Daily Rhythmicity of Clock Gene Transcript Levels in Fast and Slow
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SHARP1 (BHLHE41) Mouse Monoclonal Antibody [Clone ID: OTI3H4] Product Data
OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for TA806354 SHARP1 (BHLHE41) Mouse Monoclonal Antibody [Clone ID: OTI3H4] Product data: Product Type: Primary Antibodies Clone Name: OTI3H4 Applications: IHC, WB Recommended Dilution: WB 1:2000, IHC 1:150 Reactivity: Human Host: Mouse Isotype: IgG1 Clonality: Monoclonal Immunogen: Human recombinant protein fragment corresponding to amino acids 1-297 of human BHLHE41(NP_110389) produced in E.coli. Formulation: PBS (PH 7.3) containing 1% BSA, 50% glycerol and 0.02% sodium azide. Concentration: 1 mg/ml Purification: Purified from mouse ascites fluids or tissue culture supernatant by affinity chromatography (protein A/G) Conjugation: Unconjugated Storage: Store at -20°C as received. Stability: Stable for 12 months from date of receipt. Predicted Protein Size: 50.3 kDa Gene Name: basic helix-loop-helix family member e41 Database Link: NP_110389 Entrez Gene 79365 Human Q9C0J9 Background: This gene encodes a basic helix-loop-helix protein expressed in various tissues. The encoded protein can interact with ARNTL or compete for E-box binding sites in the promoter of PER1 and repress CLOCK/ARNTL's transactivation of PER1. This gene is believed to be involved in the control of circadian rhythm and cell differentiation. Defects in this gene are associated with the short sleep phenotype. [provided by RefSeq, Feb 2014] This product is to be used for laboratory only. Not for diagnostic or therapeutic use. View online » ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 1 / 2 SHARP1 (BHLHE41) Mouse Monoclonal Antibody [Clone ID: OTI3H4] – TA806354 Synonyms: BHLHB3; DEC2; hDEC2; SHARP1 Protein Families: Transcription Factors Protein Pathways: Circadian rhythm - mammal Product images: HEK293T cells were transfected with the pCMV6- ENTRY control (Left lane) or pCMV6-ENTRY BHLHE41 ([RC206882], Right lane) cDNA for 48 hrs and lysed. -
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. -
P53 Regulates Myogenesis by Triggering the Differentiation
CORE Metadata, citation and similar papers at core.ac.uk Provided by PubMed Central p53 Regulates Myogenesis by Triggering the Differentiation Activity of pRb Alessandro Porrello, Maria Antonietta Cerone, Sabrina Coen, Aymone Gurtner, Giulia Fontemaggi, Letizia Cimino, Giulia Piaggio, Ada Sacchi, and Silvia Soddu Molecular Oncogenesis Laboratory, Regina Elena Cancer Institute, Center for Experimental Research, 00158 Rome, Italy Abstract. The p53 oncosuppressor protein regulates mary myoblasts, pRb is hypophosphorylated and prolif- cell cycle checkpoints and apoptosis, but increasing evi- eration stops. However, these cells do not upregulate dence also indicates its involvement in differentiation pRb and have reduced MyoD activity. The transduction and development. We had previously demonstrated of exogenous TP53 or Rb genes in p53-defective myo- that in the presence of differentiation-promoting stim- blasts rescues MyoD activity and differentiation poten- uli, p53-defective myoblasts exit from the cell cycle but tial. Additionally, in vivo studies on the Rb promoter do not differentiate into myocytes and myotubes. To demonstrate that p53 regulates the Rb gene expression identify the pathways through which p53 contributes at transcriptional level through a p53-binding site. to skeletal muscle differentiation, we have analyzed Therefore, here we show that p53 regulates myoblast the expression of a series of genes regulated during differentiation by means of pRb without affecting its myogenesis in parental and dominant–negative p53 cell cycle–related functions. (dnp53)-expressing C2C12 myoblasts. We found that in dnp53-expressing C2C12 cells, as well as in p53Ϫ/Ϫ pri- Key words: p53 • Rb • MyoD • differentiation • muscle Introduction The differentiation of skeletal myoblasts is characterized review, see Wright, 1992). -
