Cited2 Modulates TGF-B-Mediated Upregulation of MMP9
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LHX2 (NM 004789) Human Tagged ORF Clone 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 RC210786L4 LHX2 (NM_004789) Human Tagged ORF Clone Product data: Product Type: Expression Plasmids Product Name: LHX2 (NM_004789) Human Tagged ORF Clone Tag: mGFP Symbol: LHX2 Synonyms: hLhx2; LH2 Vector: pLenti-C-mGFP-P2A-Puro (PS100093) E. coli Selection: Chloramphenicol (34 ug/mL) Cell Selection: Puromycin ORF Nucleotide The ORF insert of this clone is exactly the same as(RC210786). Sequence: Restriction Sites: SgfI-MluI Cloning Scheme: ACCN: NM_004789 ORF Size: 1218 bp 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 LHX2 (NM_004789) Human Tagged ORF Clone – RC210786L4 OTI Disclaimer: The molecular sequence of this clone aligns with the gene accession number as a point of reference only. However, individual transcript sequences of the same gene can differ through naturally occurring variations (e.g. polymorphisms), each with its own valid existence. This clone is substantially in agreement with the reference, but a complete review of all prevailing variants is recommended prior to use. More info OTI Annotation: This clone was engineered to express the complete ORF with an expression tag. Expression varies depending on the nature of the gene. RefSeq: NM_004789.3 RefSeq Size: 2416 bp RefSeq ORF: 1221 bp Locus ID: 9355 UniProt ID: P50458, B3KNJ5 Domains: homeobox, LIM Protein Families: Transcription Factors MW: 44.4 kDa Gene Summary: This gene encodes a protein belonging to a large protein family, members of which carry the LIM domain, a unique cysteine-rich zinc-binding domain. -
Cited2 Controls Left-Right Patterning and Heart Development Through a Nodal-Pitx2c Pathway
ARTICLES Cited2 controls left-right patterning and heart development through a Nodal-Pitx2c pathway Simon D Bamforth1,6,Jose´ Braganc¸a1,6, Cassandra R Farthing1,6,Ju¨rgen E Schneider1, Carol Broadbent1, Anna C Michell1, Kieran Clarke2, Stefan Neubauer1, Dominic Norris3, Nigel A Brown4, Robert H Anderson5 & Shoumo Bhattacharya1 Malformations of the septum, outflow tract and aortic arch are the most common congenital cardiovascular defects and occur in mice lacking Cited2, a transcriptional coactivator of TFAP2. Here we show that Cited2–/– mice also develop laterality defects, including right isomerism, abnormal cardiac looping and hyposplenia, which are suppressed on a mixed http://www.nature.com/naturegenetics genetic background. Cited2–/– mice lack expression of the Nodal target genes Pitx2c, Nodal and Ebaf in the left lateral plate mesoderm, where they are required for establishing laterality and cardiovascular development. CITED2 and TFAP2 were detected at the Pitx2c promoter in embryonic hearts, and they activate Pitx2c transcription in transient transfection assays. We propose that an abnormal Nodal-Pitx2c pathway represents a unifying mechanism for the cardiovascular malformations observed in Cited2–/– mice, and that such malformations may be the sole manifestation of a laterality defect. Genetic, developmental and molecular studies over the past decade transcription factors by linking them to EP300 and CREBBP9,15,16. have identified a number of DNA-binding transcription factors that Mutations in Tcfap2a and TFAP2B (Char syndrome) result in cardiac have key roles in cardiac morphogenesis and in the pathogenesis of and aortic arch malformations17,18, suggesting that coactivation of common congenital heart defects1. The role of transcriptional coacti- TFAP2 by CITED2, EP300 and CREBBP is necessary for the normal vators, molecules that connect DNA-binding transcription factors to development of these structures9. -
Absence of S100A4 in the Mouse Lens Induces an Aberrant Retina-Specific Differentiation Program and Cataract
