinn (a.k.a Prof. Quinny) and Dr Jill Bubb for all of their support, guidance, wisdom (thank you Jill) and encouragement throughout my PhD; I could not have wished for a better pair. I am also extremely grateful to the BBSRC for funding my PhD project. I would also like to extend my thanks to Dr Graeme Sills for providing samples and assistance with my work on the SANAD epilepsy project, Dr Fabio Miyajima for offering his knowledge and knowhow on many occasions, Dr Gerome Breen for being a bioinformatics wizard and providing support on several projects, Dr Minyan Wang’s lab for their help and hospitality during my 3 month visit to Xi'an Jiaotong-Liverpool University, Dr Roshan Koron for assisting with the breast cancer study, Dr Chris Murgatroyd for his invaluable advice on ChIP and Professor Dan Rujescu’s lab for providing clinical samples and support with statistical analyses on the schizophrenia project. -
Identification of SNP-Containing Regulatory Motifs in the Myelodysplastic Syndromes Model Using SNP Arrays Ad Gene Expression Arrays" (2013)
University of Central Florida STARS Faculty Bibliography 2010s Faculty Bibliography 1-1-2013 Identification of SNP-containing egulatr ory motifs in the myelodysplastic syndromes model using SNP arrays ad gene expression arrays Jing Fan Jennifer G. Dy Chung-Che Chang University of Central Florida Xiaoboo Zhou Find similar works at: https://stars.library.ucf.edu/facultybib2010 University of Central Florida Libraries http://library.ucf.edu This Article is brought to you for free and open access by the Faculty Bibliography at STARS. It has been accepted for inclusion in Faculty Bibliography 2010s by an authorized administrator of STARS. For more information, please contact [email protected]. Recommended Citation Fan, Jing; Dy, Jennifer G.; Chang, Chung-Che; and Zhou, Xiaoboo, "Identification of SNP-containing regulatory motifs in the myelodysplastic syndromes model using SNP arrays ad gene expression arrays" (2013). Faculty Bibliography 2010s. 3960. https://stars.library.ucf.edu/facultybib2010/3960 Chinese Journal of Cancer Original Article Jing Fan 1, Jennifer G. Dy 1, Chung鄄Che Chang 2 and Xiaobo Zhou 3 Abstract Myelodysplastic syndromes have increased in frequency and incidence in the American population, but patient prognosis has not significantly improved over the last decade. Such improvements could be realized if biomarkers for accurate diagnosis and prognostic stratification were successfully identified. In this study, we propose a method that associates two state鄄of 鄄th e鄄ar t array technologies single nucleotide polymor鄄 要 phism (SNP) array and gene expression array with gene motifs considered transcription factor -binding 要 sites (TFBS). We are particularly interested in SNP鄄co ntaining motifs introduced by genetic variation and mutation as TFBS. -
Id Proteins Promote a Cancer Stem Cell Phenotype in Triple Negative Breast
bioRxiv preprint doi: https://doi.org/10.1101/497313; this version posted March 11, 2020. 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 4.0 International license. 1 Id proteins promote a cancer stem cell phenotype in triple negative 2 breast cancer via negative regulation of Robo1 3 Wee S. Teo1,2, Holly Holliday1,2#, Nitheesh Karthikeyan3#, Aurélie S. Cazet1,2, Daniel L. 4 Roden1,2, Kate Harvey1, Christina Valbirk Konrad1, Reshma Murali3, Binitha Anu Varghese3, 5 Archana P. T.3,4, Chia-Ling Chan1,2, Andrea McFarland1, Simon Junankar1,2, Sunny Ye1, 6 Jessica Yang1, Iva Nikolic1,2, Jaynish S. Shah5, Laura A. Baker1,2, Ewan K.A. Millar1,6,7,8, 7 Mathew J. Naylor1,2,10, Christopher J. Ormandy1,2, Sunil R. Lakhani11, Warren Kaplan1,12, 8 Albert S. Mellick13,14, Sandra A. O’Toole1,9, Alexander Swarbrick1,2*, Radhika Nair1,2,3* 9 Affiliations 10 1Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia 11 2St Vincent’s Clinical School, Faculty of Medicine, UNSW Sydney, New South Wales, 12 Australia 13 3 Cancer Research Program, Rajiv Gandhi Centre for Biotechnology, Kerala, India 14 4Manipal Academy of Higher Education, Manipal, Karnataka, India 15 5Centenary Institute, The University of Sydney, New South Wales, Australia 16 6 Department of Anatomical Pathology, NSW Health Pathology, St George Hospital, 17 Kogarah, NSW, Australia 18 7 School of Medical Sciences, UNSW Sydney, Kensington NSW, Australia. -
Human Transcription Factor Protein-Protein Interactions in Health and Disease
