ZBTB7B Antibody Cat

Total Page：16

File Type：pdf, Size：1020Kb

ZBTB7B Antibody Cat. No.: 58-864 ZBTB7B Antibody Western blot analysis of ZBTB7B using rabbit polyclonal ZBTB7B Antibody using 293 cell lysates (2 ug/lane) either nontransfected (Lane 1) or transiently transfected (Lane 2) with the ZBTB7B gene. Specifications HOST SPECIES: Rabbit SPECIES REACTIVITY: Human This ZBTB7B antibody is generated from rabbits immunized with a KLH conjugated IMMUNOGEN: synthetic peptide between 315-343 amino acids from the Central region of human ZBTB7B. TESTED APPLICATIONS: WB APPLICATIONS: For WB starting dilution is: 1:1000 PREDICTED MOLECULAR 58 kDa WEIGHT: September 30, 2021 1 https://www.prosci-inc.com/zbtb7b-antibody-58-864.html Properties This antibody is purified through a protein A column, followed by peptide affinity PURIFICATION: purification. CLONALITY: Polyclonal ISOTYPE: Rabbit Ig CONJUGATE: Unconjugated PHYSICAL STATE: Liquid BUFFER: Supplied in PBS with 0.09% (W/V) sodium azide. CONCENTRATION: batch dependent Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies STORAGE CONDITIONS: care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures. Additional Info OFFICIAL SYMBOL: ZBTB7B Zinc finger and BTB domain-containing protein 7B, Krueppel-related zinc finger protein cKrox, hcKrox, T-helper-inducing POZ/Krueppel-like factor, Zinc finger and BTB domain- ALTERNATE NAMES: containing protein 15, Zinc finger protein 67 homolog, Zfp-67, Zinc finger protein 857B, Zinc finger protein Th-POK, ZBTB7B, ZBTB15, ZFP67, ZNF857B ACCESSION NO.: O15156 GENE ID: 51043 USER NOTE: Optimal dilutions for each application to be determined by the researcher. Background and References ZFP67 is an early growth response gene that encodes a zinc finger-containing BACKGROUND: transcription factor that binds to the promoter regions of type I collagen genes (e.g., COL1A1; MIM 120150) and has a role in development. 1) Zhang, M., et al. J. Immunol. 185(7):3960-3969(2010) Yerges, L.M., et al. J. Bone Miner. Res. 24(12):2039-2049(2009) Egawa, T. J. Cell. Biochem. 107(6):1037-1045(2009) Tokunaga, REFERENCES: T., et al. Autoimmunity 42(8):653-660(2009) Renard, E., et al. J. Cell. Mol. Med. 12 (6B), 2836-2847 (2008) : ANTIBODIES FOR RESEARCH USE ONLY. For additional information, visit ProSci's Terms & Conditions Page. September 30, 2021 2 https://www.prosci-inc.com/zbtb7b-antibody-58-864.html.

Copy Link

Recommended publications

A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated.
[Show full text]
Tu Cornellgrad 0058F 10421.Pdf (5.371Mb)
MOLECULAR FUNCTION OF MAMMALIAN TRANSLOCATOR PROTEIN (TSPO) A Dissertation Presented to the Faculty of the Graduate School of Cornell University In Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy by Lan Ngoc Ly Tu August 2017 © 2017 Lan Ngoc Ly Tu MOLECULAR FUNCTION OF MAMMALIAN TRANSLOCATOR PROTEIN (TSPO) Lan Ngoc Ly Tu, Ph. D. Cornell University 2017 Translocator protein (TSPO), previously known as the peripheral benzodiazepine receptor (PBR), is a mitochondrial outer membrane protein highly conserved from bacteria to humans. TSPO is found to be upregulated in many pathological conditions, making it an attractive target for both diagnostic and therapeutic purposes in human medicine. However, the exact molecular function of TSPO remained unclear. For the past 25 years, TSPO was depicted to transport cholesterol from the cytosol to the inner mitochondrial membrane, the rate-limiting step in steroid hormone biosynthesis. Its critical role in survival and development was reinforced by a report that claimed TSPO knockout (Tspo-/-) mice were embryonic lethal. Therefore, there had been no genetic models to study the function of TSPO and all functional interpretations of TSPO were based on in vitro experiments using pharmacological tools. Our lab generated the first global Tspo-/- mice which surprisingly were healthy with no apparent abnormalities. Deletion of TSPO in different steroidogenic cell lines also did not affect cell viability. Furthermore, steroid hormone production was not affected in Tspo-/- mice or in steroidogenic cells lacking TSPO compared to the controls, indicating that TSPO is not involved in steroidogenesis. The stimulating effect of some TSPO binding chemicals on steroid hormone production that formed the early basis for linking TSPO and steroidogenesis was also found to be inaccurate.
