TEF Antibody Cat

Total Page：16

File Type：pdf, Size：1020Kb

TEF Antibody Cat. No.: 28-837 TEF Antibody Antibody used in IHC on Human Skeletal muscle at 5 ug/ml. Specifications HOST SPECIES: Rabbit SPECIES REACTIVITY: Human Antibody produced in rabbits immunized with a synthetic peptide corresponding a region IMMUNOGEN: of human TEF. TESTED APPLICATIONS: ELISA, WB TEF antibody can be used for detection of TEF by ELISA at 1:312500. TEF antibody can be APPLICATIONS: used for detection of TEF by western blot at 1.0 μg/mL, and HRP conjugated secondary antibody should be diluted 1:50,000 - 100,000. POSITIVE CONTROL: 1) Cat. No. 1211 - HepG2 Cell Lysate PREDICTED MOLECULAR 33 kDa WEIGHT: September 29, 2021 1 https://www.prosci-inc.com/tef-antibody-28-837.html Properties PURIFICATION: Antibody is purified by peptide affinity chromatography method. CLONALITY: Polyclonal CONJUGATE: Unconjugated PHYSICAL STATE: Liquid Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% BUFFER: sucrose. CONCENTRATION: batch dependent For short periods of storage (days) store at 4˚C. For longer periods of storage, store TEF STORAGE CONDITIONS: antibody at -20˚C. As with any antibody avoid repeat freeze-thaw cycles. Additional Info OFFICIAL SYMBOL: TEF ALTERNATE NAMES: TEF, KIAA1655 ACCESSION NO.: NP_003207 PROTEIN GI NO.: 4507431 GENE ID: 7008 USER NOTE: Optimal dilutions for each application to be determined by the researcher. Background and References TEF (thyrotroph embryonic factor) is a member of the PAR bZip (proline and acidic amino acid-rich basic leucine zipper) transcription factor family. It accumulates with robust circadian rhythms in tissues with high amplitudes of clock gene expression.Thyrotroph embryonic factor (TEF), a transcription factor, is a member of the PAR (proline and acidic amino acid-rich) subfamily of basic region/leucine zipper (bZIP) transcription factors. It is expressed in a broad range of cells and tissues in adult animals, however, during embryonic development, TEF expression appears to be restricted to the developing BACKGROUND: anterior pituitary gland, coincident with the appearance of thyroid-stimulating hormone, beta (TSHB). Indeed, TEF can bind to, and transactivate the TSHB promoter. It shows homology (in the functional domains) with other members of the PAR-bZIP subfamily of transcription factors, which include albumin D box-binding protein (DBP), human hepatic leukemia factor (HLF) and chicken vitellogenin gene-binding protein (VBP); VBP is considered the chicken homologue of TEF. Different members of the subfamily can readily form heterodimers, and share DNA-binding, and transcriptional regulatory properties. REFERENCES: 1) Inukai, T., (2005) Blood 105 (11), 4437-4444. ANTIBODIES FOR RESEARCH USE ONLY. September 29, 2021 2 https://www.prosci-inc.com/tef-antibody-28-837.html For additional information, visit ProSci's Terms & Conditions Page. September 29, 2021 3 https://www.prosci-inc.com/tef-antibody-28-837.html.

Copy Link

Recommended publications

A Molecular Switch for Photoperiod Responsiveness in Mammals
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Current Biology 20, 2193–2198, December 21, 2010 ª2010 Elsevier Ltd All rights reserved DOI 10.1016/j.cub.2010.10.048 Report A Molecular Switch for Photoperiod Responsiveness in Mammals Hugues Dardente,1,* Cathy A. Wyse,1 Mike J. Birnie,1 type 2 thyroid hormone deiodinase (Dio2) expression in the Sandrine M. Dupre´,2 Andrew S.I. Loudon,2 hypothalamus [6]. This enzyme is a gatekeeper for the effects Gerald A. Lincoln,3 and David G. Hazlerigg1,* of thyroid hormone in the hypothalamus, controlling the avail- 1Institute of Biological and Environmental Sciences, Zoology ability of the active form of thyroid hormone, triiodothyronine, Building, Tillydrone Avenue, University of Aberdeen, and dictating the expression of summer phenotypes [7, 8]. Aberdeen AB24 2TZ, UK A unique feature of mammalian seasonal biology [2–5] is that 2Faculty of Life Sciences, University of Manchester, these effects of day length on PT function depend on the pineal Manchester M13 9PT, UK hormone melatonin, which acts via a high density of melatonin 3Queen’s Medical Research Institute, University of Edinburgh, receptors localized in the PT [ 9, 10]. Melatonin is a circadian Edinburgh EH16 4SB, UK signal, with a nocturnal waveform proportional to the length of the night, and consequently, in the PT, melatonin controls the rhythmical expression of multiple transcription factors Summary implicated in circadian function [11–15]. Hence, we hypothe- sized that photoperiodic effects on TSHb expression in the Seasonal synchronization based on day length (photope- PT are initiated through melatonin’s effects on circadian tran- riod) allows organisms to anticipate environmental change.
