Cited2, an Autoregulated Transcriptional Modulator, in TGF-Β Signaling
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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. -
Cited1 (NM 001276466) Mouse 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 MR228487 Cited1 (NM_001276466) Mouse Tagged ORF Clone Product data: Product Type: Expression Plasmids Product Name: Cited1 (NM_001276466) Mouse Tagged ORF Clone Tag: Myc-DDK Symbol: Cited1 Synonyms: AI316840; AU019144; Msg1 Vector: pCMV6-Entry (PS100001) E. coli Selection: Kanamycin (25 ug/mL) Cell Selection: Neomycin ORF Nucleotide >MR228487 representing NM_001276466 Sequence: Red=Cloning site Blue=ORF Green=Tags(s) TTTTGTAATACGACTCACTATAGGGCGGCCGGGAATTCGTCGACTGGATCCGGTACCGAGGAGATCTGCC GCCGCGATCGCC ATGCCAACTATGTCGAGGCCTGCACTTGATGTCAAGGGTGGCACCACCTCTGGGAAGGAGGATGCCAACC AGGAGATGAACTCTCTGGCCTACTCCAACCTTGGAGTGAAGGATCGCAAGGCAGTGACTGTCCTGCACTA CCCCGGGGTCACCGCAAATGGAGCCAAAGCCAACGGAGTTCCCACTAGCTCCTCTGGATCGACATCTCCA ATAGGCTCTCCTACTGCCACCCCTTCTTCCAAACCCCCATCCTTCAACCTGCATCCTACCCCTCACCTGA TGGCCAGCATGCAGCTTCAGAAGCTTAATAGCCAGTACCAAGGGGCTGCGGCTACTGCTGCTGCTGCCCT CACTGGTGCAGGCCTACCAGGGGAGGAAGAGCCCATGCAAAACTGGGTCACCGCCCCTCTGGTAGTGGGA GGGTCTCCGGGATCTGTCTCTCCTCCTGCTGGTGCCCAGAGCCCTGCTCTCATTGATTCTGACCCGGTGG ATGAGGAGGTGCTGATGTCTCTGGTGGTTGAATTGGGGCTAGACCGAGCCAATGAGCTTCCCGAGCTGTG GCTGGGGCAGAATGAGTTTGATTTCACTGCAGATTTTCCCTCTGGCTGC ACGCGTACGCGGCCGCTCGAGCAGAAACTCATCTCAGAAGAGGATCTGGCAGCAAATGATATCCTGGATT ACAAGGATGACGACGATAAGGTTTAA Protein Sequence: >MR228487 representing NM_001276466 Red=Cloning site Green=Tags(s) MPTMSRPALDVKGGTTSGKEDANQEMNSLAYSNLGVKDRKAVTVLHYPGVTANGAKANGVPTSSSGSTSP -
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. -
HSPA8 Antibody (C-Term) Purified Rabbit Polyclonal Antibody (Pab) Catalog # Ap2872b
10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 HSPA8 Antibody (C-term) Purified Rabbit Polyclonal Antibody (Pab) Catalog # AP2872b Specification HSPA8 Antibody (C-term) - Product Information Application IF, WB, IHC-P, FC,E Primary Accession P11142 Other Accession P63018, P63017, P19378, P19120, A2Q0Z1 Reactivity Human, Mouse Predicted Bovine, Hamster, Horse, Rat Host Rabbit Clonality Polyclonal Isotype Rabbit Ig Antigen Region 539-569 HSPA8 Antibody (C-term) - Additional Information Confocal immunofluorescent analysis of Gene ID 3312 HSPA8 Antibody (C-term)(Cat#AP2872b) with Hela cell followed by Alexa Fluor Other Names 488-conjugated goat anti-rabbit lgG (green). Heat shock cognate 71 kDa protein, Heat Actin filaments have been labeled with Alexa shock 70 kDa protein 8, Fluor 555 phalloidin (red). Lipopolysaccharide-associated protein 1, LAP-1, LPS-associated protein 1, HSPA8, HSC70, HSP73, HSPA10 Target/Specificity This HSPA8 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 539-569 amino acids from the C-terminal region of human HSPA8. Dilution IF~~1:10~50 WB~~1:1000 IHC-P~~1:10~50 FC~~1:10~50 Format Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This Western blot analysis of lysates from rat antibody is prepared by Saturated H-4-II-E, mouse NIH/3T3 cell line (from left to Ammonium Sulfate (SAS) precipitation right), using HSPA8 Antibody (C-term) (Cat. # followed by dialysis against PBS. AP2872b). AP2872b was diluted at 1:1000 at each lane. A goat anti-rabbit IgG H&L(HRP) at Page 1/5 10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 Storage 1:5000 dilution was used as the secondary Maintain refrigerated at 2-8°C for up to 2 antibody. -
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, -
TOX3 Is Expressed in Mammary ER+ Epithelial Cells and Regulates ER
