The NANOG Transcription Factor Induces Type 2 Deiodinase Expression and Regulates the Intracellular Activation of Thyroid Hormone in Keratinocyte Carcinomas
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
ATRX Induction by Mutant Huntingtin Via Cdx2 Modulates Heterochromatin Condensation and Pathology in Huntington’S Disease
Cell Death and Differentiation (2012) 19, 1109–1116 & 2012 Macmillan Publishers Limited All rights reserved 1350-9047/12 www.nature.com/cdd ATRX induction by mutant huntingtin via Cdx2 modulates heterochromatin condensation and pathology in Huntington’s disease J Lee1,2, YK Hong3, GS Jeon4, YJ Hwang4, KY Kim4, KH Seong4, M-K Jung4, DJ Picketts5, NW Kowall1,2, KS Cho3 and H Ryu*,1,2,4 Aberrant chromatin remodeling is involved in the pathogenesis of Huntington’s disease (HD) but the mechanism is not known. Herein, we report that mutant huntingtin (mtHtt) induces the transcription of alpha thalassemia/mental retardation X linked (ATRX), an ATPase/helicase and SWI/SNF-like chromatin remodeling protein via Cdx-2 activation. ATRX expression was elevated in both a cell line model and transgenic model of HD, and Cdx-2 occupancy of the ATRX promoter was increased in HD. Induction of ATRX expanded the size of promyelocytic leukemia nuclear body (PML-NB) and increased trimethylation of H3K9 (H3K9me3) and condensation of pericentromeric heterochromatin, while knockdown of ATRX decreased PML-NB and H3K9me3 levels. Knockdown of ATRX/dXNP improved the hatch rate of fly embryos expressing mtHtt (Q127). ATRX/dXNP overexpression exacerbated eye degeneration of eye-specific mtHtt (Q127) expressing flies. Our findings suggest that transcriptional alteration of ATRX by mtHtt is involved in pericentromeric heterochromatin condensation and contributes to the pathogenesis of HD. Cell Death and Differentiation (2012) 19, 1109–1116; doi:10.1038/cdd.2011.196; published -
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. -
Down-Regulation of Stem Cell Genes, Including Those in a 200-Kb Gene Cluster at 12P13.31, Is Associated with in Vivo Differentiation of Human Male Germ Cell Tumors
Research Article Down-Regulation of Stem Cell Genes, Including Those in a 200-kb Gene Cluster at 12p13.31, Is Associated with In vivo Differentiation of Human Male Germ Cell Tumors James E. Korkola,1 Jane Houldsworth,1,2 Rajendrakumar S.V. Chadalavada,1 Adam B. Olshen,3 Debbie Dobrzynski,2 Victor E. Reuter,4 George J. Bosl,2 and R.S.K. Chaganti1,2 1Cell Biology Program and Departments of 2Medicine, 3Epidemiology and Biostatistics, and 4Pathology, Memorial Sloan-Kettering Cancer Center, New York, New York Abstract on the degree and type of differentiation (i.e., seminomas, which Adult male germ cell tumors (GCTs) comprise distinct groups: resemble undifferentiated primitive germ cells, and nonseminomas, seminomas and nonseminomas, which include pluripotent which show varying degrees of embryonic and extraembryonic embryonal carcinomas as well as other histologic subtypes patterns of differentiation; refs. 2, 3). Nonseminomatous GCTs are exhibiting various stages of differentiation. Almost all GCTs further subdivided into embryonal carcinomas, which show early show 12p gain, but the target genes have not been clearly zygotic or embryonal-like differentiation, yolk sac tumors and defined. To identify 12p target genes, we examined Affymetrix choriocarcinomas, which exhibit extraembryonal forms of differ- (Santa Clara, CA) U133A+B microarray (f83% coverage of 12p entiation, and teratomas, which show somatic differentiation along genes) expression profiles of 17 seminomas, 84 nonseminoma multiple lineages (3). Both seminomas and embryonal carcinoma GCTs, and 5 normal testis samples. Seventy-three genes on 12p are known to express stem cell markers, such as POU5F1 (4) and were significantly overexpressed, including GLUT3 and REA NANOG (5). -
Interaction Network of Immune‑Associated Genes Affecting the Prognosis of Patients with Glioblastoma
EXPERIMENTAL AND THERAPEUTIC MEDICINE 21: 61, 2021 Interaction network of immune‑associated genes affecting the prognosis of patients with glioblastoma XIAOHONG HOU1*, JIALIN CHEN2*, QIANG ZHANG1, YINCHUN FAN1, CHENGMING XIANG1, GUIYIN ZHOU1, FANG CAO1 and SHENGTAO YAO1 1Department of Cerebrovascular Disease, Affiliated Hospital of Zunyi Medical University;2 Department of Neonatology, The First People' s Hospital of Zunyi Affiliated to Zunyi Medical University, Zunyi, Guizhou 563000, P.R. China Received October 15, 2019; Accepted October 6, 2020 DOI: 10.3892/etm.2020.9493 Abstract. Glioblastoma multiforme (GBM) is a common and immune genes of interest. The interaction network of malignant tumor type of the nervous system. The purpose immune‑regulatory genes constructed in the present study of the present study was to establish a regulatory network of enhances the current understanding of mechanisms associated immune‑associated genes affecting the prognosis of patients with poor prognosis of patients with GBM. The risk score with GBM. The GSE4290, GSE50161 and GSE2223 datasets model established in the present study may be used to evaluate from the Gene Expression Omnibus database were screened the prognosis of patients with GBM. to identify common differentially expressed genes (co‑DEGs). A functional enrichment analysis indicated that the co‑DEGs Introduction were mainly enriched in cell communication, regulation of enzyme activity, immune response, nervous system, cytokine Glioblastoma multiforme (GBM) is one of the most malig‑ signaling in immune system and the AKT signaling pathway. nant tumor types of the central nervous system, with short The co‑DEGs accumulated in immune response were then median survival and poor prognosis. -