www.nature.com/scientificreports OPEN Absence of S100A4 in the mouse lens induces an aberrant retina‑specifc diferentiation program and cataract Rupalatha Maddala1*, Junyuan Gao2, Richard T. Mathias2, Tylor R. Lewis1, Vadim Y. Arshavsky1,3, Adriana Levine4, Jonathan M. Backer4,5, Anne R. Bresnick4 & Ponugoti V. Rao1,3* S100A4, a member of the S100 family of multifunctional calcium‑binding proteins, participates in several physiological and pathological processes. In this study, we demonstrate that S100A4 expression is robustly induced in diferentiating fber cells of the ocular lens and that S100A4 (−/−) knockout mice develop late‑onset cortical cataracts. Transcriptome profling of lenses from S100A4 (−/−) mice revealed a robust increase in the expression of multiple photoreceptor‑ and Müller glia‑specifc genes, as well as the olfactory sensory neuron‑specifc gene, S100A5. This aberrant transcriptional profle is characterized by corresponding increases in the levels of proteins encoded by the aberrantly upregulated genes. Ingenuity pathway network and curated pathway analyses of diferentially expressed genes in S100A4 (−/−) lenses identifed Crx and Nrl transcription factors as the most signifcant upstream regulators, and revealed that many of the upregulated genes possess promoters containing a high‑density of CpG islands bearing trimethylation marks at histone H3K27 and/or H3K4, respectively. In support of this fnding, we further documented that S100A4 (−/−) knockout lenses have altered levels of trimethylated H3K27 and H3K4. Taken together, -
Exploring the Relationship Between Gut Microbiota and Major Depressive Disorders
E3S Web of Conferences 271, 03055 (2021) https://doi.org/10.1051/e3sconf/202127103055 ICEPE 2021 Exploring the Relationship between Gut Microbiota and Major Depressive Disorders Catherine Tian1 1Shanghai American School, Shanghai, China Abstract. Major Depressive Disorder (MDD) is a psychiatric disorder accompanied with a high rate of suicide, morbidity and mortality. With the symptom of an increasing or decreasing appetite, there is a possibility that MDD may have certain connections with gut microbiota, the colonies of microbes which reside in the human digestive system. In recent years, more and more studies started to demonstrate the links between MDD and gut microbiota from animal disease models and human metabolism studies. However, this relationship is still largely understudied, but it is very innovative since functional dissection of this relationship would furnish a new train of thought for more effective treatment of MDD. In this study, by using multiple genetic analytic tools including Allen Brain Atlas, genetic function analytical tools, and MicrobiomeAnalyst, I explored the genes that shows both expression in the brain and the digestive system to affirm that there is a connection between gut microbiota and the MDD. My approach finally identified 7 MDD genes likely to be associated with gut microbiota, implicating 3 molecular pathways: (1) Wnt Signaling, (2) citric acid cycle in the aerobic respiration, and (3) extracellular exosome signaling. These findings may shed light on new directions to understand the mechanism of MDD, potentially facilitating the development of probiotics for better psychiatric disorder treatment. 1 Introduction 1.1 Major Depressive Disorder Major Depressive Disorder (MDD) is a mood disorder that will affect the mood, behavior and other physical parts. -
Wilms' Tumor Gene 1 in Different Types of Cancer
UMEÅ UNIVERSITY MEDICAL DISSERTATIONS New Series No.1717 ISSN 0346-6612 ISBN 978-91-7601-263-5 Wilms’ tumor gene 1 in different types of cancer Xingru Li Department of Medical Biosciences, Clinical Chemistry Umeå University, Sweden Umeå 2015 Copyright © 2015 Xingru Li ISBN: 978-91-7601-263-5 ISSN: 0346-6612 Printed by: Print & Media Umeå, Sweden, 2015 To my family Table of Contents Abstract .......................................................................................................... 1 Original Articles ............................................................................................. 2 Abbreviations ................................................................................................. 3 Introduction .................................................................................................... 4 WT1 (Wilms’ tumor gene 1) ...................................................................... 