Targeting Glioblastoma Stem Cells Through Disruption of the Circadian Clock
Published OnlineFirst August 27, 2019; DOI: 10.1158/2159-8290.CD-19-0215 RESEARCH ARTICLE Targeting Glioblastoma Stem Cells through Disruption of the Circadian Clock Zhen Dong1, Guoxin Zhang1, Meng Qu2, Ryan C. Gimple1,3, Qiulian Wu1, Zhixin Qiu1, Briana C. Prager1,3, Xiuxing Wang1, Leo J.Y. Kim1,3, Andrew R. Morton3, Deobrat Dixit1, Wenchao Zhou4, Haidong Huang4, Bin Li5, Zhe Zhu1, Shideng Bao4, Stephen C. Mack6, Lukas Chavez7, Steve A. Kay2, and Jeremy N. Rich1 Downloaded from cancerdiscovery.aacrjournals.org on September 24, 2021. © 2019 American Association for Cancer Research. Published OnlineFirst August 27, 2019; DOI: 10.1158/2159-8290.CD-19-0215 ABSTRACT Glioblastomas are highly lethal cancers, containing self-renewing glioblastoma stem cells (GSC). Here, we show that GSCs, differentiated glioblastoma cells (DGC), and nonmalignant brain cultures all displayed robust circadian rhythms, yet GSCs alone displayed exquisite dependence on core clock transcription factors, BMAL1 and CLOCK, for optimal cell growth. Downregulation of BMAL1 or CLOCK in GSCs induced cell-cycle arrest and apoptosis. Chromatin immu- noprecipitation revealed that BMAL1 preferentially bound metabolic genes and was associated with active chromatin regions in GSCs compared with neural stem cells. Targeting BMAL1 or CLOCK attenu- ated mitochondrial metabolic function and reduced expression of tricarboxylic acid cycle enzymes. Small-molecule agonists of two independent BMAL1–CLOCK negative regulators, the cryptochromes and REV-ERBs, downregulated stem cell factors and reduced GSC growth. Combination of cryp- tochrome and REV-ERB agonists induced synergistic antitumor effi cacy. Collectively, these fi ndings show that GSCs co-opt circadian regulators beyond canonical circadian circuitry to promote stemness maintenance and metabolism, offering novel therapeutic paradigms. -
Investigation of the Underlying Hub Genes and Molexular Pathogensis in Gastric Cancer by Integrated Bioinformatic Analyses
bioRxiv preprint doi: https://doi.org/10.1101/2020.12.20.423656; this version posted December 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. Investigation of the underlying hub genes and molexular pathogensis in gastric cancer by integrated bioinformatic analyses Basavaraj Vastrad1, Chanabasayya Vastrad*2 1. Department of Biochemistry, Basaveshwar College of Pharmacy, Gadag, Karnataka 582103, India. 2. Biostatistics and Bioinformatics, Chanabasava Nilaya, Bharthinagar, Dharwad 580001, Karanataka, India. * Chanabasayya Vastrad [email protected] Ph: +919480073398 Chanabasava Nilaya, Bharthinagar, Dharwad 580001 , Karanataka, India bioRxiv preprint doi: https://doi.org/10.1101/2020.12.20.423656; this version posted December 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. Abstract The high mortality rate of gastric cancer (GC) is in part due to the absence of initial disclosure of its biomarkers. The recognition of important genes associated in GC is therefore recommended to advance clinical prognosis, diagnosis and and treatment outcomes. The current investigation used the microarray dataset GSE113255 RNA seq data from the Gene Expression Omnibus database to diagnose differentially expressed genes (DEGs). Pathway and gene ontology enrichment analyses were performed, and a proteinprotein interaction network, modules, target genes - miRNA regulatory network and target genes - TF regulatory network were constructed and analyzed. Finally, validation of hub genes was performed. The 1008 DEGs identified consisted of 505 up regulated genes and 503 down regulated genes. -
Cellular and Developmental Control of O2 Homeostasis by Hypoxia-Inducible Factor 1␣