[Show full text]
Pancreatic Cancer Prognosis Is Predicted by a Novel ATAC-Array Technology For
bioRxiv preprint doi: https://doi.org/10.1101/2021.01.21.427604; this version posted January 22, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Pancreatic cancer prognosis is predicted by a novel ATAC-array technology for assessing chromatin accessibility Authors: Dhara S1, Chhangawala S2,3, Chintalapudi H1, Askan G4, Aveson V4,5, Massa AL1, Zhang L4, Torres D1, Makohon-Moore AP4, Lecomte N4, Melchor JP4, Bermeo J4, Cardenas III A4, Sinha S4, Glassman D4, Nicolle R7, Moffitt R6, Yu KH4, Leppanen S8, Laderman S8, Curry B8, Gui J1, Balachandran VP4, Iacobuzio-Donahue C4, Chandwani R5, Leslie CS3* and Leach SD1* Author affiliations: 1, Dartmouth Geisel School of Medicine and Norris Cotton Cancer Center, Hanover, NH, USA 2, Weill Cornell Graduate School of Medical Sciences, New York, NY, USA. 3, Computational Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA. 4, David M. Rubenstein Center for Pancreatic Cancer Research, Memorial Sloan Kettering Cancer Center, New York, NY, USA 5, Weill Cornell Medicine, New York, NY, USA 6, Stony Brook University, Stony Brook, NY, USA 7, Programme Cartes d'Identité des Tumeurs, Ligue Nationale Contre Le Cancer, Paris, France 8, Agilent Technologies Inc. Santa Clara, CA, USA (* Co-corresponding author e-mails: [email protected]; [email protected]) (First two authors contributed equally to this work) 1 bioRxiv preprint doi: https://doi.org/10.1101/2021.01.21.427604; this version posted January 22, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder.
[Show full text]
Figure S17 Figure S16
immune responseregulatingcellsurfacereceptorsignalingpathway ventricular cardiacmuscletissuedevelopment t cellactivationinvolvedinimmuneresponse intrinsic apoptoticsignalingpathway single organismalcelladhesion cholesterol biosyntheticprocess myeloid leukocytedifferentiation determination ofadultlifespan response tointerferongamma muscle organmorphogenesis endothelial celldifferentiation brown fatcelldifferentiation mitochondrion organization myoblast differentiation response toprotozoan amino acidtransport leukocyte migration cytokine production t celldifferentiation protein secretion response tovirus angiogenesis Scrt1 Tcf25 Dpf1 Sap30 Ing2 Zfp654 Sp9 Zfp263 Mxi1 Hes6 