Table S7. Gene Ontology Category Membership for Genes Down-Regulated in Arctic Charr (Salvelinus Alpinus) Family 10 Gill Tissue

Total Page:16

File Type:pdf, Size:1020Kb

Table S7. Gene Ontology Category Membership for Genes Down-Regulated in Arctic Charr (Salvelinus Alpinus) Family 10 Gill Tissue Table S7. Gene Ontology category membership for genes down-regulated in Arctic charr (Salvelinus alpinus) family 10 gill tissue. GO ID GO category description FDR P-value Genes within GO category 32501 multicellular organismal process 2.96E-08 SEPT5, MEF2C, ACVRL1, NRP1, PTGS2, PDGFA, FGFRL1, TGFB3, POSTN, PAX1, GSR, DAB2, FLI1, HEY1, CTGF, COL12A1, HTRA3, LMOD1, ERRFI1, COL11A1, PLD2, MINPP1, ARHGAP24, MYH9, PPDPF, SCEL, FMN1, ARVCF, G6PD, RHCG, GNAQ, NAV2, DLL4, OTOF, VEGFA, VAMP5, SHOX, PDGFRB, CAMK1, PRDM1, WNT9A, IQCB1, IRX3, RBP4, GCLC, CLCN2, LUM, MYL1, NTAN1, KEAP1, TIMP2, ITGB1, TIMP3, GCGR, MYOT, PAQR5, HCRTR2, FOXQ1, HOXA3, NDRG3, COL6A3, GPSM1, TGM2, CSDE1, LHX6, COL8A1, ZNF423, DNMT3A, COL4A1, LGALS3, MYO1E, NLK, FBN1, ITGA1, COL15A1, RCAN1, DPYSL3, ATP1A1, COL5A2, FURIN, COL5A1, SLC17A7, ATP7A, GCM2, LAMA4, NEDD4, ITGA5, ULK2, PTP4A1, JAK2, TCF12, MYLK, SNTA1, PLEKHA1, CACNA1B, ABCC6 32502 developmental process 4.00E-07 MEF2C, ACVRL1, NRP1, PTGS2, PDGFA, FGFRL1, TGFB3, POSTN, PAX1, DAB2, FLI1, HEY1, CTGF, COL12A1, HTRA3, ERRFI1, PLD2, MINPP1, ALDH6A1, ARHGAP24, MYH9, PPDPF, SCEL, FMN1, ARVCF, G6PD, RHCG, GNAQ, NAV2, DLL4, VEGFA, VAMP5, SHOX, PDGFRB, CAMK1, PRDM1, WNT9A, SLC40A1, IQCB1, IRX3, FRK, RBP4, SHROOM1, GCLC, CLCN2, MYL1, KEAP1, TIMP2, ITGB1, TIMP3, PAQR5, FOXQ1, HOXA3, NDRG3, COL6A3, GPSM1, TGM2, CSDE1, LHX6, COL8A1, ZNF423, DNMT3A, COL4A1, LGALS3, MYO1E, NLK, FBN1, ITGA1, COL15A1, RCAN1, DPYSL3, COL5A2, FURIN, COL5A1, ATP7A, GCM2, LAMA4, NEDD4, ITGA5, ULK2, PTP4A1, JAK2, TCF12, SNTA1, PLEKHA1 7275 multicellular organismal development 8.36E-07 MEF2C, ACVRL1, NRP1, PTGS2, PDGFA, FGFRL1, TGFB3, POSTN, PAX1, DAB2, FLI1, HEY1, CTGF, COL12A1, HTRA3, ERRFI1, PLD2, MINPP1, ARHGAP24, MYH9, PPDPF, SCEL, FMN1, ARVCF, G6PD, RHCG, GNAQ, NAV2, DLL4, VEGFA, VAMP5, SHOX, PDGFRB, CAMK1, PRDM1, WNT9A, IQCB1, IRX3, RBP4, CLCN2, GCLC, MYL1, KEAP1, TIMP2, ITGB1, TIMP3, PAQR5, FOXQ1, HOXA3, COL6A3, GPSM1, TGM2, CSDE1, LHX6, COL8A1, ZNF423, DNMT3A, COL4A1, LGALS3, MYO1E, NLK, FBN1, ITGA1, COL15A1, RCAN1, DPYSL3, COL5A2, COL5A1, ATP7A, GCM2, LAMA4, NEDD4, ITGA5, ULK2, PTP4A1, JAK2, TCF12, SNTA1, PLEKHA1 