Downloaded from genesdev.cshlp.org on September 28, 2021 - Published by Cold Spring Harbor Laboratory Press Cellular and developmental control of O2 homeostasis by hypoxia-inducible factor 1a Narayan V. Iyer,1,5 Lori E. Kotch,1,5 Faton Agani,1 Sandra W. Leung,1 Erik Laughner,1 Roland H. Wenger,2 Max Gassmann,2 John D. Gearhart,3 Ann M. Lawler,3 Aimee Y. Yu,1 and Gregg L. Semenza1,4 1Center for Medical Genetics, Departments of Pediatrics and Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287-3914 USA; 2Institute of Physiology, University of Zurich-Irchel, 8057 Zurich, Switzerland; 3Department of Gynecology and Obstetrics, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 USA Hypoxia is an essential developmental and physiological stimulus that plays a key role in the pathophysiology of cancer, heart attack, stroke, and other major causes of mortality. Hypoxia-inducible factor 1 (HIF-1) is the only known mammalian transcription factor expressed uniquely in response to physiologically relevant levels −/− of hypoxia. We now report that in Hif1a embryonic stem cells that did not express the O2-regulated HIF-1a subunit, levels of mRNAs encoding glucose transporters and glycolytic enzymes were reduced, and cellular proliferation was impaired. Vascular endothelial growth factor mRNA expression was also markedly decreased in hypoxic Hif1a−/− embryonic stem cells and cystic embryoid bodies. Complete deficiency of HIF-1a resulted in developmental arrest and lethality by E11 of Hif1a−/− embryos that manifested neural tube defects, cardiovascular malformations, and marked cell death within the cephalic mesenchyme. In Hif1a+/+ embryos, HIF-1a expression increased between E8.5 and E9.5, coincident with the onset of developmental defects and cell death in Hif1a−/− embryos. -
The MCK Enhancer Contains a P53 Responsive Element (P53/Anti-Oncogene/Trans-Activation) HAROLD WEINTRAUB*, STEPHEN Hauschkat, and STEPHEN J
Proc. Natl. Acad. Sci. USA Vol. 88, pp. 4570-4571, June 1991 Biochemistry The MCK enhancer contains a p53 responsive element (p53/anti-oncogene/trans-activation) HAROLD WEINTRAUB*, STEPHEN HAUSCHKAt, AND STEPHEN J. TAPSCOTT* *Howard Hughes Medical Institute, Fred Hutchinson Cancer Research Center, 1124 Columbia Street, Seattle, WA 98104; and tDepartment of Biochemistry, University of Washington, Seattle, WA 98195 Contributed by Harold Weintraub, March 4, 1991 ABSTRACT p53 is an antioncogene that is defective or suggesting that activation may be species specific; however, absent in a large number of human tumors. Its function in levels ofprotein produced by the expression vectors were not normal cells is not known. We show that co-transfection of directly assayed in these experiments. By using an MCK- mouse p53 with muscle-specific creatine kinase-chloramphen- specific antibody, we have not been able to demonstrate icol acetyltransferase reporter gene, containing 3.3 kilobase of activation of the endogenous MCK gene in 10T1/2 cells upstream control sequence for the muscle-specfic creatine transfected with p53; in contrast 10T'/2 cells transfected with kinase gene, results in a 10- to 80-fold activation. The p53 MyoD express endogenous MCK immunoreactivity. responsive element maps to a region disinguhed from the Table 2 shows that a transforming mutant of murine p53 known MyoD binding region. Identification ofa p53 responsive (Ala -3 Val at position 135) fails to activate MCK-CAT in element should allow a more focused analysis of the effects of CV1 cells. A related mutation has lost its capacity for p53 in controlling gene activity. transactivation when fused to the DNA binding domain of GaI4 (5, 6). -
Role of the Nuclear Receptor Rev-Erb Alpha in Circadian Food Anticipation and Metabolism Julien Delezie
Role of the nuclear receptor Rev-erb alpha in circadian food anticipation and metabolism Julien Delezie To cite this version: Julien Delezie. Role of the nuclear receptor Rev-erb alpha in circadian food anticipation and metabolism. Neurobiology. Université de Strasbourg, 2012. English. NNT : 2012STRAJ018. tel- 00801656 HAL Id: tel-00801656 https://tel.archives-ouvertes.fr/tel-00801656 Submitted on 10 Apr 2013 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. UNIVERSITÉ DE STRASBOURG ÉCOLE DOCTORALE DES SCIENCES DE LA VIE ET DE LA SANTE CNRS UPR 3212 · Institut des Neurosciences Cellulaires et Intégratives THÈSE présentée par : Julien DELEZIE soutenue le : 29 juin 2012 pour obtenir le grade de : Docteur de l’université de Strasbourg Discipline/ Spécialité : Neurosciences Rôle du récepteur nucléaire Rev-erbα dans les mécanismes d’anticipation des repas et le métabolisme THÈSE dirigée par : M CHALLET Etienne Directeur de recherche, université de Strasbourg RAPPORTEURS : M PFRIEGER Frank Directeur de recherche, université de Strasbourg M KALSBEEK Andries -
Androgen-Dependent Pathology Demonstrates Myopathic
Research article Androgen-dependent pathology demonstrates myopathic contribution to the Kennedy disease phenotype in a mouse knock-in model Zhigang Yu,1 Nahid Dadgar,1 Megan Albertelli,2 Kirsten Gruis,3 Cynthia Jordan,4 Diane M. Robins,2 and Andrew P. Lieberman1 1Department of Pathology, 2Department of Human Genetics, and 3Department of Neurology, University of Michigan Medical School, Ann Arbor, Michigan, USA. 4Department of Psychology and Neuroscience Program, Michigan State University, East Lansing, Michigan, USA. Kennedy disease, a degenerative disorder characterized by androgen-dependent neuromuscular weakness, is caused by a CAG/glutamine tract expansion in the androgen receptor (Ar) gene. We developed a mouse model of Kennedy disease, using gene targeting to convert mouse androgen receptor (AR) to human sequence while introducing 113 glutamines. AR113Q mice developed hormone and glutamine length–dependent neuromus- cular weakness characterized by the early occurrence of myopathic and neurogenic skeletal muscle pathology and by the late development of neuronal intranuclear inclusions in spinal neurons. AR113Q males unexpect- edly died at 2–4 months. We show that this androgen-dependent death reflects decreased expression of skeletal muscle chloride channel 1 (CLCN1) and the skeletal muscle sodium channel α-subunit, resulting in myotonic discharges in skeletal muscle of the lower urinary tract. AR113Q limb muscles show similar myopathic features and express decreased levels of mRNAs encoding neurotrophin-4 and glial cell line–derived neurotrophic fac- tor. These data define an important myopathic contribution to the Kennedy disease phenotype and suggest a role for muscle in non–cell autonomous toxicity of lower motor neurons. Introduction dent on the presence of androgen (13–16) and is regulated, in Kennedy disease, or spinal and bulbar muscular atrophy, is one part, by hormone-dependent retrograde transport (17, 18). -
Circadian Rhythmicity and the Influence of 'Clock
2311 Z Kiss and P M Ghosh Prostate cancer and the 23:11 T123–T134 Thematic Review ‘clock’ genes WOMEN IN CANCER THEMATIC REVIEW Circadian rhythmicity and the influence of ‘clock’ genes on prostate cancer Zsofia Kiss1,2 and Paramita M Ghosh1,2,3 1VA Northern California Health Care System, Mather, California, USA Correspondence 2Department of Urology, University of California at Davis, Sacramento, California, USA should be addressed 3Department of Biochemistry and Molecular Medicine, University of California at Davis, Sacramento, to P M Ghosh California, USA Email [email protected] Abstract Key Words The androgen receptor (AR) plays a key role in the development and progression f circadian clock of prostate cancer (CaP). Since the mid-1990s, reports in the literature pointed out f androgen receptor higher incidences of CaP in some select groups, such as airline pilots and night shift f melatonin workers in comparison with those working regular hours. The common finding in these f per1 ‘high-risk’ groups was that they all experienced a deregulation of the body’s internal f bmal1 circadian rhythm. Here, we discuss how the circadian rhythm affects androgen levels and modulates CaP development and progression. Circadian rhythmicity of androgen Endocrine-Related Cancer Endocrine-Related production is lost in CaP patients, with the clock genes Per1 and Per2 decreasing, and Bmal1 increasing, in these individuals. Periodic expression of the clock genes was restored upon administration of the neurohormone melatonin, thereby suppressing CaP progression. Activation of the melatonin receptors and the AR antagonized each other, and therefore the tumour-suppressive effects of melatonin and the clock genes were most clearly observed in the absence of androgens, that is, in conjunction with androgen deprivation therapy (ADT). -
Myod-Cre Driven Alterations in K-Ras and P53 Lead to a Mouse Model
bioRxiv preprint doi: https://doi.org/10.1101/2021.06.15.448607; this version posted June 15, 2021. 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. MyoD-Cre driven alterations in K-Ras and p53 lead to a mouse model with histological and molecular characteristics of human rhabdomyosarcoma with direct translational applications Kengo Nakahata1, Brian W. Simons2, Enrico Pozzo3, Ryan Shuck1, Lyazat Kurenbekova1, Cristian Coarfa4,6 Tajhal D. Patel1, and Jason T. Yustein*1,5,6 1Texas Children’s Cancer and Hematology Centers and The Faris D. Virani Ewing Sarcoma Center, Baylor College of Medicine, Houston, TX 77030 2Center for Comparative Medicine, Baylor College of Medicine, Houston, TX 77030 3Translational Cardiomyology Laboratory, Stem Cell Research Institute, Stem Cell Biology and Embryology Unit, Department of Development and Regeneration, KU Leuven, Leuven, Belgium. 4Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030 5Cancer and Cell Biology Program, Baylor College of Medicine, Houston, TX 77030 6Dan L. Duncan Cancer Comprehensive Center, Baylor College of Medicine, Houston, TX 77030 *Corresponding Author Corresponding Author: Jason T. Yustein, MD, PhD 1102 Bates St., Suite 1025.07 Houston, Texas 77030 832-824-4601 (Office) [email protected] ORCID: https://orcid.org/0000-0002-2052-0527 - 1 - bioRxiv preprint doi: https://doi.org/10.1101/2021.06.15.448607; this version posted June 15, 2021. 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. -
Hypoxia and Aging Eui-Ju Yeo1
Yeo Experimental & Molecular Medicine (2019) 51:67 https://doi.org/10.1038/s12276-019-0233-3 Experimental & Molecular Medicine REVIEW ARTICLE Open Access Hypoxia and aging Eui-Ju Yeo1 Abstract Eukaryotic cells require sufficient oxygen (O2) for biological activity and survival. When the oxygen demand exceeds its supply, the oxygen levels in local tissues or the whole body decrease (termed hypoxia), leading to a metabolic crisis, threatening physiological functions and viability. Therefore, eukaryotes have developed an efficient and rapid oxygen sensing system: hypoxia-inducible factors (HIFs). The hypoxic responses are controlled by HIFs, which induce the expression of several adaptive genes to increase the oxygen supply and support anaerobic ATP generation in eukaryotic cells. Hypoxia also contributes to a functional decline during the aging process. In this review, we focus on the molecular mechanisms regulating HIF-1α and aging-associated signaling proteins, such as sirtuins, AMP-activated protein kinase, mechanistic target of rapamycin complex 1, UNC-51-like kinase 1, and nuclear factor κB, and their roles in aging and aging-related diseases. In addition, the effects of prenatal hypoxia and obstructive sleep apnea (OSA)- induced intermittent hypoxia have been reviewed due to their involvement in the progression and severity of many diseases, including cancer and other aging-related diseases. The pathophysiological consequences and clinical manifestations of prenatal hypoxia and OSA-induced chronic intermittent hypoxia are discussed in detail. Introduction chemoreceptors stimulates the neurotransmitter release 3 1234567890():,; 1234567890():,; 1234567890():,; 1234567890():,; Oxygen (O2) plays critical roles in aerobic respiration pathway and modulates the activity of a neutral endo- and metabolism as the final electron acceptor of the peptidase, neprilysin (NEP), which modifies the cellular mitochondrial electron transport chain, which is respon- response to hypoxia by hydrolyzing substance P4.