Ncomms2254.Pdf
ARTICLE Received 3 May 2012 | Accepted 5 Nov 2012 | Published 4 Dec 2012 DOI: 10.1038/ncomms2254 The RB family is required for the self-renewal and survival of human embryonic stem cells Jamie F. Conklin1,2,3, Julie Baker2,3 & Julien Sage1,2,3 The mechanisms ensuring the long-term self-renewal of human embryonic stem cells are still only partly understood, limiting their use in cellular therapies. Here we found that increased activity of the RB cell cycle inhibitor in human embryonic stem cells induces cell cycle arrest, differentiation and cell death. Conversely, inactivation of the entire RB family (RB, p107 and p130) in human embryonic stem cells triggers G2/M arrest and cell death through functional activation of the p53 pathway and the cell cycle inhibitor p21. Differences in E2F target gene activation upon loss of RB family function between human embryonic stem cells, mouse embryonic stem cells and human fibroblasts underscore key differences in the cell cycle regulatory networks of human embryonic stem cells. Finally, loss of RB family function pro- motes genomic instability in both human and mouse embryonic stem cells, uncoupling cell cycle defects from chromosomal instability. These experiments indicate that a homeostatic level of RB activity is essential for the self-renewal and the survival of human embryonic stem cells. 1 Department of Pediatrics, Stanford Medical School, Stanford, California 94305, USA. 2 Department of Genetics, Stanford Medical School, Stanford, California 94305, USA. 3 Institute for Stem Cell Biology and Regenerative Medicine, Stanford Medical School, Stanford, California 94305, USA. Correspondence and requests for materials should be addressed to J.S. -
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. -
Selective Estrogen Receptor Modulators: Discrimination of Agonistic Versus Antagonistic Activities by Gene Expression Profiling in Breast Cancer Cells
[CANCER RESEARCH 64, 1522–1533, February 15, 2004] Selective Estrogen Receptor Modulators: Discrimination of Agonistic versus Antagonistic Activities by Gene Expression Profiling in Breast Cancer Cells Jonna Frasor,1 Fabio Stossi,1 Jeanne M. Danes,1 Barry Komm,2 C. Richard Lyttle,2 and Benita S. Katzenellenbogen1 1Department of Molecular and Integrative Physiology, University of Illinois and College of Medicine, Urbana, Illinois, and 2Women’s Health Research Institute, Wyeth Research, Collegeville, Pennsylvania ABSTRACT tures in these women; however, some detrimental side effects such as an increased risk of endometrial cancer, stroke, and pulmonary embolism Selective estrogen receptor modulators (SERMs) such as tamoxifen are were also associated with tamoxifen treatment (7). Ral was examined in effective in the treatment of many estrogen receptor-positive breast cancers the Multiple Outcomes of Raloxifene Evaluation trial and found to be and have also proven to be effective in the prevention of breast cancer in women at high risk for the disease. The comparative abilities of tamoxifen effective in reducing the incidence of osteoporosis in postmenopausal versus raloxifene in breast cancer prevention are currently being compared in women, as well as the incidence of breast cancer but, unlike tamoxifen, the Study of Tamoxifen and Raloxifene trial. To better understand the actions without the increased risk of endometrial cancer (8, 9). On the basis of the of these compounds in breast cancer, we have examined their effects on the positive outcome of these trials, the Study of Tamoxifen and Raloxifene expression of ϳ12,000 genes, using Affymetrix GeneChip microarrays, with trial was begun in 1999 to directly compare the effects of these two quantitative PCR verification in many cases, categorizing their actions as SERMs, tamoxifen and Ral, in prevention of breast cancer (10, 11). -
Derivation of Stable Microarray Cancer-Differentiating Signatures Using Consensus Scoring of Multiple Random Sampling and Gene-Ranking Consistency Evaluation
Research Article Derivation of Stable Microarray Cancer-Differentiating Signatures Using Consensus Scoring of Multiple Random Sampling and Gene-Ranking Consistency Evaluation Zhi Qun Tang,1,2 Lian Yi Han,1,2 Hong Huang Lin,1,2 Juan Cui,1,2 Jia Jia,1,2 Boon Chuan Low,2,3 Bao Wen Li,2,4 and Yu Zong Chen1,2 1Bioinformatics and Drug Design Group, Department of Pharmacy; 2Center for Computational Science and Engineering; and Departments of 3Biological Sciences and 4Physics, National University of Singapore, Singapore, Singapore Abstract sampling methods. Only 1 to 5 of the 4 to 60 selected predictor Microarrays have been explored for deriving molecular genes in each of these sets are present in more than half of the signatures to determine disease outcomes, mechanisms, other nine sets (Table 1), and 2 to 20 of the predictor genes in each targets, and treatment strategies. Although exhibiting good set are cancer related (Table 2). Despite the use of sophisticated predictive performance, some derived signatures are unstable class differentiation and signature selection methods, the selected due to noises arising from measurement variability and signatures show few overlapping predictor genes, as in the case of biological differences. Improvements in measurement, anno- other microarray data sets including non–Hodgkin lymphoma, tation, and signature selection methods have been proposed. acute lymphocytic leukemia, breast cancer, lung adenocarcinoma, We explored a new signature selection method that incorpo- medulloblastoma, hepatocellular carcinoma, and acute myeloid rates consensus scoring of multiple random sampling and leukemia (9, 15). multistep evaluation of gene-ranking consistency for maxi- Although these signatures display high cancer differentiation mally avoiding erroneous elimination of predictor genes. -
TRANSCRIPTIONAL REGULATION of Hur in RENAL STRESS
TRANSCRIPTIONAL REGULATION OF HuR IN RENAL STRESS DISSERTATION Presented in Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy in the Graduate School of The Ohio State University By Sudha Suman Govindaraju Graduate Program in Biochemistry The Ohio State University 2014 Dissertation Committee: Dr. Beth S. Lee, Ph.D., Advisor Dr. Kathleen Boris-Lawrie, Ph.D. Dr. Sissy M. Jhiang, Ph.D. Dr. Arthur R. Strauch, Ph.D Abstract HuR is a ubiquitously expressed RNA-binding protein that affects the post- transcriptional life of thousands of cellular mRNAs by regulating transcript stability and translation. HuR can post-transcriptionally regulate gene expression and modulate cellular responses to stress, differentiation, proliferation, apoptosis, senescence, inflammation, and the immune response. It is an important mediator of survival during cellular stress, but when inappropriately expressed, can promote oncogenic transformation. Not surprisingly, the expression of HuR itself is tightly regulated at multiple transcriptional and post-transcriptional levels. Previous studies demonstrated the existence of two alternate HuR transcripts that differ in their 5’ untranslated regions and have markedly different translatabilities. These forms were also found to be reciprocally expressed following cellular stress in kidney proximal tubule cell lines, and the shorter, more readily translatable variant was shown to be regulated by Smad 1/5/8 pathway and bone morphogenetic protein-7 (BMP-7) signaling. In this study, the factors that promote transcription of the longer alternate form were identified. NF-κB was shown to be important for expression of the long HuR mRNA, as was a newly identified region with potential for binding the Sp/KLF families of transcription factors. -
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. -
KLF2 Induced
UvA-DARE (Digital Academic Repository) The transcription factor KLF2 in vascular biology Boon, R.A. Publication date 2008 Link to publication Citation for published version (APA): Boon, R. A. (2008). The transcription factor KLF2 in vascular biology. General rights It is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulations If you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: https://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. UvA-DARE is a service provided by the library of the University of Amsterdam (https://dare.uva.nl) Download date:23 Sep 2021 Supplementary data: Genes induced by KLF2 Dekker et al. LocusLink Accession Gene Sequence Description Fold p-value ID number symbol change (FDR) 6654 AK022099 SOS1 cDNA FLJ12037 fis, clone HEMBB1001921. 100.00 5.9E-09 56999 AF086069 ADAMTS9 full length insert cDNA clone YZ35C05. 100.00 1.2E-09 6672 AF085934 SP100 full length insert cDNA clone YR57D07. 100.00 6.7E-13 9031 AF132602 BAZ1B Williams Syndrome critical region WS25 mRNA, partial sequence. -
Molecular Profile of Tumor-Specific CD8+ T Cell Hypofunction in a Transplantable Murine Cancer Model
Downloaded from http://www.jimmunol.org/ by guest on September 25, 2021 T + is online at: average * The Journal of Immunology , 34 of which you can access for free at: 2016; 197:1477-1488; Prepublished online 1 July from submission to initial decision 4 weeks from acceptance to publication 2016; doi: 10.4049/jimmunol.1600589 http://www.jimmunol.org/content/197/4/1477 Molecular Profile of Tumor-Specific CD8 Cell Hypofunction in a Transplantable Murine Cancer Model Katherine A. Waugh, Sonia M. Leach, Brandon L. Moore, Tullia C. Bruno, Jonathan D. Buhrman and Jill E. Slansky J Immunol cites 95 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html http://www.jimmunol.org/content/suppl/2016/07/01/jimmunol.160058 9.DCSupplemental This article http://www.jimmunol.org/content/197/4/1477.full#ref-list-1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material References Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2016 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 25, 2021. The Journal of Immunology Molecular Profile of Tumor-Specific CD8+ T Cell Hypofunction in a Transplantable Murine Cancer Model Katherine A.