DOCSLIB.ORG

N-Terminal Region (ARP31090 P050) Data Sheet

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
N-Terminal Region (ARP31090 P050) Data Sheet NR3C1 antibody - N-terminal region (ARP31090_P050) Data Sheet Product Number ARP31090_P050 Product Name NR3C1 antibody - N-terminal region (ARP31090_P050) Size 50ug Gene Symbol NR3C1 Alias Symbols GCCR; GCR; GR; GRL Nucleotide Accession# NM_001018076 Protein Size (# AA) 777 amino acids Molecular Weight 86kDa Product Format Lyophilized powder NCBI Gene Id 2908 Host Rabbit Clonality Polyclonal Official Gene Full Name Nuclear receptor subfamily 3, group C, member 1 (glucocorticoid receptor) Gene Family NR This is a rabbit polyclonal antibody against NR3C1. It was validated on Western Blot by Aviva Systems Biology. At Aviva Systems Biology we manufacture rabbit polyclonal antibodies on a large scale (200-1000 Description products/month) of high throughput manner. Our antibodies are peptide based and protein family oriented. We usually provide antibodies covering each member of a whole protein family of your interest. We also use our best efforts to provide you antibodies recognize various epitopes of a target protein. For availability of antibody needed for your experiment, please inquire (). Peptide Sequence Synthetic peptide located within the following region: MDSKESLTPGREENPSSVLAQERGDVMDFYKTLRGGATVKVSASSPSLAV NR3C1 is a receptor for glucocorticoids that can act as both a transcription factor and as a regulator of other transcription factors. This protein can also be found in heteromeric cytoplasmic complexes along with heat Description of Target shock factors and immunophilins. The protein is typically found in the cytoplasm until it binds a ligand, which induces transport into the nucleus. Mutations in this gene are a cause of glucocorticoid resistance, or cortisol, resistance. KDM5A, NCOA2, TP53, ADA, AR, BAG1, CALM1, CALR, CEBPA, CEBPB, CHD9, COPS6, CREB1, CREBBP, DAP3, DCAF6, DDX54, ECD, ETS1, ETS2, FKBP4, FYN, GRIP1, HNRNPU, HSP90AA1, HSPA1A, IDE, IFNGR2, JUN, KDM5A, KPNA2, LCK, MAPK1, MAPK15, MAPK8, MDM2, MED14, NCL, NCOA1, NCOA2, NCOA6, NCOR1, NCOR2, NFKB1, NFKB2, NR2F2, NR2F6, NR3C1, NR3C2, NRIP1, ONECUT1, PBX1, POU1F1, POU2F1, POU2F2, PPARGC1A, PRKACA, PRKDC, PSMC3IP, PTGES3, PTMS, RAF1, RELA, RNF14, SFN, SLC25A4, SMAD3, SMARCA2, SMARCA4, SMARCB1, SMARCC1, SMARCD1, SMARCE1, STAT3, STAT5A, STAT5B, SUMO1, SUMO4, SYT1, TBP, TGFB1I1, TP53, TRIM24, Partner Proteins TRIM28, TSG101, TXN, UBB, UBE2I, YWHAH, ZBTB16, ADA, ARPC5, BAG1, CALR, CEBPA, CEBPB, CREB1, CREBBP, DAP3, DAXX, DDX54, ECD, EP300, ETS2, FKBP4, GRIP1, HDAC1, HDAC2, HMGB1, HMGB2, HNRNPU, HOXB1, HSP82, HSP90AA1, HSPA1A, HSPD1, JUN, KDM5A, LRIF1, MAFF, MDM2, MED1, MED14, MSX2, NCL, NCOA1, NCOA2, NCOA3, NCOA4, NCOA6, NCOR1, NCOR2, NEDD4L, NFKB1, NFKB2, NR2E3, NR2F2, NR2F6, NR3C1, NR3C2, NRIP1, ONECUT1, PBX1, PIAS2, PML, POU1F1, POU2F1, POU2F2, PPARGC1A, PSMC3IP, PTGES3, PTMS, Psmc3ip, RAD9A, RAF1, RAN, RANBP9, RBM14, RELA, RXRB, SET, SFN, SFPQ, SMAD3, SMARCA2, SMARCA4, SMARCC1, SMARCD1, SMARCE1, SRC, STAT3, STAT5B, SVIL, TADA2A, TBP, TDG, TGFB1I1, TP53, TRIM24, TRIM28, TSG101, TXN, UBC, YWHAH, ZBTB16, ZBTB20, ZBTB3, ZBTB9, ZNF496 Reconstitution and Add 50 ul of distilled water. Final anti-NR3C1 antibody concentration is 1 mg/ml in PBS buffer with 2% sucrose. Storage For longer periods of storage, store at -20C. Avoid repeat freeze-thaw cycles. Lead Time Domestic: within 24 hours delivery International: 3-5 business days Blocking Peptide For anti-NR3C1 antibody is Catalog # AAP31090 Immunogen The immunogen for anti-NR3C1 antibody: synthetic peptide directed towards the N terminal of human NR3C1 Swissprot Id P04150 Protein Name Glucocorticoid receptor Protein Accession # NP_001018086 Purification Affinity Purified Species Reactivity Human, Rabbit, Rat, Sheep, Mouse, Bovine, Pig, Horse Application WB Predicted Homology Based on Immunogen Human: 100%; Rat: 86%; Rabbit: 86%; Pig: 79%; Horse: 79%; Mouse: 79%; Sheep: 79%; Bovine: 79% Sequence Human HepG2 WB Suggested Anti-NR3C1 Antibody Image 1 Titration: 1.0 ug/ml Positive Control: HepG2 Whole Cell __________________________________________________________________________________________________________________________________________________________________ This product is for Research Use Only. Not for diagnostic, human, or veterinary use. Optimal conditions of its use should be determined by end users..
Load more

Recommended publications
  • Table 2. Functional Classification of Genes Differentially Regulated After HOXB4 Inactivation in HSC/Hpcs
    Table 2. Functional classification of genes differentially regulated after HOXB4 inactivation in HSC/HPCs Symbol Gene description Fold-change (mean ± SD) Signal transduction Adam8 A disintegrin and metalloprotease domain 8 1.91 ± 0.51 Arl4 ADP-ribosylation factor-like 4 - 1.80 ± 0.40 Dusp6 Dual specificity phosphatase 6 (Mkp3) - 2.30 ± 0.46 Ksr1 Kinase suppressor of ras 1 1.92 ± 0.42 Lyst Lysosomal trafficking regulator 1.89 ± 0.34 Mapk1ip1 Mitogen activated protein kinase 1 interacting protein 1 1.84 ± 0.22 Narf* Nuclear prelamin A recognition factor 2.12 ± 0.04 Plekha2 Pleckstrin homology domain-containing. family A. (phosphoinosite 2.15 ± 0.22 binding specific) member 2 Ptp4a2 Protein tyrosine phosphatase 4a2 - 2.04 ± 0.94 Rasa2* RAS p21 activator protein 2 - 2.80 ± 0.13 Rassf4 RAS association (RalGDS/AF-6) domain family 4 3.44 ± 2.56 Rgs18 Regulator of G-protein signaling - 1.93 ± 0.57 Rrad Ras-related associated with diabetes 1.81 ± 0.73 Sh3kbp1 SH3 domain kinase bindings protein 1 - 2.19 ± 0.53 Senp2 SUMO/sentrin specific protease 2 - 1.97 ± 0.49 Socs2 Suppressor of cytokine signaling 2 - 2.82 ± 0.85 Socs5 Suppressor of cytokine signaling 5 2.13 ± 0.08 Socs6 Suppressor of cytokine signaling 6 - 2.18 ± 0.38 Spry1 Sprouty 1 - 2.69 ± 0.19 Sos1 Son of sevenless homolog 1 (Drosophila) 2.16 ± 0.71 Ywhag 3-monooxygenase/tryptophan 5- monooxygenase activation protein. - 2.37 ± 1.42 gamma polypeptide Zfyve21 Zinc finger. FYVE domain containing 21 1.93 ± 0.57 Ligands and receptors Bambi BMP and activin membrane-bound inhibitor - 2.94 ± 0.62
    [Show full text]
  • Cross-Talk Between HER2 and MED1 Regulates Tamoxifen Resistance of Human Breast Cancer Cells