4 Structure of WT1 ..................................................................................... 4 WT1, the transcription factor ................................................................. 5 WT1 and its interacting partners ............................................................ 5 WT1 function .......................................................................................... 8 The tumor suppressor ........................................................................ 8 An oncogene ...................................................................................... 8 Mutations and -
Brief Report
BRIEF REPORT CITED2 mutations potentially cause idiopathic premature ovarian failure DORA JANETH FONSECA, DIEGO OJEDA, BESMA LAKHAL, RIM BRAHAM, STEFANIE EGGERS, ERIN TURBITT, STEFAN WHITE, SONIA GROVER, GARRY WARNE, MARGARET ZACHARIN, ^ ALEXANDRA NEVIN LAM, HANENE LANDOLSI, HATEM ELGHEZAL, ALI SAAD, CARLOS MARTIN RESTREPO, MARC FELLOUS, ANDREW SINCLAIR, PETER KOOPMAN, and PAUL LAISSUE BOGOTA, COLOMBIA; SOUSSE, TUNISIA; MELBOURNE AND BRISBANE, AUSTRALIA; AND PARIS, FRANCE Anomalies in gonadal development in a mouse knockout model of Cited2 have been recently described. In Cited2 2/2 female gonads, an ectopic cell migration was observed and the female program of sex determination was transiently delayed. We hypothesize that, in humans, this temporary inhibition of genes should be sufficient to provoke a developmental impairment of the female gonads, conducive to prema- ture ovarian failure (POF). To establish whether CITED2 mutations are a common cause of the disease, we performed a mutational analysis of this gene in a panel of patients with POF and in a group of control women with normal fertility. We amplified and di- rectly sequenced the complete open reading frame of CITED2 in 139 patients with POF and 290 controls. This study revealed 5 synonymous and 3 nonsynonymous vari- ants. Among these, 7 are novel. The nonsynonymous variant c.604C.A (p.Pro202Thr) was found uniquely in 1 woman from the POF group. In silico analysis of this mutation indicated a potential deleterious effect. We conclude that mutations in CITED2 may be involved -
Action by CITED2 in the Nucleus B Κ
Negative Feedback Regulation of NF-κB Action by CITED2 in the Nucleus Xiwen Lou, Shaogang Sun, Wei Chen, Yi Zhou, Yuefeng Huang, Xing Liu, Yufei Shan and Chen Wang This information is current as of September 29, 2021. J Immunol 2011; 186:539-548; Prepublished online 22 November 2010; doi: 10.4049/jimmunol.1001650 http://www.jimmunol.org/content/186/1/539 Downloaded from Supplementary http://www.jimmunol.org/content/suppl/2010/11/22/jimmunol.100165 Material 0.DC1 References This article cites 45 articles, 19 of which you can access for free at: http://www.jimmunol.org/ http://www.jimmunol.org/content/186/1/539.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists by guest on September 29, 2021 • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Negative Feedback Regulation of NF-kB Action by CITED2 in the Nucleus Xiwen Lou, Shaogang Sun, Wei Chen, Yi Zhou, Yuefeng Huang, Xing Liu, Yufei Shan, and Chen Wang NF-kB is a family of important transcription factors that modulate immunity, development, inflammation, and cancer. -
Thelhx2transcription Factor Controls Thalamocortical Axonal
4372 • The Journal of Neuroscience, March 28, 2012 • 32(13):4372–4385 Development/Plasticity/Repair The Lhx2 Transcription Factor Controls Thalamocortical Axonal Guidance by Specific Regulation of Robo1 and Robo2 Receptors Paula Marcos-Monde´jar,1 Sandra Peregrín,1 James Y. Li,2 Leif Carlsson,3 Shubha Tole,4 and Guillermina Lo´pez-Bendito1 1Instituto de Neurociencias de Alicante, Consejo Superior de Investigaciones Científicas and Universidad Miguel Herna´ndez, 03550 Sant Joan d’Alacant, Spain, 2Department of Genetics and Developmental Biology, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, Connecticut 06030-6403, 3Umeå Center for Molecular Medicine, Umeå University, 901 87 Umeå, Sweden, and 4Department of Biological Sciences, Tata Institute of Fundamental Research, Colaba, Mumbai 