Seksenyan et al. BMC Cancer (2015) 15:22 DOI 10.1186/s12885-015-1018-2 RESEARCH ARTICLE Open Access TOX3 is expressed in mammary ER+ epithelial cells and regulates ER target genes in luminal breast cancer Akop Seksenyan1, Asha Kadavallore1, Ann E Walts2, Brian de la Torre1, Dror Berel3,4, Samuel P Strom5,6, Parinaz Aliahmad1, Vincent A Funari5 and Jonathan Kaye1,3,7* Abstract Background: A breast cancer susceptibility locus has been mapped to the gene encoding TOX3. Little is known regarding the expression pattern or biological role of TOX3 in breast cancer or in the mammary gland. Here we analyzed TOX3 expression in murine and human mammary glands and in molecular subtypes of breast cancer, and assessed its ability to alter the biology of breast cancer cells. Methods: We used a cell sorting strategy, followed by quantitative real-time PCR, to study TOX3 gene expression in the mouse mammary gland. To study the expression of this nuclear protein in human mammary glands and breast tumors, we generated a rabbit monoclonal antibody specific for human TOX3. In vitro studies were performed on MCF7, BT474 and MDA-MB-231 cell lines to study the effects of TOX3 modulation on gene expression in the context of breast cancer cells. Results: We found TOX3 expression in estrogen receptor-positive mammary epithelial cells, including progenitor cells. A subset of breast tumors also highly expresses TOX3, with poor outcome associated with high expression of TOX3 in luminal B breast cancers. We also demonstrate the ability of TOX3 to alter gene expression in MCF7 luminal breast cancer cells, including cancer relevant genes TFF1 and CXCR4. -
HSPA8 Antibody (N-Term) Purified Rabbit Polyclonal Antibody (Pab) Catalog # AW5209
10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 HSPA8 Antibody (N-term) Purified Rabbit Polyclonal Antibody (Pab) Catalog # AW5209 Specification HSPA8 Antibody (N-term) - Product Information Application IF, WB, IHC-P, FC,E Primary Accession P11142 Other Accession P63018, P63017, P19378, O73885, P19120, A2Q0Z1 Reactivity Human, Mouse, Rat Predicted Bovine, Chicken, Hamster, Horse Host Rabbit Clonality Polyclonal Calculated MW H=71;M=71;Rat= 71 KDa Isotype Rabbit Ig Antigen Source HUMAN Confocal immunofluorescent analysis of HSPA8 Antibody (N-term)(Cat#AW5209) with HSPA8 Antibody (N-term) - Additional Information A2058 cell followed by Alexa Fluor 488-conjugated goat anti-rabbit lgG (green). Actin filaments have been labeled with Alexa Gene ID 3312 Fluor 555 phalloidin (red).DAPI was used to Antigen Region stain the cell nuclear (blue). 82-110 Other Names HSPA8; HSC70; HSP73; HSPA10; Heat shock cognate 71 kDa protein; Heat shock 70 kDa protein 8 Dilution IF~~1:10~50 WB~~1:1000 IHC-P~~1:10~50 FC~~1:10~50 Target/Specificity This HSPA8 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 82-110 amino acids from the N-terminal region of human HSPA8. Western blot analysis of lysates from Hela,A431,mouse NIH/3T3,rat H-4-Ⅱ-E cell line Format (from left to right), using HSPA8 Antibody Purified polyclonal antibody supplied in PBS (N-term)(Cat. #AW5209). AW5209 was Page 1/5 10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 with 0.09% (W/V) sodium azide. -
A Genomic Atlas of Human Adrenal and Gonad Development [Version 2; Referees: 4 Approved] Ignacio Del Valle1, Federica Buonocore1, Andrew J