    Published OnlineFirst September 10, 2012; DOI: 10.1158/0008-5472.CAN-12-1305 Cancer Tumor and Stem Cell Biology Research Cross-talk between HER2 and MED1 Regulates Tamoxifen Resistance of Human Breast Cancer Cells Jiajun Cui1, Katherine Germer1, Tianying Wu2, Jiang Wang3, Jia Luo5, Shao-chun Wang1, Qianben Wang4, and Xiaoting Zhang1 Abstract Despite the fact that most breast cancer patients have estrogen receptor (ER) a-positive tumors, up to 50% of the patients are or soon develop resistance to endocrine therapy. It is recognized that HER2 activation is one of the major mechanisms contributing to endocrine resistance. In this study, we report that the ER coactivator MED1 is a novel cross-talk point for the HER2 and ERa pathways. Tissue microarray analysis of human breast cancers revealed that MED1 expression positively correlates most strongly with HER2 status of the tumors. MED1 was highly phosphorylated, in a HER2-dependent manner, at the site known to be critical for its activation. Importantly, RNAi-mediated attenuation of MED1 sensitized HER2-overexpressing cells to tamoxifen treatment. MED1 and its phosphorylated form, but not the corepressors N-CoR and SMRT, were recruited to the ERa target gene promoter by tamoxifen in HER2-overexpressing cells. Significantly, MED1 attenuation or mutation of MED1 phosphorylation sites was sufficient to restore the promoter recruitment of N-CoR and SMRT. Notably, we found that MED1 is required for the expression of not only traditional E2-ERa target genes but also the newly described EGF-ERa target genes. Our results additionally indicated that MED1 is recruited to the HER2 gene and required for its expression.
    [Show full text]
  • Cisplatin and Phenanthriplatin Modulate Long-Noncoding
    www.nature.com/scientificreports OPEN Cisplatin and phenanthriplatin modulate long‑noncoding RNA expression in A549 and IMR90 cells revealing regulation of microRNAs, Wnt/β‑catenin and TGF‑β signaling Jerry D. Monroe1,2, Satya A. Moolani2,3, Elvin N. Irihamye2,4, Katheryn E. Lett1, Michael D. Hebert1, Yann Gibert1* & Michael E. Smith2* The monofunctional platinum(II) complex, phenanthriplatin, acts by blocking transcription, but its regulatory efects on long‑noncoding RNAs (lncRNAs) have not been elucidated relative to traditional platinum‑based chemotherapeutics, e.g., cisplatin. Here, we treated A549 non‑small cell lung cancer and IMR90 lung fbroblast cells for 24 h with either cisplatin, phenanthriplatin or a solvent control, and then performed microarray analysis to identify regulated lncRNAs. RNA22 v2 microRNA software was subsequently used to identify microRNAs (miRNAs) that might be suppressed by the most regulated lncRNAs. We found that miR‑25‑5p, ‑30a‑3p, ‑138‑5p, ‑149‑3p, ‑185‑5p, ‑378j, ‑608, ‑650, ‑708‑5p, ‑1253, ‑1254, ‑4458, and ‑4516, were predicted to target the cisplatin upregulated lncRNAs, IMMP2L‑1, CBR3‑1 and ATAD2B‑5, and the phenanthriplatin downregulated lncRNAs, AGO2‑1, COX7A1‑2 and SLC26A3‑1. Then, we used qRT‑PCR to measure the expression of miR‑25‑5p, ‑378j, ‑4516 (A549) and miR‑149‑3p, ‑608, and ‑4458 (IMR90) to identify distinct signaling efects associated with cisplatin and phenanthriplatin. The signaling pathways associated with these miRNAs suggests that phenanthriplatin may modulate Wnt/β‑catenin and TGF‑β signaling through the MAPK/ ERK and PTEN/AKT pathways diferently than cisplatin. Further, as some of these miRNAs may be subject to dissimilar lncRNA targeting in A549 and IMR90 cells, the monofunctional complex may not cause toxicity in normal lung compared to cancer cells by acting through distinct lncRNA and miRNA networks.
    [Show full text]
  • Transcription Factor P73 Regulates Th1 Differentiation
    ARTICLE https://doi.org/10.1038/s41467-020-15172-5 OPEN Transcription factor p73 regulates Th1 differentiation Min Ren1, Majid Kazemian 1,4, Ming Zheng2, JianPing He3, Peng Li1, Jangsuk Oh1, Wei Liao1, Jessica Li1, ✉ Jonathan Rajaseelan1, Brian L. Kelsall 3, Gary Peltz 2 & Warren J. Leonard1 Inter-individual differences in T helper (Th) cell responses affect susceptibility to infectious, allergic and autoimmune diseases. To identify factors contributing to these response differ- 1234567890():,; ences, here we analyze in vitro differentiated Th1 cells from 16 inbred mouse strains. Haplotype-based computational genetic analysis indicates that the p53 family protein, p73, affects Th1 differentiation. In cells differentiated under Th1 conditions in vitro, p73 negatively regulates IFNγ production. p73 binds within, or upstream of, and modulates the expression of Th1 differentiation-related genes such as Ifng and Il12rb2. Furthermore, in mouse experimental autoimmune encephalitis, p73-deficient mice have increased IFNγ production and less dis- ease severity, whereas in an adoptive transfer model of inflammatory bowel disease, transfer of p73-deficient naïve CD4+ T cells increases Th1 responses and augments disease severity. Our results thus identify p73 as a negative regulator of the Th1 immune response, suggesting that p73 dysregulation may contribute to susceptibility to autoimmune disease. 1 Laboratory of Molecular Immunology and the Immunology Center, National Heart, Lung, and Blood Institute, Bethesda, MD 20892-1674, USA. 2 Department of Anesthesia, Stanford University School of Medicine, Stanford, CA 94305, USA. 3 Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA. 4Present address: Department of Biochemistry and Computer Science, Purdue University, West ✉ Lafayette, IN 37906, USA.
    [Show full text]
  • Mechanical Forces Induce an Asthma Gene Signature in Healthy Airway Epithelial Cells Ayşe Kılıç1,10, Asher Ameli1,2,10, Jin-Ah Park3,10, Alvin T
    www.nature.com/scientificreports OPEN Mechanical forces induce an asthma gene signature in healthy airway epithelial cells Ayşe Kılıç1,10, Asher Ameli1,2,10, Jin-Ah Park3,10, Alvin T. Kho4, Kelan Tantisira1, Marc Santolini 1,5, Feixiong Cheng6,7,8, Jennifer A. Mitchel3, Maureen McGill3, Michael J. O’Sullivan3, Margherita De Marzio1,3, Amitabh Sharma1, Scott H. Randell9, Jefrey M. Drazen3, Jefrey J. Fredberg3 & Scott T. Weiss1,3* Bronchospasm compresses the bronchial epithelium, and this compressive stress has been implicated in asthma pathogenesis. However, the molecular mechanisms by which this compressive stress alters pathways relevant to disease are not well understood. Using air-liquid interface cultures of primary human bronchial epithelial cells derived from non-asthmatic donors and asthmatic donors, we applied a compressive stress and then used a network approach to map resulting changes in the molecular interactome. In cells from non-asthmatic donors, compression by itself was sufcient to induce infammatory, late repair, and fbrotic pathways. Remarkably, this molecular profle of non-asthmatic cells after compression recapitulated the profle of asthmatic cells before compression. Together, these results show that even in the absence of any infammatory stimulus, mechanical compression alone is sufcient to induce an asthma-like molecular signature. Bronchial epithelial cells (BECs) form a physical barrier that protects pulmonary airways from inhaled irritants and invading pathogens1,2. Moreover, environmental stimuli such as allergens, pollutants and viruses can induce constriction of the airways3 and thereby expose the bronchial epithelium to compressive mechanical stress. In BECs, this compressive stress induces structural, biophysical, as well as molecular changes4,5, that interact with nearby mesenchyme6 to cause epithelial layer unjamming1, shedding of soluble factors, production of matrix proteins, and activation matrix modifying enzymes, which then act to coordinate infammatory and remodeling processes4,7–10.
    [Show full text]
  • Key Roles for MED1 Lxxll Motifs in Pubertal Mammary Gland Development and Luminal-Cell Differentiation
    Key roles for MED1 LxxLL motifs in pubertal mammary gland development and luminal-cell differentiation Pingping Jianga,b,1, Qiuping Hua,1, Mitsuhiro Itoc,1,3, Sara Meyera, Susan Waltza, Sohaib Khana, Robert G. Roederc,2, and Xiaoting Zhanga,2 aDepartment of Cancer and Cell Biology, College of Medicine, University of Cincinnati, 3125 Eden Avenue, OH 45267; bCollege of Life Sciences, Zhejiang University, 388 Yuhangtang Road, Hangzhou 310058, China; and cLaboratory of Biochemistry and Molecular Biology, The Rockefeller University, 1230 York Avenue, New York, NY 10065 Contributed by Robert G. Roeder, February 16, 2010 (sent for review January 18, 2010) Mediator recently has emerged as a central player in the direct (7–9). In general, individual Mediator subunits interact transduction of signals from transcription factors to the general specifically with their corresponding transcription factors and de- transcriptional machinery. In the case of nuclear receptors, in vitro letions of these Mediator subunits often affect expression primar- studies have shown that the transcriptional coactivator function of ily of target genes and pathways controlled by their corresponding the Mediator involves direct ligand-dependent interactions of the transcription factor(s) (9). In the case of nuclear receptors, the MED1 subunit, through its two classical LxxLL motifs, with the re- Mediator interactions are ligand- and AF-2-dependent and ceptor AF2 domain. However, despite the strong in vitro evidence, mediated through the LxxLL motifs in the MED1 (a.k.a. there currently is little information regarding in vivo functions of TRAP220/PBP/DRIP205) subunit (10–13). Importantly, in rela- the LxxLL motifs either in MED1 or in other coactivators.
    [Show full text]
  • Rabbit Anti-RNF14/FITC Conjugated Antibody
    SunLong Biotech Co.,LTD Tel: 0086-571- 56623320 Fax:0086-571- 56623318 E-mail:[email protected] www.sunlongbiotech.com Rabbit Anti-RNF14/FITC Conjugated antibody SL9225R-FITC Product Name: Anti-RNF14/FITC Chinese Name: FITC标记的Ring finger protein14抗体 Androgen receptor associated protein 54; Androgen receptor-associated protein 54; ARA 54; ARA54; E3 ubiquitin protein ligase RNF14; E3 ubiquitin-protein ligase Alias: RNF14; FLJ26004; HFB 30; HFB30; HRIHFB2038; RING finger protein 14; RNF 14; Rnf14; RNF14_HUMAN; TRIAD 2; TRIAD2; Triad2 protein. Organism Species: Rabbit Clonality: Polyclonal React Species: Human,Mouse,Rat,Dog,Pig,Cow,Rabbit,Sheep, IF=1:50-200 Applications: not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. Molecular weight: 54kDa Form: Lyophilized or Liquid Concentration: 1mg/ml immunogen: KLH conjugated synthetic peptide derived from human RNF14 Lsotype: IgG Purification: affinitywww.sunlongbiotech.com purified by Protein A Storage Buffer: 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year Storage: when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. background: Might act as an E3 ubiquitin-protein ligase which accepts ubiquitin from specific E2 ubiquitin-conjugating enzymes and then transfers it to substrates, which could be Product Detail: nuclear proteins. Could play a role as a coactivator for androgen- and, to a lesser extent, progesterone-dependent transcription.
    [Show full text]
  • Tamoxifen Erythroid Toxicity Revealed by Studying the Role of Nuclear
    COMMENT as in Santana-Codina et al.1 Briefly, 12-week old Sv129/J Tamoxifen erythroid toxicity revealed by studying Ncoa4-ko and wild-type littermates received 200 mg/kg the role of nuclear receptor co-activator 4 in tamoxifen via oral gavage daily for five consecutive days erythropoiesis (day 0-4) and complete blood count was obtained at days 0, 4, 11 and 21. We chose mice on Sv129/J background We read with great interest the paper recently pub- that, unlike C57BL/6 Ncoa4-ko animals,4 do not show lished by Santana-Codina et al.1 about the cell anemia or alterations of iron parameters but only mild autonomous and non-autonomous role of nuclear recep- microcytosis (Figure 1 and Nai et al., 2019, manuscript in tor co-activator 4 (NCOA4). NCOA4 is a cargo receptor preparation). At day 4, only Ncoa4-ko mice showed a sta- that, in conditions of iron deficiency, promotes fer- tistically significant decrease in red blood cell (RBC) ritinophagy to release iron from ferritin.2,3 Inactivation of count, and hematocrit (Hct) and hemoglobin (Hb) levels. Ncoa4 in C57BL/6 mice causes mild microcytic anemia and increases the susceptibility to iron-deficiency anemia At day 11, also wild-type mice showed a reduction in due to iron being trapped in ferritin in several organs.3,4 To RBC count and decreased Hb and Hct, although for the formally prove the role of Ncoa4 inactivation on erythro- latter two parameters levels were higher than those of poiesis, a tamoxifen-inducible CRE-dependent Ncoa4-ko mice.
    [Show full text]
  • Molecular Profile of Tumor-Specific CD8+ T Cell Hypofunction in a Transplantable Murine Cancer Model
    Downloaded from http://www.jimmunol.org/ by guest on September 25, 2021 T + is online at: average * The Journal of Immunology , 34 of which you can access for free at: 2016; 197:1477-1488; Prepublished online 1 July from submission to initial decision 4 weeks from acceptance to publication 2016; doi: 10.4049/jimmunol.1600589 http://www.jimmunol.org/content/197/4/1477 Molecular Profile of Tumor-Specific CD8 Cell Hypofunction in a Transplantable Murine Cancer Model Katherine A. Waugh, Sonia M. Leach, Brandon L. Moore, Tullia C. Bruno, Jonathan D. Buhrman and Jill E. Slansky J Immunol cites 95 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html http://www.jimmunol.org/content/suppl/2016/07/01/jimmunol.160058 9.DCSupplemental This article http://www.jimmunol.org/content/197/4/1477.full#ref-list-1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material References Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2016 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 25, 2021. The Journal of Immunology Molecular Profile of Tumor-Specific CD8+ T Cell Hypofunction in a Transplantable Murine Cancer Model Katherine A.
    [Show full text]
  • Brd4 Bridges the Transcriptional Regulators, Aire and P-Tefb, to Promote Elongation of Peripheral-Tissue Antigen Transcripts In
    Brd4 bridges the transcriptional regulators, Aire and PNAS PLUS P-TEFb, to promote elongation of peripheral-tissue antigen transcripts in thymic stromal cells Hideyuki Yoshidaa, Kushagra Bansala, Uwe Schaeferb, Trevor Chapmanc, Inmaculada Riojac, Irina Proektd, Mark S. Andersone, Rab K. Prinjhac, Alexander Tarakhovskyb, Christophe Benoista,f,1, and Diane Mathisa,f,1 aDivision of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115; bLaboratory of Immune Cell Epigenetics and Signaling, The Rockefeller University, New York, NY 10065; cEpinova Discovery Performance Unit, Immuno-Inflammation Therapy Area, Medicines Research Centre, GlaxoSmithKline, Stevenage SG1 2NY, United Kingdom; dDepartment of Microbiology and Immunology, University of California, San Francisco, CA 94143; eDiabetes Center, University of California, San Francisco, CA 94143; and fEvergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women’s Hospital, Boston, MA 02115 Contributed by Diane Mathis, June 22, 2015 (sent for review April 20, 2015; reviewed by Leslie J. Berg and Tadatsugu Taniguchi) Aire controls immunologic tolerance by inducing a battery of turning transcription up or down. Indeed, recent data derived thymic transcripts encoding proteins characteristic of peripheral from a variety of experimental approaches argue that Aire’smajor tissues. Its unusually broad effect is achieved by releasing RNA modus operandi is to release promoter-proximal RNA polymerase II polymerase II paused just downstream of transcriptional start (Pol-II) pausing (11–13). sites. We explored Aire’s collaboration with the bromodomain- It has become increasingly clear that the regulation of Pol-II containing protein, Brd4, uncovering an astonishing correspon- pausing is a major nexus of transcriptional control (14), and the dencebetweenthosegenesinducedbyAireandthoseinhibited focus of transcription factors as diverse as NF-κB (15), c-Myc (16), by a small-molecule bromodomain blocker.
    [Show full text]
  • Overlap of Vitamin a and Vitamin D Target Genes with CAKUT- Related Processes [Version 1; Peer Review: 1 Approved with Reservations]
    F1000Research 2021, 10:395 Last updated: 21 JUL 2021 BRIEF REPORT Overlap of vitamin A and vitamin D target genes with CAKUT- related processes [version 1; peer review: 1 approved with reservations] Ozan Ozisik1, Friederike Ehrhart 2,3, Chris T Evelo 2, Alberto Mantovani4, Anaı̈s Baudot 1,5 1Aix Marseille University, Inserm, MMG, Marseille, 13385, France 2Department of Bioinformatics - BiGCaT, Maastricht University, Maastricht, 6200 MD, The Netherlands 3Department of Bioinformatics, NUTRIM/MHeNs, Maastricht University, Maastricht, 6200 MD, The Netherlands 4Istituto Superiore di Sanità, Rome, 00161, Italy 5Barcelona Supercomputing Center (BSC), Barcelona, 08034, Spain v1 First published: 18 May 2021, 10:395 Open Peer Review https://doi.org/10.12688/f1000research.51018.1 Latest published: 18 May 2021, 10:395 https://doi.org/10.12688/f1000research.51018.1 Reviewer Status Invited Reviewers Abstract Congenital Anomalies of the Kidney and Urinary Tract (CAKUT) are a 1 group of abnormalities affecting the kidneys and their outflow tracts, which include the ureters, the bladder, and the urethra. CAKUT version 1 patients display a large clinical variability as well as a complex 18 May 2021 report aetiology, as only 5% to 20% of the cases have a monogenic origin. It is thereby suspected that interactions of both genetic and 1. Elena Menegola, Università degli Studi di environmental factors contribute to the disease. Vitamins are among the environmental factors that are considered for CAKUT aetiology. In Milano, Milan, Italy this study, we collected vitamin A and vitamin D target genes and Any reports and responses or comments on the computed their overlap with CAKUT-related gene sets.
    [Show full text]
  • In Acute Myeloid Leukemia
    7283 Original Article Comprehensively analyze the expression and prognostic role for ten-eleven translocations (TETs) in acute myeloid leukemia Yan Huang1#, Jie Wei1#, Xunjun Huang1, Weijie Zhou1, Yuling Xu2, Dong-Hong Deng2, Peng Cheng2 1Department of Hematology and Rheumatology, People’s Hospital of Baise, Baise, China; 2Department of Hematology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China Contributions: (I) Conception and design: J Wei, Y Huang; (II) Administrative support: X Huang, Y Xu; (III) Provision of study materials or patients: W Zhou; (IV) Collection and assembly of data: J Wei, Y Huang; (V) Data analysis and interpretation: DH Deng, P Cheng; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors. #These authors contributed equally to this work. Correspondence to: Yuling Xu. Department of Hematology, The First Affiliated Hospital of Guangxi Medical University, Nanning, China. Email: [email protected]; Dong-Hong Deng. Department of Hematology, The First Affiliated Hospital of Guangxi Medical University, Nanning, China. Email: [email protected]; Peng Cheng. Department of Hematology, The First Affiliated Hospital of Guangxi Medical University, Nanning 530000, China. Email: [email protected]. Background: The ten-eleven translocation (TET) family oxidize 5-methylcytosines (5mCs) and promote the locus-specific reversal of DNA. The role of TETs in acute myeloid leukemia (AML) is mostly unknown. Methods: TETs mRNA expression levels were analyzed via Gene Expression Profiling Interactive Analysis (GEPIA). The association TETs expression levels and methylation with prognosis by UALCAN GenomicScape, and METHsurv. We analyzed TETs’ aberration types, located mutations, and structures via cBioPortal. GeneMANIA performed the functional network. Gene ontology (GO) enrichment was analyzed via LinkedOmics.
    [Show full text]