[Show full text]
Structural and Numerical Changes of Chromosome X in Patients with Esophageal Atresia
European Journal of Human Genetics (2014) 22, 1077–1084 & 2014 Macmillan Publishers Limited All rights reserved 1018-4813/14 www.nature.com/ejhg ARTICLE Structural and numerical changes of chromosome X in patients with esophageal atresia Erwin Brosens*,1,2,5, Elisabeth M de Jong1,2,5, Tahsin Stefan Barakat3, Bert H Eussen1, Barbara D’haene4, Elfride De Baere4, Hannah Verdin4, Pino J Poddighe1, Robert-Jan Galjaard1, Joost Gribnau3, Alice S Brooks1, Dick Tibboel2 and Annelies de Klein1 Esophageal atresia with or without tracheoesophageal fistula (EA/TEF) is a relatively common birth defect often associated with additional congenital anomalies such as vertebral, anal, cardiovascular, renal and limb defects, the so-called VACTERL association. Yet, little is known about the causal genetic factors. Rare case reports of gastrointestinal anomalies in children with triple X syndrome prompted us to survey the incidence of structural and numerical changes of chromosome X in patients with EA/TEF. All available (n ¼ 269) karyotypes of our large (321) EA/TEF patient cohort were evaluated for X-chromosome anomalies. If sufficient DNA material was available, we determined genome-wide copy number profiles with SNP array and identified subtelomeric aberrations on the difficult to profile PAR1 region using telomere-multiplex ligation-dependent probe amplification. In addition, we investigated X-chromosome inactivation (XCI) patterns and mode of inheritance of detected aberrations in selected patients. Three EA/TEF patients had an additional maternally inherited X chromosome. These three female patients had normal random XCI patterns. Two male EA/TEF patients had small inherited duplications of the XY-linked SHOX (Short stature HOmeoboX-containing) locus.
[Show full text]
Transcription Mediated Insulation and Interference Direct Gene Cluster
1 Transcription mediated insulation and interference direct gene 2 cluster expression switches 3 Tania Nguyen1, Harry Fischl1#, Françoise S. Howe1#, Ronja Woloszczuk1#, Ana Serra 4 Barros1*, Zhenyu Xu2*, David Brown1, Struan C. Murray1, Simon Haenni1, James M. 5 Halstead1, Leigh O’Connor1, Gergana Shipkovenska1, Lars M. Steinmetz2 and Jane Mellor1§ 6 1Department of Biochemistry, South Parks Road, Oxford, OX1 3QU, UK 7 2European Molecular Biology Laboratory (EMBL), Genome Biology Unit, 69117 Heidelberg, 8 Germany 9 10 . 11 # , * Equal contribution 12 § Corresponding author: [email protected] 13 14 Competing interests statement: JM is an advisor to Oxford Biodynamics Ltd and Sibelius Ltd and sits 15 on the board of Chronos Therapeutics Ltd. OBD supported this work but have no commercial 16 interest in the study design, data collection and interpretation, or the decision to submit the work 17 for publication. 1 18 Abstract 19 In yeast, many tandemly arranged genes show peak expression in different phases of the 20 metabolic cycle (YMC) or in different carbon sources, indicative of regulation by a bi- 21 modal switch, but it is not clear how these switches are controlled. Using native 22 elongating transcript analysis (NET-seq), we show that transcription itself is a component 23 of bi-modal switches, facilitating reciprocal expression in gene clusters. HMS2, encoding a 24 growth-regulated transcription factor, switches between sense- or antisense-dominant 25 states that also coordinate up- and down-regulation of transcription at neighbouring 26 genes. Engineering HMS2 reveals alternative mono-, di- or tri-cistronic and antisense 27 transcription units (TUs), using different promoter and terminator combinations, that 28 underlie state-switching.