400 005, India The assembly of neural circuits is dependent upon the generation of specific neuronal subtypes, each subtype displaying unique prop- erties that direct the formation of selective connections with appropriate target cells. Actions of transcription factors in neural progen- itors and postmitotic cells are key regulators in this process. LIM-homeodomain transcription factors control crucial aspects of neuronal differentiation, including subtype identity and axon guidance. Nonetheless, their regulation during development is poorly understood and the identity of the downstream molecular effectors of their activity remains largely unknown. Here, we demonstrate that the Lhx2 transcription factor is dynamically regulated in distinct pools of thalamic neurons during the development of thalamocortical connec- tivity in mice. Indeed, overexpression of Lhx2 provokes defective thalamocortical axon guidance in vivo, while specific conditional deletion of Lhx2 in the thalamus produces topographic defects that alter projections from the medial geniculate nucleus and from the caudal ventrobasal nucleus in particular. -
CITED2 Functions As a Molecular Switch of Cytokine-Induced Proliferation and Quiescence
Cell Death and Differentiation (2012) 19, 2015–2028 & 2012 Macmillan Publishers Limited All rights reserved 1350-9047/12 www.nature.com/cdd CITED2 functions as a molecular switch of cytokine-induced proliferation and quiescence Y-T Chou1,10, C-H Hsieh2,10, S-H Chiou3,4,10, C-F Hsu1, Y-R Kao1, C-C Lee1, C-H Chung1, Y-H Wang5, H-S Hsu4,6, S-T Pang7, Y-S Shieh8 and C-W Wu*,1,2,4,9 Transforming growth factor-a (TGF-a)-induced proliferation and transforming growth factor-b (TGF-b)-mediated quiescence are intricately balanced in normal lung-tissue homeostasis but are deregulated during neoplastic progression of lung cancer. Here, we show that Cbp/p300-interacting transactivator with Glu/Asp-rich carboxy-terminal domain 2 (CITED2), a novel MYC- interacting transcriptional modulator, responds to TGF-a induction and TGF-b suppression to orchestrate cellular proliferation and quiescence, respectively. Upon TGF-a induction, CITED2 was induced by MYC and further modulated MYC-mediated transcription in a feed-forward manner. CITED2 recruited p300 to promote MYC-p300-mediated transactivation of E2F3, leading to increased G1/S cell cycle progression. Moreover, CITED2 inhibited cellular quiescence by enhancing MYC-mediated suppression of p21CIP1. CITED2 interacted with histone deacetylase 1 (HDAC1) and potentiated MYC–HDAC1 complex formation. TGF-b stimulation provoked downregulation of CITED2, which abrogated MYC-HDAC1-mediated p21CIP1 suppression, causing cellular quiescence. Ectopic CITED2 expression enhanced tumor growth in nude mice; furthermore, CITED2 knockdown caused tumor shrinkage and increased overall host mouse survival rates. Expression of CITED2/MYC/E2F3/ p21CIP1 signaling molecules was associated with poor prognosis of lung cancer patients. -
Wt1 Directs the Lineage Specification of Sertoli and Granulosa Cells By
© 2017. Published by The Company of Biologists Ltd | Development (2017) 144, 44-53 doi:10.1242/dev.144105 RESEARCH ARTICLE Wt1 directs the lineage specification of sertoli and granulosa cells by repressing Sf1 expression Min Chen1,*, Lianjun Zhang1,2,*, Xiuhong Cui1, Xiwen Lin1, Yaqiong Li1,2, Yaqing Wang3, Yanbo Wang1,2, Yan Qin1,2, Dahua Chen1, Chunsheng Han1, Bin Zhou4, Vicki Huff5 and Fei Gao1,‡ ABSTRACT Leydig cells and theca-interstitial cells are the steroidogenic cells Supporting cells (Sertoli and granulosa) and steroidogenic cells in male and female gonads, respectively. The steroid hormones (Leydig and theca-interstitium) are two major somatic cell types in produced by steroidogenic cells play essential roles in germ cell mammalian gonads, but the mechanisms that control their development and in maintaining secondary sexual characteristics. differentiation during gonad development remain elusive. In this Leydig cells first appear in testes at E12.5, whereas theca-interstitial study, we found that deletion of Wt1 in the ovary after sex cells are observed postnatally