HELKA GÖÖS GÖÖS HELKA Recent Publications in this Series 45/2019 Mgbeahuruike Eunice Ego Evaluation of the Medicinal Uses and Antimicrobial Activity of Piper guineense (Schumach & Thonn) 46/2019 Suvi Koskinen AND DISEASE IN HEALTH INTERACTIONS PROTEIN-PROTEIN FACTOR HUMAN TRANSCRIPTION Near-Occlusive Atherosclerotic Carotid Artery Disease: Study with Computed Tomography Angiography 47/2019 Flavia Fontana DISSERTATIONES SCHOLAE DOCTORALIS AD SANITATEM INVESTIGANDAM Biohybrid Cloaked Nanovaccines for Cancer Immunotherapy UNIVERSITATIS HELSINKIENSIS 48/2019 Marie Mennesson Kainate Receptor Auxiliary Subunits Neto1 and Neto2 in Anxiety and Fear-Related Behaviors 49/2019 Zehua Liu Porous Silicon-Based On-Demand Nanohybrids for Biomedical Applications 50/2019 Veer Singh Marwah Strategies to Improve Standardization and Robustness of Toxicogenomics Data Analysis HELKA GÖÖS 51/2019 Iryna Hlushchenko Actin Regulation in Dendritic Spines: From Synaptic Plasticity to Animal Behavior and Human HUMAN TRANSCRIPTION FACTOR PROTEIN-PROTEIN Neurodevelopmental Disorders 52/2019 Heini Liimatta INTERACTIONS IN HEALTH AND DISEASE Efectiveness of Preventive Home Visits among Community-Dwelling Older People 53/2019 Helena Karppinen Older People´s Views Related to Their End of Life: Will-to-Live, Wellbeing and Functioning 54/2019 Jenni Laitila Elucidating Nebulin Expression and Function in Health and Disease 55/2019 Katarzyna Ciuba Regulation of Contractile Actin Structures in Non-Muscle Cells 56/2019 Sami Blom Spatial Characterisation of Prostate Cancer by Multiplex -
Chip Validated H4k5ac (Clone RM140) Antibody with Positive and Negative Primer Sets
www.chromatrap.com Clywedog Rd South Wrexham Industrial Estate Wrexham LL13 9XS, United Kingdom Tel: +44 (0) 1978 666239/40 Email: [email protected] ChIP Validated H4K5ac (Clone RM140) Antibody with Positive and Negative Primer Sets Catalogue no: 900029 Chromatrap®’s ChIP Validated H4K5ac Antibody with Positive Primer Set provides a complete set of tools to assist with a successful ChIP assay. Including: H4K5ac antibody, control rabbit IgG, and positive primer set. The ChIP Validated H4K5ac Antibody with Positive Primer Set is not suitable for use with non-human species. Background: Histone 4 (H4) is one of the five core histone proteins, comprising the protein component of chromatin. H4 is ubiquitous within chromosomes and can be found bound to most gene sequences throughout the genome. Acetylation of lysine 5 on histone 4 (H4K5ac) is associated with open chromatin and active gene transcription. H4K5ac has been shown to have roles in epigenetic bookmarking, a process where genetic information is passed onto daughter cells during cell division. A rabbit IgG is included in this Antibody Primer Set as a negative control for the ChIP experiment. The H4K5ac positive primer set recognises the promoter of the GAPDH gene, associated with active transcription and is a suitable target for this antibody. Suggested Usage: Component Suggested Dilution Figure H4K5ac 2:1 (antibody: chromatin) 1 Rabbit IgG 2:1 (antibody: chromatin) 1 Positive Primer Set Dilute from 4M (provided) to 1M working concentration Please note: Optimal dilutions should be determined by the user. These volumes are stated as guidelines only. Advancements in Epigenetics *This product is for research use only. -
Mediator of DNA Damage Checkpoint 1 (MDC1) Is a Novel Estrogen Receptor Co-Regulator in Invasive 6 Lobular Carcinoma of the Breast 7 8 Evelyn K
bioRxiv preprint doi: https://doi.org/10.1101/2020.12.16.423142; this version posted December 16, 2020. 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 4.0 International license. 1 Running Title: MDC1 co-regulates ER in ILC 2 3 Research article 4 5 Mediator of DNA damage checkpoint 1 (MDC1) is a novel estrogen receptor co-regulator in invasive 6 lobular carcinoma of the breast 7 8 Evelyn K. Bordeaux1+, Joseph L. Sottnik1+, Sanjana Mehrotra1, Sarah E. Ferrara2, Andrew E. Goodspeed2,3, James 9 C. Costello2,3, Matthew J. Sikora1 10 11 +EKB and JLS contributed equally to this project. 12 13 Affiliations 14 1Dept. of Pathology, University of Colorado Anschutz Medical Campus 15 2Biostatistics and Bioinformatics Shared Resource, University of Colorado Comprehensive Cancer Center 16 3Dept. of Pharmacology, University of Colorado Anschutz Medical Campus 17 18 Corresponding author 19 Matthew J. Sikora, PhD.; Mail Stop 8104, Research Complex 1 South, Room 5117, 12801 E. 17th Ave.; Aurora, 20 CO 80045. Tel: (303)724-4301; Fax: (303)724-3712; email: [email protected]. Twitter: 21 @mjsikora 22 23 Authors' contributions 24 MJS conceived of the project. MJS, EKB, and JLS designed and performed experiments. JLS developed models 25 for the project. EKB, JLS, SM, and AEG contributed to data analysis and interpretation. SEF, AEG, and JCC 26 developed and performed informatics analyses. MJS wrote the draft manuscript; all authors read and revised the 27 manuscript and have read and approved of this version of the manuscript.