[Show full text]
273.Full-Text.Pdf
Copyright 2001 by the Genetics Society of America The te¯on Gene Is Required for Maintenance of Autosomal Homolog Pairing at Meiosis I in Male Drosophila melanogaster John E. Tomkiel,* Barbara T. Wakimoto² and Albert Briscoe, Jr.* *Center for Molecular Medicine and Genetics, Wayne State University, Detroit, Michigan 48202 and ²Departments of Zoology and Genetics, University of Washington, Seattle, Washington 98195 Manuscript received July 10, 2000 Accepted for publication September 29, 2000 ABSTRACT In recombination-pro®cient organisms, chiasmata appear to mediate associations between homologs at metaphase of meiosis I. It is less clear how homolog associations are maintained in organisms that lack recombination, such as male Drosophila. In lieu of chiasmata and synaptonemal complexes, there must be molecules that balance poleward forces exerted across homologous centromeres. Here we describe the genetic and cytological characterization of four EMS-induced mutations in te¯on (tef), a gene involved in this process in Drosophila melanogaster. All four alleles are male speci®c and cause meiosis I-speci®c nondisjunction of the autosomes. They do not measurably perturb sex chromosome segregation, suggesting that there are differences in the genetic control of autosome and sex chromosome segregation in males. Meiotic transmission of univalent chromosomes is unaffected in tef mutants, implicating the tef product in a pairing-dependent process. The segregation of translocations between sex chromosomes and autosomes is altered in tef mutants in a manner that supports this hypothesis. Consistent with these genetic observations, cytological examination of meiotic chromosomes suggests a role of tef in regulating or mediating pairing of autosomal bivalents at meiosis I.
[Show full text]
A Detailed Genome-Wide Reconstruction of Mouse Metabolism Based on Human Recon 1
UC San Diego UC San Diego Previously Published Works Title A detailed genome-wide reconstruction of mouse metabolism based on human Recon 1 Permalink https://escholarship.org/uc/item/0ck1p05f Journal BMC Systems Biology, 4(1) ISSN 1752-0509 Authors Sigurdsson, Martin I Jamshidi, Neema Steingrimsson, Eirikur et al. Publication Date 2010-10-19 DOI http://dx.doi.org/10.1186/1752-0509-4-140 Supplemental Material https://escholarship.org/uc/item/0ck1p05f#supplemental Peer reviewed eScholarship.org Powered by the California Digital Library University of California Sigurdsson et al. BMC Systems Biology 2010, 4:140 http://www.biomedcentral.com/1752-0509/4/140 RESEARCH ARTICLE Open Access A detailed genome-wide reconstruction of mouse metabolism based on human Recon 1 Martin I Sigurdsson1,2,3, Neema Jamshidi4, Eirikur Steingrimsson1,3, Ines Thiele3,5*, Bernhard Ø Palsson3,4* Abstract Background: Well-curated and validated network reconstructions are extremely valuable tools in systems biology. Detailed metabolic reconstructions of mammals have recently emerged, including human reconstructions. They raise the question if the various successful applications of microbial reconstructions can be replicated in complex organisms. Results: We mapped the published, detailed reconstruction of human metabolism (Recon 1) to other mammals. By searching for genes homologous to Recon 1 genes within mammalian genomes, we were able to create draft metabolic reconstructions of five mammals, including the mouse. Each draft reconstruction was created in compartmentalized and non-compartmentalized version via two different approaches. Using gap-filling algorithms, we were able to produce all cellular components with three out of four versions of the mouse metabolic reconstruction.