in the ovaries along with the determination caused ectopic development of steroidogenic cells at development of ovarian follicles. The origins of Leydig cells the embryonic stage. Furthermore, differentiation of both Sertoli and (Weaver et al., 2009; Barsoum and Yao, 2010; DeFalco et al., 2011) granulosa cells was blocked when Wt1 was deleted before sex and theca cells (Liu et al., 2015) have been studied previously. determination and most genital ridge somatic cells differentiated into However, the underlying mechanism that regulates the steroidogenic cells in both male and female gonads. Further studies differentiation between supporting cells and steroidogenic cells revealed that WT1 repressed Sf1 expression by directly binding to the during gonad development is poorly understood. -
CITED2-Mediated Mechanotransduction and Its Use for Chondroprotection
City University of New York (CUNY) CUNY Academic Works All Dissertations, Theses, and Capstone Projects Dissertations, Theses, and Capstone Projects 10-2014 CITED2-Mediated Mechanotransduction and its use for Chondroprotection Daniel J. Leong Graduate Center, City University of New York How does access to this work benefit ou?y Let us know! More information about this work at: https://academicworks.cuny.edu/gc_etds/444 Discover additional works at: https://academicworks.cuny.edu This work is made publicly available by the City University of New York (CUNY). Contact: [email protected] CITED2-Mediated Mechanotransduction and its use for Chondroprotection By Daniel J. Leong A dissertation submitted to the Graduate Faculty in Biomedical Engineering in partial fulfillment of the requirements for the degree of Doctor of Philosophy, The City University of New York 2014 Copyright by Daniel Leong 2014 This manuscript has been read and accepted for the Graduate Faculty in Biomedical Engineering in satisfaction of the dissertation requirement for the degree of Doctor of Philosophy. ____________________________________________________________________________ Sihong Wang, PhD – Chair of Examining Committee Date Department of Biomedical Engineering, The City University of New York ____________________________________________________________________________ Ardie Walser, PhD, Executive Officer Date The City University of New York Hui (Herb) B. Sun, PhD – Dissertation Advisor Departments of Orthopaedic Surgery and Radiation Oncology Albert Einstein College of Medicine Luis Cardoso, PhD – Dissertation Advisor Department of Biomedical Engineering, The City University of New York Mitchell B. Schaffler, PhD – Dissertation Committee Member Department of Biomedical Engineering, The City University of New York Robert J. Majeska, PhD – Dissertation Committee Member Department of Biomedical Engineering, The City University of New York Abstract of the Dissertation CITED2-Mediated Mechanotransduction and its use for Chondroprotection By Daniel J. -
Gene Dosage Effects and Transcriptional Regulation of Early Mammalian Adrenal Cortex Development Pierre Val, & Amanda Swain
Gene dosage effects and transcriptional regulation of early mammalian adrenal cortex development Pierre Val, & Amanda Swain To cite this version: Pierre Val, & Amanda Swain. Gene dosage effects and transcriptional regulation of early mammalian adrenal cortex development. Molecular and Cellular Endocrinology, Elsevier, 2010, 323 (1), pp.105. 10.1016/j.mce.2009.12.010. hal-00593434 HAL Id: hal-00593434 https://hal.archives-ouvertes.fr/hal-00593434 Submitted on 16 May 2011 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. Accepted Manuscript Title: Gene dosage effects and transcriptional regulation of early mammalian adrenal cortex development Authors: Pierre VAL, & Amanda Swain PII: S0303-7207(09)00618-2 DOI: doi:10.1016/j.mce.2009.12.010 Reference: MCE 7391 To appear in: Molecular and Cellular Endocrinology Please cite this article as: VAL, P., Swain, A., Gene dosage effects and transcriptional regulation of early mammalian adrenal cortex development, Molecular and Cellular Endocrinology (2008), doi:10.1016/j.mce.2009.12.010 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript.