DOCSLIB.ORG

Transcription Factor Activity ELISA

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Transcription Factor Activity ELISA Transcription Factor Activity ELISA Measure DNA-Binding Activity Quickly & Simply! SIMPLE Measure Transcription Factor DNA-Binding Activity with our qualitative in-direct ELISA technology FLEXIBLE Use cell or nuclear lysates to measure the activity of wild-type or phosphorylated transcription factors RAPID SCREENING Screen transcriptional inhibitors/activators rapidly in a 96-well format SPECIFIC Kits use highly validated antibodies available separately for further studies Simple Protocol Great Data Phospho-CREB Transcription Factor Activity Assay c-Jun Transcription Factor Activity Assay To learn more visit: www.assaygenie.com Phosphorylated Transcription Factor Activity ELISA Myc (Phospho-Ser62) Transcription Factor Phospho-SMAD1 Activity Assay Transcription Factor Activity Assay PHOSPHORYLATED TRANSCRIPTION FACTOR ACTIVITY ELISA CODE PRODUCT CODE PRODUCT CODE PRODUCT TFAB00001 AML1 (Phospho-Ser303) TFAB00059 ER-alpha (Phospho-Ser118) TFAB00038 NF-kB p100 (Phospho-Ser872) TFAB00002 AML1 (Phospho-Ser435) TFAB00020 ER-beta (Phospho-Ser105) TFAB00043 NF-kB p65 (Phospho-Ser276) TFAB00012 AR (Phospho-Ser650) TFAB00025 ETS1 (Phospho-Thr38) TFAB00065 NF-kB p65 (Phospho-Ser311) TFAB00013 AR (Phospho-Tyr363) TFAB00028 FKHRL1 (Phospho-Ser253) TFAB00044 NF-kB p65 (Phospho-Ser468) TFAB00014 ATF2 (Phospho-Ser480) TFAB00026 FOXO1 (Phospho-Ser256) TFAB00042 NF-kB p65 (Phospho-Ser529) TFAB00015 ATF2 (Phospho-Thr69 or 51) TFAB00027 FOXO1 (Phospho-Ser319) TFAB00070 p53 (Acetyl-Lys317) TFAB00016 ATF2 (Phospho-Thr71 or 53) TFAB00029 GATA1 (Phospho-Ser142) TFAB00067 p53 (Phospho-Ser20) TFAB00006 c-Jun (Phospho-Ser243) TFAB00030 GATA1 (Phospho-Ser310) TFAB00046 p53 (Phospho-Ser315) TFAB00003 c-Jun (Phospho-Ser249) TFAB00032 GATA4 (Phospho-Ser105) TFAB00068 p53 (Phospho-Ser33) TFAB00004 c-Jun (Phospho-Ser63) TFAB00031 GATA4 (Phospho-Ser262) TFAB00047 p53 (Phospho-Ser376) TFAB00005 c-Jun (Phospho-Ser73) TFAB00033 GR (Phospho-Ser211) TFAB00045 p53 (Phospho-Ser392) TFAB00007 c-Jun (Phospho-Thr239) TFAB00034 HSF1 (Phospho-Ser303) TFAB00069 p53 (Phospho-Thr18) TFAB00008 c-Jun (Phospho-Thr91) TFAB00010 JunB (Phospho-Ser259) TFAB00048 RAR alpha (Phospho-Ser77) TFAB00009 c-Jun (Phospho-Thr93) TFAB00011 JunD (Phospho-Ser255) TFAB00049 Smad1 (Phospho-Ser187) TFAB00017 CREB (Phospho-Ser121) TFAB00051 MEF2A (Phospho-Ser408) TFAB00063 Smad1 (Phospho-Ser465) TFAB00018 CREB (Phospho-Ser129) TFAB00052 MEF2A (Phospho-Thr312) TFAB00050 Smad2 (Phospho-Ser250) TFAB00019 CREB (Phospho-Ser133) TFAB00054 MEF2C (Phospho-Ser396) TFAB00064 Smad3 (Phospho-Ser213) TFAB00021 Elk1 (Phospho-Ser383) TFAB00055 MEF2D (Phospho-Ser444) TFAB00066 SOX-9 (Phospho-Ser181) TFAB00022 Elk1 (Phospho-Ser389) TFAB00035 MYB (Phospho-Ser12) TFAB00056 STAT1 (Phospho-Ser727) TFAB00023 Elk1 (Phospho-Thr417) TFAB00036 Myc (Phospho-Ser62) TFAB00062 STAT1 (Phospho-Tyr701) TFAB00024 Elk3 (Phospho-Ser357) TFAB00037 Myc (Phospho-Thr58) TFAB00057 STAT5A (Phospho-Ser780) To learn more visit: www.assaygenie.com Transcription Factor Activity ELISA TRANSCRIPTION FACTOR ACTIVITY ELISA TRANSCRIPTION FACTOR ACTIVITY ELISA CODE PRODUCT CODE PRODUCT CODE PRODUCT CODE PRODUCT TFAB00134 ADA2L TFAB00077 Fos TFAB00205 Maf TFAB00155 RREB1 TFAB00104 AFX TFAB00107 FOXB2 TFAB00204 MAFF TFAB00075 RUNX3 TFAB00074 AML1 TFAB00108 FOXC1/2 TFAB00163 MEF2A TFAB00176 RXR gamma TFAB00080 AP-2 TFAB00109 FOXD3 TFAB00133 Meis1 TFAB00202 SIX5 TFAB00081 AR TFAB00110 FOXH1 TFAB00135 MYB TFAB00158 Smad1 TFAB00082 ATF1 TFAB00113 FOXK1 TFAB00138 MYC TFAB00159 Smad2 TFAB00083 ATF2 TFAB00111 FOXL1 TFAB00189 MYSM1 TFAB00187 Smad3 TFAB00084 ATF3 TFAB00105 FOXO1 TFAB00136 NCoR1 TFAB00190 SMRC2 TFAB00085 ATF5 TFAB00112 FOXO1A TFAB00137 NCOR2 TFAB00199 SOX12 TFAB00086 ATF7 TFAB00078 Fra-2 TFAB00183 NFAT3 TFAB00200 SOX6 TFAB00072 B-Myb TFAB00114 GATA1 TFAB00139 NF-kB p100/p52 TFAB00160 SP1 TFAB00089 CDX2 TFAB00115 GATA3 TFAB00140 NF-kB p105/p50 TFAB00161 SP2 TFAB00181 CEBPB TFAB00116 GATA4 TFAB00141 NF-kB p65 TFAB00162 SP3/4 TFAB00197 CEBPD/E TFAB00117 GATA6 TFAB00142 NFYA TFAB00102 SPI1 TFAB00196 CEBPZ TFAB00118 GR TFAB00188 NFYB TFAB00103 SPIC TFAB00076 c-Jun TFAB00119 GTF2IRD1 TFAB00178 NR1I3 TFAB00164 SRF TFAB00087 CREB TFAB00192 HBP1 TFAB00143 NR2F6 TFAB00127 SRY TFAB00088 CREB3L2 TFAB00120 HIF-1a TFAB00144 NRF1 TFAB00165 STAT1 TFAB00207 DLX3 TFAB00182 HNF4a/g TFAB00208 NRL TFAB00184 STAT2 TFAB00090 DLX5 TFAB00121 HOXA1 TFAB00145 OCT-1 TFAB00185 STAT3 TFAB00091 DP-2 TFAB00122 HOXA1/B1/D1 TFAB00150 OCT-2 TFAB00166 STAT5A TFAB00092 E2F-5 TFAB00123 HOXA11/D11 TFAB00198 OCT-3 TFAB00186 STAT5B TFAB00177 EGR1/2 TFAB00124 HOXB2 TFAB00146 p53 TFAB00167 TBX1 TFAB00094 ELF1 TFAB00125 HOXD10 TFAB00147 p63 TFAB00168 TBX18 TFAB00095 ELF5 TFAB00126 HOXD12 TFAB00148 p73 TFAB00169 TBX2 TFAB00096 Elk1 TFAB00128 HOXD8 TFAB00149 Pax-8 TFAB00170 TBX3 TFAB00179 ER-alpha TFAB00129 HSF1 TFAB00151 POU4F1 TFAB00132 TCF7 TFAB00093 ER-beta TFAB00130 IKZF2 TFAB00152 PPAR-alpha TFAB00201 TCFL5 TFAB00097 ERF TFAB00203 IKZF4 TFAB00153 PPAR-gamma TFAB00175 TEAD3 TFAB00098 ETS1 TFAB00131 IRF2 TFAB00154 PR TFAB00180 TFE3 TFAB00099 ETV4 TFAB00079 JunB TFAB00171 RAR alpha TFAB00173 TR alpha TFAB00100 ETV6 TFAB00193 KLF TFAB00172 RAR beta TFAB00174 TRbeta TFAB00106 FKHRL1 TFAB00195 KLF10/11 TFAB00156 RFX2 TFAB00073 TRF1 TFAB00101 FLI1 TFAB00194 KLF7 TFAB00156 RFX2 TFAB00191 TTF1 To learn more visit: www.assaygenie.com Transcription Factor Activity ELISA Search Assay Genie for over 1,500 Transcription Factor DNA-Binding Activity & Phospho- Specific Cell-Based ELISA! www.assaygenie.com Quote: [email protected] | Dublin, Ireland | London, UK .
Load more

Recommended publications
  • SOX12 Contributes to the Activation of the JAK2/STAT3 Pathway and Malignant Transformation of Esophageal Squamous Cell Carcinoma
    ONCOLOGY REPORTS 45: 129-138, 2021 SOX12 contributes to the activation of the JAK2/STAT3 pathway and malignant transformation of esophageal squamous cell carcinoma CHUNGUANG LI1*, MAOLING ZHU2*, JI ZHU1, QIJUE LU1, BOWEN SHI1, BIN SUN3 and HEZHONG CHEN1 1Department of Thoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai 200438; 2Department of Gastroenterology, Yangpu Hospital, Tongji University School of Medicine, Shanghai 200090; 3Molecular Oncology Laboratory, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai 200438, P.R. China Received May 15, 2020; Accepted October 6, 2020 DOI: 10.3892/or.2020.7863 Abstract. As a crucial transcription factor, sex-determining cells in vitro. Recombinant protein of SOX12 could restore the region Y box 12 (SOX12) is closely related with tumorigenesis aggressive phenotype of ESCC cells. Furthermore, knockdown and malignant transformation in various malignant tumor of the expression of SOX12 inhibited the activation of the Janus types. To date, the specific function of SOX12 in esophageal kinase 2 (JAK2)/signal transducer and activator of transcrip- squamous cell carcinoma (ESCC) has remained largely tion 3 (STAT3) signaling pathway by decreasing the expression elusive and requires further investigation. The present study of the JAK2/STAT3 signaling pathway. Recombinant protein aimed to determine whether aberrant expression of SOX12 is of SOX12 could recover the activation of the JAK2/STAT3 associated with malignant development of ESCC. The expres- signaling pathway. Analysis of the clinical data revealed that sion level of SOX12 in ESCC cells and tissues was analyzed overexpression of SOX12 indicated shorter overall survival by RT-qPCR and western blotting. Short hairpin RNA time (OS; P=0.0341) and disease-free survival time (DFS; (shRNA) targeting SOX12 was transfected into ESCC cells to P=0.04).
    [Show full text]
  • 4-6 Weeks Old Female C57BL/6 Mice Obtained from Jackson Labs Were Used for Cell Isolation
    Methods Mice: 4-6 weeks old female C57BL/6 mice obtained from Jackson labs were used for cell isolation. Female Foxp3-IRES-GFP reporter mice (1), backcrossed to B6/C57 background for 10 generations, were used for the isolation of naïve CD4 and naïve CD8 cells for the RNAseq experiments. The mice were housed in pathogen-free animal facility in the La Jolla Institute for Allergy and Immunology and were used according to protocols approved by the Institutional Animal Care and use Committee. Preparation of cells: Subsets of thymocytes were isolated by cell sorting as previously described (2), after cell surface staining using CD4 (GK1.5), CD8 (53-6.7), CD3ε (145- 2C11), CD24 (M1/69) (all from Biolegend). DP cells: CD4+CD8 int/hi; CD4 SP cells: CD4CD3 hi, CD24 int/lo; CD8 SP cells: CD8 int/hi CD4 CD3 hi, CD24 int/lo (Fig S2). Peripheral subsets were isolated after pooling spleen and lymph nodes. T cells were enriched by negative isolation using Dynabeads (Dynabeads untouched mouse T cells, 11413D, Invitrogen). After surface staining for CD4 (GK1.5), CD8 (53-6.7), CD62L (MEL-14), CD25 (PC61) and CD44 (IM7), naïve CD4+CD62L hiCD25-CD44lo and naïve CD8+CD62L hiCD25-CD44lo were obtained by sorting (BD FACS Aria). Additionally, for the RNAseq experiments, CD4 and CD8 naïve cells were isolated by sorting T cells from the Foxp3- IRES-GFP mice: CD4+CD62LhiCD25–CD44lo GFP(FOXP3)– and CD8+CD62LhiCD25– CD44lo GFP(FOXP3)– (antibodies were from Biolegend). In some cases, naïve CD4 cells were cultured in vitro under Th1 or Th2 polarizing conditions (3, 4).
    [Show full text]
  • Supplemental Information
    Supplemental information Dissection of the genomic structure of the miR-183/96/182 gene. Previously, we showed that the miR-183/96/182 cluster is an intergenic miRNA cluster, located in a ~60-kb interval between the genes encoding nuclear respiratory factor-1 (Nrf1) and ubiquitin-conjugating enzyme E2H (Ube2h) on mouse chr6qA3.3 (1). To start to uncover the genomic structure of the miR- 183/96/182 gene, we first studied genomic features around miR-183/96/182 in the UCSC genome browser (http://genome.UCSC.edu/), and identified two CpG islands 3.4-6.5 kb 5’ of pre-miR-183, the most 5’ miRNA of the cluster (Fig. 1A; Fig. S1 and Seq. S1). A cDNA clone, AK044220, located at 3.2-4.6 kb 5’ to pre-miR-183, encompasses the second CpG island (Fig. 1A; Fig. S1). We hypothesized that this cDNA clone was derived from 5’ exon(s) of the primary transcript of the miR-183/96/182 gene, as CpG islands are often associated with promoters (2). Supporting this hypothesis, multiple expressed sequences detected by gene-trap clones, including clone D016D06 (3, 4), were co-localized with the cDNA clone AK044220 (Fig. 1A; Fig. S1). Clone D016D06, deposited by the German GeneTrap Consortium (GGTC) (http://tikus.gsf.de) (3, 4), was derived from insertion of a retroviral construct, rFlpROSAβgeo in 129S2 ES cells (Fig. 1A and C). The rFlpROSAβgeo construct carries a promoterless reporter gene, the β−geo cassette - an in-frame fusion of the β-galactosidase and neomycin resistance (Neor) gene (5), with a splicing acceptor (SA) immediately upstream, and a polyA signal downstream of the β−geo cassette (Fig.
    [Show full text]
  • Appendix 2. Significantly Differentially Regulated Genes in Term Compared with Second Trimester Amniotic Fluid Supernatant
    Appendix 2. Significantly Differentially Regulated Genes in Term Compared With Second Trimester Amniotic Fluid Supernatant Fold Change in term vs second trimester Amniotic Affymetrix Duplicate Fluid Probe ID probes Symbol Entrez Gene Name 1019.9 217059_at D MUC7 mucin 7, secreted 424.5 211735_x_at D SFTPC surfactant protein C 416.2 206835_at STATH statherin 363.4 214387_x_at D SFTPC surfactant protein C 295.5 205982_x_at D SFTPC surfactant protein C 288.7 1553454_at RPTN repetin solute carrier family 34 (sodium 251.3 204124_at SLC34A2 phosphate), member 2 238.9 206786_at HTN3 histatin 3 161.5 220191_at GKN1 gastrokine 1 152.7 223678_s_at D SFTPA2 surfactant protein A2 130.9 207430_s_at D MSMB microseminoprotein, beta- 99.0 214199_at SFTPD surfactant protein D major histocompatibility complex, class II, 96.5 210982_s_at D HLA-DRA DR alpha 96.5 221133_s_at D CLDN18 claudin 18 94.4 238222_at GKN2 gastrokine 2 93.7 1557961_s_at D LOC100127983 uncharacterized LOC100127983 93.1 229584_at LRRK2 leucine-rich repeat kinase 2 HOXD cluster antisense RNA 1 (non- 88.6 242042_s_at D HOXD-AS1 protein coding) 86.0 205569_at LAMP3 lysosomal-associated membrane protein 3 85.4 232698_at BPIFB2 BPI fold containing family B, member 2 84.4 205979_at SCGB2A1 secretoglobin, family 2A, member 1 84.3 230469_at RTKN2 rhotekin 2 82.2 204130_at HSD11B2 hydroxysteroid (11-beta) dehydrogenase 2 81.9 222242_s_at KLK5 kallikrein-related peptidase 5 77.0 237281_at AKAP14 A kinase (PRKA) anchor protein 14 76.7 1553602_at MUCL1 mucin-like 1 76.3 216359_at D MUC7 mucin 7,
    [Show full text]
  • Directing an Artificial Zinc Finger Protein to New Targets by Fusion to a Non-DNA Binding Domain
    Directing an artificial zinc finger protein to new targets by fusion to a non-DNA binding domain Wooi Fang (Catheryn) Lim A thesis in fulfilment of the requirements for the degree of Doctor of Philosophy School of Biotechnology and Biomolecular Sciences Faculty of Science March 2016 Page | 0 THESIS/ DISSERTATION SHEET Page | i ORIGINALITY STATEMENT ‘I hereby declare that this submission is my own work and to the best of my knowledge it contains no materials previously published or written by another person, or substantial proportions of material which have been accepted for the award of any other degree or diploma at UNSW or any other educational institution, except where due acknowledgement is made in the thesis. Any contribution made to the research by others, with whom I have worked at UNSW or elsewhere, is explicitly acknowledged in the thesis. I also declare that the intellectual content of this thesis is the product of my own work, except to the extent that assistance from others in the project's design and conception or in style, presentation and linguistic expression is acknowledged.’ WOOI FANG LIM Signed …………………………………………….............. 31-03-2016 Date …………………………………………….............. Page | i COPYRIGHT STATEMENT ‘I hereby grant the University of New South Wales or its agents the right to archive and to make available my thesis or dissertation in whole or part in the University libraries in all forms of media, now or here after known, subject to the provisions of the Copyright Act 1968. I retain all proprietary rights, such as patent rights. I also retain the right to use in future works (such as articles or books) all or part of this thesis or dissertation.
    [Show full text]
  • SOX2 and SOX12 Are Predictive of Prognosis in Patients with Clear Cell Renal Cell Carcinoma
    4564 ONCOLOGY LETTERS 15: 4564-4570, 2018 SOX2 and SOX12 are predictive of prognosis in patients with clear cell renal cell carcinoma WEIJIE GU1,2*, BEIHE WANG1,2*, FANGNING WAN1,2*, JUNLONG WU1,2, XIAOLIN LU1,2, HONGKAI WANG1,2, YAO ZHU1,2, HAILIANG ZHANG1,2, GUOHAI SHI1,2, BO DAI1,2 and DINGWEI YE1,2 1Department of Urology, Fudan University Shanghai Cancer Center; 2Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, P.R. China Received October 21, 2016; Accepted September 28, 2017 DOI: 10.3892/ol.2018.7828 Abstract. Sex-determining region Y-box protein (SOX) genes were associated with poor prognosis for OS (log-rank test, all serve an important role in cancer growth and metastasis. P<0.05). SOX2 and SOX12 were identified as independent The present study aimed to determine the predictive ability prognostic factors of OS in clear cell RCC. of SOX and associated genes identified through molecular network in clear cell renal cell carcinoma (RCC). A total of Introduction 505 patients with clear cell RCC from The Cancer Genome Atlas (TCGA) cohorts were collected in this study. The Renal cell carcinoma (RCC) accounts for ~2-3% of all malig- expression profile of SOX and associated genes were obtained nancies worldwide (1). Despite an increasing proportion of from the TCGA RNAseq database. Clinicopathological patients with early stage tumors at diagnosis and the develop- characteristics, including age, gender, tumor grade, stage, ment of novel treatment strategies, a quarter still present with laterality disease-free-survival and overall survival (OS) were locally advanced or metastatic disease, and eventually, one collected.
    [Show full text]
  • Multi-Omics Analysis of SOX4, SOX11, and SOX12 Expression and the Associated Pathways in Human Cancers
    Journal of Personalized Medicine Article Multi-Omics Analysis of SOX4, SOX11, and SOX12 Expression and the Associated Pathways in Human Cancers Jaekwon Seok †, Minchan Gil †, Ahmed Abdal Dayem , Subbroto Kumar Saha and Ssang-Goo Cho * Department of Stem Cell and Regenerative Biotechnology, Incurable Disease Animal Model & Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul 05029, Korea; [email protected] (J.S.); [email protected] (M.G.); [email protected] (A.A.D.); [email protected] (S.K.S.) * Correspondence: [email protected]; Tel.: +82-2-450-4207 or +82-2-444-4207 † These authors contributed equally to this study. Abstract: The Sry-related HMG BOX (SOX) gene family encodes transcription factors containing highly conserved high-mobility group domains that bind to the minor groove in DNA. Although some SOX genes are known to be associated with tumorigenesis and cancer progression, their expression and prognostic value have not been systematically studied. We performed multi-omic analysis to investigate the expression of SOX genes in human cancers. Expression and phylogenetic tree analyses of the SOX gene family revealed that the expression of three closely related SOX members, SOX4, SOX11, and SOX12, was increased in multiple cancers. Expression, mutation, and alteration of the three SOX members were evaluated using the Oncomine and cBioPortal databases, and the correlation between these genes and clinical outcomes in various cancers was examined using the Kaplan–Meier, PrognoScan, and R2 database analyses. The genes commonly correlated Citation: Seok, J.; Gil, M.; Dayem, with the three SOX members were categorized in key pathways related to the cell cycle, mitosis, A.A.; Saha, S.K.; Cho, S.-G.
    [Show full text]
  • SOX12 Upregulation Is Associated with Metastasis of Hepatocellular Carcinoma and Increases CDK4 and IGF2BP1 Expression
    European Review for Medical and Pharmacological Sciences 2017; 21: 3821-3826 SOX12 upregulation is associated with metastasis of hepatocellular carcinoma and increases CDK4 and IGF2BP1 expression P. Y UA N1, L. MENG2, N. WANG3 1Department of Interventional Therapy, the People’s Hospital of Jianhu, Jianhu, Jiangsu, China 2Clinical Laboratory, the People’s Hospital of Lanling, Linyi, Shandong, China 3Department of Ultrasound, the First Hospital of Hebei Medical University, Shijiazhuang, Hebei, China Introduction Abstract. – OBJECTIVE: In this study, we studied the expression profile of SOX12 gene in different pathological stages of hepatocellular Hepatocellular carcinoma (HCC) is one of carcinoma (HCC) and explored the possible the most common cancers and is also a leading downstream genes related to its regulation of cause of cancer-related death worldwide1. Local HCC invasion and migration. and distant metastases are indicators of poor MATERIALS AND METHODS: Bioinformatic prognosis and are also the main causes of can- data mining was performed in liver cancer co- cer-related death2,3. Therefore, elucidating the hort in TCGA. HepG2 cells were used as in vitro cell model to assess the effect of SOX12 on molecular mechanisms underlying HCC metas- CDK4 and IGF2BP1 expression. The association tasis is critical for identifying novel therapeutic between the expression of SOX12, CDK4 or IG- targets. F2BP1 and survival time in HCC patients was SYR-related high mobility group (HMG) box also assessed based on the data in TCGA. (SOX) family proteins are a conserved group RESULTS: The regional lymph node metasta- of transcriptional factors widely participate in sis (N1) and distant metastasis (M1) cases had both normal embryonic development and onco- significantly increased SOX12 expression than 4,5 5,6 the lymph node negative (N0) and distant metas- genic processes .
    [Show full text]
  • Sox12 Promotes T Reg Differentiation in the Periphery During Colitis
    Published Online: 6 September, 2018 | Supp Info: http://doi.org/10.1084/jem.20172082 Downloaded from jem.rupress.org on September 10, 2018 BRIEF DEFINITIVE REPORT Sox12 promotes T reg differentiation in the periphery during colitis Shigeru Tanaka1, Akira Suto1,2, Taro Iwamoto1, Takahiro Kageyama1, Tomohiro Tamachi1, Hiroaki Takatori1, Kotaro Suzuki1, Koichi Hirose1, Osamu Ohara3, Véronique Lefebvre4, and Hiroshi Nakajima1 Peripherally induced regulatory T (pT reg) cells play indispensable roles in regulating gut inflammation; however, the mechanism underling the differentiation of pT reg cells under inflammatory conditions remains largely unknown. Here, we show that the expression of Sox12, a member of SoxC family, is significantly induced in T reg cells in colitic mice. We also show that TCR–NFAT signaling induces Sox12 expression in CD4+ T cells. Although Sox12 is not required for the development of thymus-derived T reg (tT reg) cells, Sox12 is involved in the development of pT reg cells under inflammatory conditions in an adoptive transfer colitis model. Moreover, we found that enforced expression of Sox12 is sufficient to promote Foxp3 expression in CD4+ T cells even in the absence of TGF-β or IL-2 and that Sox12 binds to Foxp3 promoter and drives its transcription. These results suggest that TCR-NFAT signaling induces the development of pT reg cells in colitic mice partly through Sox12 induction. Introduction Regulatory T (T reg) cells, defined by the expression of Foxp3, 2013). Among the downstream pathways of these signals, Smad3 have a central role in the protection against excessive inflamma- and NFAT binding to conserved noncoding sequence 1 (CNS1) of tory responses caused by infections or autoimmune diseases.
    [Show full text]
  • A Grainyhead-Like 2/Ovo-Like 2 Pathway Regulates Renal Epithelial Barrier Function and Lumen Expansion
    BASIC RESEARCH www.jasn.org A Grainyhead-Like 2/Ovo-Like 2 Pathway Regulates Renal Epithelial Barrier Function and Lumen Expansion † ‡ | Annekatrin Aue,* Christian Hinze,* Katharina Walentin,* Janett Ruffert,* Yesim Yurtdas,*§ | Max Werth,* Wei Chen,* Anja Rabien,§ Ergin Kilic,¶ Jörg-Dieter Schulzke,** †‡ Michael Schumann,** and Kai M. Schmidt-Ott* *Max Delbrueck Center for Molecular Medicine, Berlin, Germany; †Experimental and Clinical Research Center, and Departments of ‡Nephrology, §Urology, ¶Pathology, and **Gastroenterology, Charité Medical University, Berlin, Germany; and |Berlin Institute of Urologic Research, Berlin, Germany ABSTRACT Grainyhead transcription factors control epithelial barriers, tissue morphogenesis, and differentiation, but their role in the kidney is poorly understood. Here, we report that nephric duct, ureteric bud, and collecting duct epithelia express high levels of grainyhead-like homolog 2 (Grhl2) and that nephric duct lumen expansion is defective in Grhl2-deficient mice. In collecting duct epithelial cells, Grhl2 inactivation impaired epithelial barrier formation and inhibited lumen expansion. Molecular analyses showed that GRHL2 acts as a transcrip- tional activator and strongly associates with histone H3 lysine 4 trimethylation. Integrating genome-wide GRHL2 binding as well as H3 lysine 4 trimethylation chromatin immunoprecipitation sequencing and gene expression data allowed us to derive a high-confidence GRHL2 target set. GRHL2 transactivated a group of genes including Ovol2, encoding the ovo-like 2 zinc finger transcription factor, as well as E-cadherin, claudin 4 (Cldn4), and the small GTPase Rab25. Ovol2 induction alone was sufficient to bypass the requirement of Grhl2 for E-cadherin, Cldn4,andRab25 expression. Re-expression of either Ovol2 or a combination of Cldn4 and Rab25 was sufficient to rescue lumen expansion and barrier formation in Grhl2-deficient collecting duct cells.
    [Show full text]
  • Discerning the Role of Foxa1 in Mammary Gland
    DISCERNING THE ROLE OF FOXA1 IN MAMMARY GLAND DEVELOPMENT AND BREAST CANCER by GINA MARIE BERNARDO Submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy Dissertation Adviser: Dr. Ruth A. Keri Department of Pharmacology CASE WESTERN RESERVE UNIVERSITY January, 2012 CASE WESTERN RESERVE UNIVERSITY SCHOOL OF GRADUATE STUDIES We hereby approve the thesis/dissertation of Gina M. Bernardo ______________________________________________________ Ph.D. candidate for the ________________________________degree *. Monica Montano, Ph.D. (signed)_______________________________________________ (chair of the committee) Richard Hanson, Ph.D. ________________________________________________ Mark Jackson, Ph.D. ________________________________________________ Noa Noy, Ph.D. ________________________________________________ Ruth Keri, Ph.D. ________________________________________________ ________________________________________________ July 29, 2011 (date) _______________________ *We also certify that written approval has been obtained for any proprietary material contained therein. DEDICATION To my parents, I will forever be indebted. iii TABLE OF CONTENTS Signature Page ii Dedication iii Table of Contents iv List of Tables vii List of Figures ix Acknowledgements xi List of Abbreviations xiii Abstract 1 Chapter 1 Introduction 3 1.1 The FOXA family of transcription factors 3 1.2 The nuclear receptor superfamily 6 1.2.1 The androgen receptor 1.2.2 The estrogen receptor 1.3 FOXA1 in development 13 1.3.1 Pancreas and Kidney
    [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]