Wellcome Open Research 2017, 2:25 Last updated: 08 NOV 2017 RESEARCH ARTICLE A genomic atlas of human adrenal and gonad development [version 2; referees: 4 approved] Ignacio del Valle1, Federica Buonocore1, Andrew J. Duncan1, Lin Lin1, Martino Barenco2, Rahul Parnaik1, Sonia Shah3,4, Mike Hubank5, Dianne Gerrelli2, John C. Achermann 1 1Genetics and Genomic Medicine, UCL Great Ormond Street Institute of Child Health, London, UK 2Developmental Biology and Cancer, UCL Great Ormond Street Institute of Child Health, London, UK 3Institute for Molecular Bioscience, University of Queensland, Brisbane, Australia 4Institute of Cardiovascular Science, University College London, London, UK 5The Centre for Molecular Pathology, Royal Marsden Hospital, Sutton, UK v2 First published: 07 Apr 2017, 2:25 (doi: 10.12688/wellcomeopenres.11253.1) Open Peer Review Latest published: 23 Oct 2017, 2:25 (doi: 10.12688/wellcomeopenres.11253.2) Referee Status: Abstract Background: In humans, the adrenal glands and gonads undergo distinct biological events between 6-10 weeks post conception (wpc), such as testis Invited Referees determination, the onset of steroidogenesis and primordial germ cell 1 2 3 4 development. However, relatively little is currently known about the genetic mechanisms underlying these processes. We therefore aimed to generate a detailed genomic atlas of adrenal and gonad development across these critical version 2 report report stages of human embryonic and fetal development. published Methods: RNA was extracted from 53 tissue samples between 6-10 wpc 23 Oct 2017 (adrenal, testis, ovary and control). Affymetrix array analysis was performed and differential gene expression was analysed using Bioconductor. A version 1 mathematical model was constructed to investigate time-series changes across published report report report report 07 Apr 2017 the dataset. -
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. -
Single Cell Regulatory Landscape of the Mouse Kidney Highlights Cellular Differentiation Programs and Disease Targets
ARTICLE https://doi.org/10.1038/s41467-021-22266-1 OPEN Single cell regulatory landscape of the mouse kidney highlights cellular differentiation programs and disease targets Zhen Miao 1,2,3,8, Michael S. Balzer 1,2,8, Ziyuan Ma 1,2,8, Hongbo Liu1,2, Junnan Wu 1,2, Rojesh Shrestha 1,2, Tamas Aranyi1,2, Amy Kwan4, Ayano Kondo 4, Marco Pontoglio 5, Junhyong Kim6, ✉ Mingyao Li 7, Klaus H. Kaestner2,4 & Katalin Susztak 1,2,4 1234567890():,; Determining the epigenetic program that generates unique cell types in the kidney is critical for understanding cell-type heterogeneity during tissue homeostasis and injury response. Here, we profile open chromatin and gene expression in developing and adult mouse kidneys at single cell resolution. We show critical reliance of gene expression on distal regulatory elements (enhancers). We reveal key cell type-specific transcription factors and major gene- regulatory circuits for kidney cells. Dynamic chromatin and expression changes during nephron progenitor differentiation demonstrates that podocyte commitment occurs early and is associated with sustained Foxl1 expression. Renal tubule cells follow a more complex differentiation, where Hfn4a is associated with proximal and Tfap2b with distal fate. Mapping single nucleotide variants associated with human kidney disease implicates critical cell types, developmental stages, genes, and regulatory mechanisms. The single cell multi-omics atlas reveals key chromatin remodeling events and gene expression dynamics associated with kidney development. 1 Renal, Electrolyte, and Hypertension Division, Department of Medicine, University of Pennsylvania, Perelman School of Medicine, Philadelphia, PA, USA. 2 Institute for Diabetes, Obesity, and Metabolism, University of Pennsylvania, Perelman School of Medicine, Philadelphia, PA, USA. -
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