Zfp395 Rlf Ppp1r13l Snapc1 C030039L03Rik Hif1a Arrb1 Glis3 Rcor2 Hif3a Fbxo21 Dnajc21 Rest Sirt6 Foxj1 Kdm5b Ankzf1 Sos2 Plscr1 Jdp2 Rbbp8 Etv4 Msh5 Mafg Tsc22d3 Nupr1 Ddit3 Cebpg Zfp790 Atf5 Cebpb Atf3 Trim21 Irf9 Irf2 Tbx21 Stat2 Stat1 Zbp1 Irf1 aGOslimPos Ikzf3 Oasl1 Irf7 Trim30a Dhx58 Txk Rorc Rora Nr1d2 Setdb2 Vdr Vax2 Nr1d1 Foxs1 Eno1 Thap3 Nfkbil1 Edf1 Srebf1 Lbr Tead1 Zfp608 Pcx Ift57 Ssbp4 Stat3 Mxd1 Pml Ssh2 Chd7 Maf Cic Bcl3 Prkdc Mbd5 Ppfibp2 Foxp2 Tal2 Mlf1 Bcl6b Zfp827 Ikzf2 Phtf2 Bmyc Plagl2 Nfkb2 Nfkb1 Tox Nrip1 Utf1 Klf3 Plagl1 Nfkbib Spib Nfkbie Akna Rbpj Ncoa3 Id1 Tnp2 Gata3 Gata1 Pparg Id2 Epas1 Zfp280b Commons Pathway Erg GO MSigDB KEGG Hhex WikiPathways SetGene Databases Batf Aff3 Zfp266 gene modules other (hypergeometric TF, from Figure Trim24 Zbtb5 Foxo3 Aebp2 XPodNet -protein-proteininteractionsinthepodocyteexpandedbySTRING Ppp1r10 Dffb Trp53 Enrichment
[Show full text]
Bioinformatic and Modelling Approaches for a System-Level Understanding of Oxidative Stress Toxicity Elias Zgheib
Bioinformatic and modelling approaches for a system-level understanding of oxidative stress toxicity Elias Zgheib To cite this version: Elias Zgheib. Bioinformatic and modelling approaches for a system-level understanding of oxidative stress toxicity. Quantitative Methods [q-bio.QM]. Université de Technologie de Compiègne, 2018. English. NNT : 2018COMP2464. tel-02088169 HAL Id: tel-02088169 https://tel.archives-ouvertes.fr/tel-02088169 Submitted on 2 Apr 2019 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. Par Elias ZGHEIB Bioinformatic and modelling approaches for a system- level understanding of oxidative stress toxicity Thèse présentée pour l’obtention du grade de Docteur de l’UTC Soutenue le 18 décembre 2018 Spécialité : Bio-ingénierie et Mathématiques Appliquées : Unité de Recherche Biomécanique et Bio-ingénierie (UMR-7338) D2464 BIOINFORMATIC AND MODELLING APPROACHES FOR A SYSTEM-LEVEL UNDERSTANDING OF OXIDATIVE STRESS TOXICITY A THESIS SUBMITTED TO THE UNIVERSITE DE TECHNOLOGIE DE COMPIEGNE SORBONNE UNIVERSITES LABORATOIRE DE BIO-MECANIQUE ET BIOINGENIERIE UMR CNRS 7338 – BMBI 18TH OF DECEMBER 2018 For the degree of Doctor Spécialité : Bio-ingénierie et Mathématiques Appliquées Elias ZGHEIB SUPERVISED BY Prof. Frédéric Y. BOIS JURY MEMBERS Mme. Karine AUDOUZE Rapporteur Mr.
[Show full text]
Integrated Transcriptomic, Phenotypic, and Functional Study Reveals Tissue-Specific Immune Properties of Mesenchymal Stromal
Integrated Transcriptomic, Phenotypic, and Functional Study Reveals Tissue-Specific Immune Properties of Mesenchymal Stromal Cells Cédric Ménard, Joelle Dulong, David Roulois, Benjamin Hebraud, Léa Verdière, Céline Pangault, Vonick Sibut, Isabelle Bezier, Nadège Bescher, Céline Monvoisin, et al. To cite this version: Cédric Ménard, Joelle Dulong, David Roulois, Benjamin Hebraud, Léa Verdière, et al.. Inte- grated Transcriptomic, Phenotypic, and Functional Study Reveals Tissue-Specific Immune Prop- erties of Mesenchymal Stromal Cells. STEM CELLS, AlphaMed Press, 2020, 38 (1), pp.146-159. 10.1002/stem.3077. hal-02282131 HAL Id: hal-02282131 https://hal-univ-rennes1.archives-ouvertes.fr/hal-02282131 Submitted on 10 Sep 2019 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. Stem Cells Integrated transcriptomic, phenotypic, and functional study reveals tissue-specific immune properties of mesenchymal stromal cells Journal: Stem Cells Manuscript ID Draft Wiley - Manuscript Type: Original Research Date Submitted by Forthe Peer Review n/a Author: Complete
[Show full text]
Engineered Type 1 Regulatory T Cells Designed for Clinical Use Kill Primary
ARTICLE Acute Myeloid Leukemia Engineered type 1 regulatory T cells designed Ferrata Storti Foundation for clinical use kill primary pediatric acute myeloid leukemia cells Brandon Cieniewicz,1* Molly Javier Uyeda,1,2* Ping (Pauline) Chen,1 Ece Canan Sayitoglu,1 Jeffrey Mao-Hwa Liu,1 Grazia Andolfi,3 Katharine Greenthal,1 Alice Bertaina,1,4 Silvia Gregori,3 Rosa Bacchetta,1,4 Norman James Lacayo,1 Alma-Martina Cepika1,4# and Maria Grazia Roncarolo1,2,4# Haematologica 2021 Volume 106(10):2588-2597 1Department of Pediatrics, Division of Stem Cell Transplantation and Regenerative Medicine, Stanford School of Medicine, Stanford, CA, USA; 2Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford School of Medicine, Stanford, CA, USA; 3San Raffaele Telethon Institute for Gene Therapy, Milan, Italy and 4Center for Definitive and Curative Medicine, Stanford School of Medicine, Stanford, CA, USA *BC and MJU contributed equally as co-first authors #AMC and MGR contributed equally as co-senior authors ABSTRACT ype 1 regulatory (Tr1) T cells induced by enforced expression of interleukin-10 (LV-10) are being developed as a novel treatment for Tchemotherapy-resistant myeloid leukemias. In vivo, LV-10 cells do not cause graft-versus-host disease while mediating graft-versus-leukemia effect against adult acute myeloid leukemia (AML). Since pediatric AML (pAML) and adult AML are different on a genetic and epigenetic level, we investigate herein whether LV-10 cells also efficiently kill pAML cells. We show that the majority of primary pAML are killed by LV-10 cells, with different levels of sensitivity to killing. Transcriptionally, pAML sensitive to LV-10 killing expressed a myeloid maturation signature.
[Show full text]
First Line of Title
β1-INTEGRIN MAY REGULATE EGR1 (EARLY GROWTH RESPONSE 1) WITHIN THE LENS by Anne M Terrell A thesis submitted to the Faculty of the University of Delaware in partial fulfillment of the requirements for the degree of Masters of Science in Biological Sciences Summer 2013 © 2013 Anne M Terrell All Rights Reserved β1-INTEGRIN MAY REGULATE EGR1 (EARLY GROWTH RESPONSE 1) WITHIN THE LENS by Anne M Terrell Approved: __________________________________________________________ Melinda K. Duncan, Ph.D. Professor in charge of thesis on behalf of the Advisory Committee Approved: __________________________________________________________ Randall L. Duncan, Ph.D. Chair of the Department of Biological Sciences Approved: __________________________________________________________ George H. Watson, Ph.D. Dean of the College of Arts and Sciences Approved: __________________________________________________________ James G. Richards, Ph.D. Vice Provost for Graduate and Professional Education ACKNOWLEDGMENTS I would like to thank my advisor, Melinda K. Duncan, for all her support throughout this project. She has helped me to become a better scientist, writer and presenter. I would also like to thank all past and present Duncan lab members, with a special thanks to Abby Manthey, Yan Wang, and Yichen Wang. Their help and guidance throughout my time in the lab was incredible. Abby Manthey was an amazing mentor in the lab and collaborator on the RNA-Seq project. Without Yan Wang’s expertise in lens cataract surgeries, I would have never been able to finish the second half of my thesis. Thank you to Yichen Wang for helping with the Egr1 staining and continuing this amazing project. I’d like to thank Shawn Polson and John H.
[Show full text]
Identification of Key Differentially Expressed Genes and Gene
Zhu et al. World Journal of Surgical Oncology (2020) 18:52 https://doi.org/10.1186/s12957-020-01820-z RESEARCH Open Access Identification of key differentially expressed genes and gene mutations in breast ductal carcinoma in situ using RNA-seq analysis Congyuan Zhu*, Hao Hu, Jianping Li*, Jingli Wang, Ke Wang and Jingqiu Sun Abstract Background: The aim of this study was to identify the key differentially expressed genes (DEGs) and high-risk gene mutations in breast ductal carcinoma in situ (DCIS). Methods: Raw data (GSE36863) were downloaded from the database of Gene Expression Omnibus (GEO), including three DCIS samples (DCIS cell lines MCF10.DCIS, Sum102, and Sum225) and one normal control sample (normal mammary epithelial cell line MCF10A). The DEGs were analyzed using NOIseq and annotated via DAVID. Motif scanning in the promoter region of DEGs was performed via SeqPos. Additionally, single nucleotide variations (SNVs) were identified via GenomeAnalysisTK and SNV risk was assessed via VarioWatch. Mutant genes with a high frequency and risk were validated by RT-PCR analyses. Results: Finally, 5391, 7073, and 7944 DEGs were identified in DCIS, Sum102, and Sum22 cell lines, respectively, when compared with MCF10A. VENN analysis of the three cell lines revealed 603 upregulated and 1043 downregulated DEGs, including 16 upregulated and 36 downregulated transcription factor (TF) genes. In addition, six TFs each (e.g., E2F1 and CREB1) were found to regulate the core up- and downregulated DEGs, respectively. Furthermore, SNV detection results revealed 1104 (MCF10.DCIS), 2833 (Sum102), and 1132 (Sum22) mutation sites. Four mutant genes (RWDD4, SDHC, SEPT7, and SFN) with high frequency and risk were identified.
[Show full text]
(12) Patent Application Publication (10) Pub. No.: US 2009/0269772 A1 Califano Et Al
US 20090269772A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2009/0269772 A1 Califano et al. (43) Pub. Date: Oct. 29, 2009 (54) SYSTEMS AND METHODS FOR Publication Classification IDENTIFYING COMBINATIONS OF (51) Int. Cl. COMPOUNDS OF THERAPEUTIC INTEREST CI2O I/68 (2006.01) CI2O 1/02 (2006.01) (76) Inventors: Andrea Califano, New York, NY G06N 5/02 (2006.01) (US); Riccardo Dalla-Favera, New (52) U.S. Cl. ........... 435/6: 435/29: 706/54; 707/E17.014 York, NY (US); Owen A. (57) ABSTRACT O'Connor, New York, NY (US) Systems, methods, and apparatus for searching for a combi nation of compounds of therapeutic interest are provided. Correspondence Address: Cell-based assays are performed, each cell-based assay JONES DAY exposing a different sample of cells to a different compound 222 EAST 41ST ST in a plurality of compounds. From the cell-based assays, a NEW YORK, NY 10017 (US) Subset of the tested compounds is selected. For each respec tive compound in the Subset, a molecular abundance profile from cells exposed to the respective compound is measured. (21) Appl. No.: 12/432,579 Targets of transcription factors and post-translational modu lators of transcription factor activity are inferred from the (22) Filed: Apr. 29, 2009 molecular abundance profile data using information theoretic measures. This data is used to construct an interaction net Related U.S. Application Data work. Variances in edges in the interaction network are used to determine the drug activity profile of compounds in the (60) Provisional application No. 61/048.875, filed on Apr.
[Show full text]
ZBTB7B Antibody Cat
ZBTB7B Antibody Cat. No.: 62-264 ZBTB7B Antibody Fluorescent confocal image of Hela cell stained with ZBTB7B Antibody .Hela cells were fixed with 4% PFA (20 min), permeabilized with Triton X-100 (0.1%, 10 min), then incubated with ZBTB7B primary antibody (1:25). For secondary antibody, Alexa Fluor 488 conjugated donkey anti-rabbit antibody (green) was used (1:400).Cytoplasmic actin was counterstained with Alexa Fluor 555 (red) conjugated Phalloidin (7units/ml). Nuclei were counterstained with DAPI (blue) (10 ug/ml, 10 min). ZBTB7B immunoreactivity is localized to Nucleus significantly. Specifications HOST SPECIES: Rabbit SPECIES REACTIVITY: Human This ZBTB7B antibody is generated from rabbits immunized with a KLH conjugated IMMUNOGEN: synthetic peptide between 440-469 amino acids from the C-terminal region of human ZBTB7B. TESTED APPLICATIONS: IF, WB For WB starting dilution is: 1:1000 APPLICATIONS: For IF starting dilution is: 1:10~50 September 29, 2021 1 https://www.prosci-inc.com/zbtb7b-antibody-62-264.html PREDICTED MOLECULAR 58 kDa WEIGHT: Properties This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by PURIFICATION: dialysis CLONALITY: Polyclonal ISOTYPE: Rabbit Ig CONJUGATE: Unconjugated PHYSICAL STATE: Liquid BUFFER: Supplied in PBS with 0.09% (W/V) sodium azide. CONCENTRATION: batch dependent Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies STORAGE CONDITIONS: care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures. Additional Info OFFICIAL SYMBOL: ZBTB7B Zinc finger and BTB domain-containing protein 7B, Krueppel-related zinc finger protein cKrox, hcKrox, T-helper-inducing POZ/Krueppel-like factor, Zinc finger and BTB domain- ALTERNATE NAMES: containing protein 15, Zinc finger protein 67 homolog, Zfp-67, Zinc finger protein 857B, Zinc finger protein Th-POK, ZBTB7B, ZBTB15, ZFP67, ZNF857B ACCESSION NO.: O15156 GENE ID: 51043 USER NOTE: Optimal dilutions for each application to be determined by the researcher.
[Show full text]
Autocrine IFN Signaling Inducing Profibrotic Fibroblast Responses By
Downloaded from http://www.jimmunol.org/ by guest on September 23, 2021 Inducing is online at: average * The Journal of Immunology , 11 of which you can access for free at: 2013; 191:2956-2966; Prepublished online 16 from submission to initial decision 4 weeks from acceptance to publication August 2013; doi: 10.4049/jimmunol.1300376 http://www.jimmunol.org/content/191/6/2956 A Synthetic TLR3 Ligand Mitigates Profibrotic Fibroblast Responses by Autocrine IFN Signaling Feng Fang, Kohtaro Ooka, Xiaoyong Sun, Ruchi Shah, Swati Bhattacharyya, Jun Wei and John Varga J Immunol cites 49 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/2013/08/20/jimmunol.130037 6.DC1 This article http://www.jimmunol.org/content/191/6/2956.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 © 2013 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 23, 2021. The Journal of Immunology A Synthetic TLR3 Ligand Mitigates Proﬁbrotic Fibroblast Responses by Inducing Autocrine IFN Signaling Feng Fang,* Kohtaro Ooka,* Xiaoyong Sun,† Ruchi Shah,* Swati Bhattacharyya,* Jun Wei,* and John Varga* Activation of TLR3 by exogenous microbial ligands or endogenous injury-associated ligands leads to production of type I IFN.
[Show full text]