[Show full text]
Antagonistic Role of E4BP4 and PAR Proteins in the Circadian Oscillatory Mechanism
Downloaded from genesdev.cshlp.org on September 26, 2021 - Published by Cold Spring Harbor Laboratory Press Antagonistic role of E4BP4 and PAR proteins in the circadian oscillatory mechanism Shigeru Mitsui,1,3 Shun Yamaguchi,1,3 Takuya Matsuo,1,2 Yoshiki Ishida,1 and Hitoshi Okamura1,4 1Department of Anatomy and Brain Science, Kobe University School of Medicine, Chuo-ku, Kobe 650-0017, Japan; 2Department of Physics, Informatics and Biology, Yamaguchi University, Yamaguchi 753-8512, Japan E4BP4, a basic leucine zipper transcription factor, contains a DNA-binding domain closely related to DBP, HLF, and TEF, which are PAR proteins. Here, we show that the phase of e4bp4 mRNA rhythm is opposite to that of the dbp, hlf, and tef rhythms in the suprachiasmatic nucleus (SCN), the mammalian circadian center, and the liver. The protein levels of E4BP4 and DBP also fluctuate in almost the opposite phase. Moreover, all PAR proteins activate, whereas E4BP4 suppresses, the transcriptional activity of the reporter gene containing a common binding sequence in transcriptional assays in vitro. An electrophoretic mobility shift assay demonstrated that E4BP4 is not able to dimerize with the PAR proteins, but is able to compete for the same binding sites with them. Furthermore, we showed sustained low e4bp4 and high dbp mRNA levels in mCry-deficient mice. These results indicate that the E4BP4 and PAR proteins are paired components of a reciprocating mechanism wherein E4BP4 suppresses the transcription of target genes during the time of day when E4BP4 is abundant, and the PAR proteins activate them at another time of day. E4BP4 and the PAR proteins may switch backand forth between the on-off conditions of the target genes.
[Show full text]
A Systematic Model to Predict Transcriptional Regulatory Mechanisms Based on Overrepresentation of Transcription Factor Binding Profiles
Downloaded from genome.cshlp.org on September 26, 2021 - Published by Cold Spring Harbor Laboratory Press Methods A systematic model to predict transcriptional regulatory mechanisms based on overrepresentation of transcription factor binding profiles Li-Wei Chang,1,2 Rakesh Nagarajan,3 Jeffrey A. Magee,3 Jeffrey Milbrandt,3 and Gary D. Stormo1,4 1Department of Genetics, Washington University School of Medicine, St. Louis, Missouri 63110, USA; 2Department of Biomedical Engineering, Washington University, St. Louis, Missouri 63130, USA; 3Department of Pathology and Immunology, Division of Laboratory Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA An important aspect of understanding a biological pathway is to delineate the transcriptional regulatory mechanisms of the genes involved. Two important tasks are often encountered when studying transcription regulation, i.e., (1) the identification of common transcriptional regulators of a set of coexpressed genes; (2) the identification of genes that are regulated by one or several transcription factors. In this study, a systematic and statistical approach was taken to accomplish these tasks by establishing an integrated model considering all of the promoters and characterized transcription factors (TFs) in the genome. A promoter analysis pipeline (PAP) was developed to implement this approach. PAP was tested using coregulated gene clusters collected from the literature. In most test cases, PAP identified the transcription regulators of the input genes accurately. When compared with chromatin immunoprecipitation experiment data, PAP’s predictions are consistent with the experimental observations. When PAP was used to analyze one published expression-profiling data set and two novel coregulated gene sets, PAP was able to generate biologically meaningful hypotheses.
[Show full text]
TEF (NM 003216) Human Tagged ORF Clone – RC205147 | Origene
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 RC205147 TEF (NM_003216) Human Tagged ORF Clone Product data: Product Type: Expression Plasmids Product Name: TEF (NM_003216) Human Tagged ORF Clone Tag: Myc-DDK Symbol: TEF Vector: pCMV6-Entry (PS100001) E. coli Selection: Kanamycin (25 ug/mL) Cell Selection: Neomycin ORF Nucleotide >RC205147 ORF sequence Sequence: Red=Cloning site Blue=ORF Green=Tags(s) TTTTGTAATACGACTCACTATAGGGCGGCCGGGAATTCGTCGACTGGATCCGGTACCGAGGAGATCTGCC GCCGCGATCGCC ATGTCCGACGCGGGCGGCGGAAAGAAGCCGCCTGTGGACCCGCAGGCAGGACCCGGTCCGGGGCCGGGGC GCGCAGCTGGGGAAAGGGGCCTGTCGGGGTCCTTCCCCCTGGTCCTGAAGAAGCTGATGGAGAACCCCCC GCGCGAGGCGCGCCTCGATAAGGAAAAGGGGAAGGAAAAGCTGGAGGAGGACGAGGCCGCAGCCGCCAGC ACCATGGCTGTCTCAGCCTCCCTCATGCCACCCATCTGGGACAAGACCATCCCATATGATGGCGAATCTT TCCACCTGGAGTACATGGACCTGGATGAGTTCCTGCTGGAGAATGGCATCCCCGCCAGCCCCACCCACCT GGCCCACAACCTGCTGCTGCCTGTAGCAGAGCTAGAAGGGAAGGAGTCTGCCAGCTCTTCCACAGCATCC CCACCATCCTCCTCCACTGCCATCTTTCAGCCCTCTGAAACTGTGTCCAGCACAGAATCTTCCCTGGAGA AGGAGAGGGAGACTCCCAGTCCCATCGACCCCAATTGTGTGGAAGTGGATGTGAACTTCAATCCGGACCC CGCCGACCTGGTGCTCTCCAGTGTGCCAGGCGGGGAGCTCTTCAACCCTCGGAAGCACAAGTTTGCTGAG GAGGACCTGAAGCCCCAGCCTATGATCAAAAAGGCCAAGAAGGTCTTTGTCCCCGACGAGCAGAAGGATG AAAAGTACTGGACAAGACGCAAGAAGAACAACGTGGCAGCTAAACGGTCACGGGATGCCCGGCGCCTGAA AGAGAATCAGATCACCATCCGGGCAGCCTTCCTGGAGAAGGAGAACACAGCCCTGCGGACGGAGGTGGCC GAGCTACGCAAGGAGGTGGGCAAGTGCAAGACCATCGTGTCCAAGTATGAGACCAAATACGGGCCCTTG
[Show full text]
Eragrostis Tef (Zucc.) Trotter]
plants Article From Traditional Breeding to Genome Editing for Boosting Productivity of the Ancient Grain Tef [Eragrostis tef (Zucc.) Trotter] Muhammad Numan 1 , Abdul Latif Khan 2 , Sajjad Asaf 2, Mohammad Salehin 1, Getu Beyene 3, Zerihun Tadele 4 and Ayalew Ligaba-Osena 1,* 1 Laboratory of Molecular Biology and Biotechnology, Department of Biology, University of North Carolina at Greensboro, Greensboro, NC 27412, USA; [email protected] (M.N.); [email protected] (M.S.) 2 Natural and Medical Sciences Research Center, Biotechnology and OMICs Laboratory, University of Nizwa, Nizwa 616, Oman; [email protected] (A.L.K.); [email protected] (S.A.) 3 Donald Danforth Plant Science Center, St. Louis, MO 63132, USA; [email protected] 4 Institute of Plant Sciences, University of Bern, Altenbergrain 21, CH-3013 Bern, Switzerland; [email protected] * Correspondence: [email protected] Abstract: Tef (Eragrostis tef (Zucc.) Trotter) is a staple food crop for 70% of the Ethiopian population and is currently cultivated in several countries for grain and forage production. It is one of the most nutritious grains, and is also more resilient to marginal soil and climate conditions than major cereals such as maize, wheat and rice. However, tef is an extremely low-yielding crop, mainly due to lodging, which is when stalks fall on the ground irreversibly, and prolonged drought during the growing season. Climate change is triggering several biotic and abiotic stresses which are Citation: Numan, M.; Khan, A.L.; expected to cause severe food shortages in the foreseeable future. This has necessitated an alternative Asaf, S.; Salehin, M.; Beyene, G.; and robust approach in order to improve resilience to diverse types of stresses and increase crop Tadele, Z.; Ligaba-Osena, A.
[Show full text]
Etiology of Esophageal Atresia and Tracheoesophageal Fistula: “Mind the Gap”
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by PubMed Central Curr Gastroenterol Rep (2010) 12:215–222 DOI 10.1007/s11894-010-0108-1 Etiology of Esophageal Atresia and Tracheoesophageal Fistula: “Mind the Gap” Elisabeth M. de Jong & Janine F. Felix & Annelies de Klein & Dick Tibboel Published online: 28 April 2010 # The Author(s) 2010. This article is published with open access at Springerlink.com Abstract Esophageal atresia and tracheoesophageal fistula 1:3500 live-born infants [1]. Five subtypes are described, (EA/TEF) are major congenital malformations affecting 1:3500 based on the location of the atresia and the type of live births. Current research efforts are focused on understand- connection between trachea and esophagus [2]. Associated ing the etiology of these defects. We describe well-known anomalies occur in 50% of patients and include vertebral, animal models, human syndromes, and associations involving anal, cardiovascular, tracheoesophageal, renal, and limb EA/TEF, indicating its etiologically heterogeneous nature. abnormalities (occurring together in the VACTERL Recent advances in genotyping technology and in knowledge association). Better surgical techniques and pre- and of human genetic variation will improve clinical counseling on postoperative care have improved the prognosis of EA/ etiologic factors. This review provides a clinical summary of TEF over the past decades, but patients still have environmental and genetic factors involved in EA/TEF. significant short- and long-term morbidity [3•]. As with other congenital malformations, EA/TEF occurs at an increased Keywords Congenital anomaly. Foregut . VACTERL . rate in twins, but usually affects only one twin [1].
[Show full text]
Development and Utilization of Human Decidualization Reporter Cell Line Uncovers New Modulators of Female Fertility
Development and utilization of human decidualization reporter cell line uncovers new modulators of female fertility Meade Hallera,1, Yan Yina,1, and Liang Maa,2 aDepartment of Internal Medicine, Division of Dermatology, Washington University in St. Louis, St. Louis, MO 63110 Edited by R. Michael Roberts, University of Missouri, Columbia, MO, and approved August 19, 2019 (received for review May 2, 2019) Failure of embryo implantation accounts for a significant percent- Decidualization involves the rapid proliferation, then differ- age of female infertility. Exquisitely coordinated molecular pro- entiation of fibroblast-like endometrial stromal cells into epithelioid- grams govern the interaction between the competent blastocyst like decidual cells, some of which become large and polyploid or and the receptive uterus. Decidualization, the rapid proliferation multinuclear. These cells become part of the decidual tissue that and differentiation of endometrial stromal cells into decidual cells, surrounds the implanting conceptus (2, 9). The maternal de- is required for implantation. Decidualization defects can cause cidual tissue plays a crucial role in the establishment of preg- poor placentation, intrauterine growth restriction, and early nancy (11, 12). Accompanying the transformation of uterine parturition leading to preterm birth. Decidualization has not yet stromal cells to decidual cells are changes occurring in the en- been systematically studied at the genetic level due to the lack of a dometrium that include extensive extracellular matrix remodel- suitable high-throughput screening tool. Herein we describe the ing, vascular remodeling, angiogenesis, and apoptosis. While generation of an immortalized human endometrial stromal cell line these are happening, the conceptus enlarges and placental de- that uses yellow fluorescent protein under the control of the prolactin velopment occurs (2, 9).
[Show full text]
Suppresses the Expression of Clock Genes by Interfering with E-Box-Mediated Transcription
TNF-␣ suppresses the expression of clock genes by interfering with E-box-mediated transcription Gionata Cavadini*, Saskia Petrzilka*, Philipp Kohler*, Corinne Jud†, Irene Tobler‡, Thomas Birchler*§, and Adriano Fontana*§ *Division of Clinical Immunology, University Hospital Zurich, Haeldeliweg 4, CH-8044 Zurich, Switzerland; †Institute of Biochemistry, University of Fribourg, Rue du Museé 5, CH-1700 Fribourg, Switzerland; and ‡Institute of Pharmacology and Toxicology, University of Zurich, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland Edited by Charles A. Dinarello, University of Colorado Health Sciences Center, Denver, CO, and approved June 15, 2007 (received for review February 22, 2007) Production of TNF-␣ and IL-1 in infectious and autoimmune dis- by the suprachiasmatic nuclei (SCN) of the hypothalamus being eases is associated with fever, fatigue, and sleep disturbances, entrained by light stimuli to the environment. This self- which are collectively referred to as sickness behavior syndrome. In sustaining circadian pacemaker uses a molecular mechanism mice TNF-␣ and IL-1 increase nonrapid eye movement sleep. Be- similar to the one used in subsidiary oscillators present in any cause clock genes regulate the circadian rhythm and thereby type of cell in the organism. The molecular clockwork involves locomotor activity and may alter sleep architecture we assessed the transcriptional repressor genes Per1, Per2, Cry1, and Cry2,as the influence of TNF-␣ on the circadian timing system. TNF-␣ is well as the transcriptional activators Bmal1 and Clock. The shown here to suppress the expression of the PAR bZip clock- heterodimerized transcription factor BMAL1:CLOCK activates controlled genes Dbp, Tef, and Hlf and of the period genes Per1, Per and Cry gene transcription by binding to E-box mo- Per2, and Per3 in fibroblasts in vitro and in vivo in the liver of mice tives in their promoters.
[Show full text]