48731 system development 8.90E-07 MEF2C, ACVRL1, NRP1, PTGS2, PDGFA, FGFRL1, TGFB3, POSTN, PAX1, FLI1, HEY1, CTGF, COL12A1, HTRA3, ERRFI1, PLD2, MINPP1, ARHGAP24, MYH9, SCEL, FMN1, G6PD, RHCG, GNAQ, NAV2, DLL4, VEGFA, VAMP5, SHOX, PDGFRB, CAMK1, PRDM1, WNT9A, IQCB1, RBP4, CLCN2, MYL1, TIMP2, TIMP3, ITGB1, FOXQ1, HOXA3, COL6A3, GPSM1, TGM2, CSDE1, LHX6, COL8A1, ZNF423, COL4A1, LGALS3, MYO1E, NLK, FBN1, ITGA1, COL15A1, RCAN1, DPYSL3, COL5A2, COL5A1, ATP7A, GCM2, LAMA4, NEDD4, ITGA5, ULK2, JAK2, TCF12, SNTA1, PLEKHA1 48856 anatomical structure development 8.90E-07 MEF2C, ACVRL1, NRP1, PTGS2, PDGFA, FGFRL1, TGFB3, POSTN, PAX1, DAB2, FLI1, HEY1, CTGF, COL12A1, HTRA3, ERRFI1, PLD2, MINPP1, ARHGAP24, MYH9, SCEL, FMN1, G6PD, RHCG, GNAQ, NAV2, DLL4, VEGFA, VAMP5, SHOX, PDGFRB, CAMK1, PRDM1, WNT9A, SLC40A1, IQCB1, RBP4, SHROOM1, CLCN2, GCLC, MYL1, TIMP2, ITGB1, TIMP3, FOXQ1, HOXA3, COL6A3, GPSM1, TGM2, CSDE1, LHX6, COL8A1, ZNF423, COL4A1, LGALS3, MYO1E, NLK, FBN1, ITGA1, COL15A1, RCAN1, DPYSL3, COL5A2, COL5A1, ATP7A, GCM2, LAMA4, NEDD4, ITGA5, ULK2, JAK2, TCF12, SNTA1, PLEKHA1 48513 organ development 2.05E-06 MEF2C, NRP1, ACVRL1, PTGS2, PDGFA, FGFRL1, TGFB3, POSTN, PAX1, FLI1, HEY1, CTGF, HTRA3, ERRFI1, MINPP1, MYH9, ARHGAP24, SCEL, FMN1, G6PD, RHCG, GNAQ, DLL4, VEGFA, VAMP5, PDGFRB, PRDM1, WNT9A, IQCB1, RBP4, CLCN2, MYL1, TIMP3, ITGB1, FOXQ1, HOXA3, GO ID GO category description FDR P-value Genes within GO category COL6A3, TGM2, CSDE1, LHX6, COL8A1, COL4A1, NLK, MYO1E, FBN1, COL15A1, RCAN1, COL5A2, COL5A1, ATP7A, LAMA4, GCM2, ITGA5, JAK2, TCF12, SNTA1, PLEKHA1 1944 vasculature development 1.58E-05 COL4A1, ACVRL1, NRP1, PDGFA, MYO1E, NLK, COL15A1, ARHGAP24, MYH9, COL5A1, ATP7A, LAMA4, HOXA3, ITGA5, CTGF, DLL4, VEGFA, TGM2, COL8A1, ERRFI1 30198 extracellular matrix organization 3.91E-05 ATP7A, COL4A2, LGALS3, CTGF, LUM, COL12A1, POSTN, VWA1, COL5A2, B4GALT7, COL11A1, COL5A1 1568 blood vessel development 4.12E-05 COL4A1, ACVRL1, NRP1, PDGFA, NLK, MYO1E, COL15A1, ARHGAP24, MYH9, COL5A1, ATP7A, LAMA4, HOXA3, ITGA5, CTGF, DLL4, VEGFA, TGM2, COL8A1 48514 blood vessel morphogenesis 5.10E-05 COL4A1, ACVRL1, NRP1, PDGFA, NLK, MYO1E, COL15A1, ARHGAP24, MYH9, ATP7A, HOXA3, ITGA5, CTGF, DLL4, VEGFA, TGM2, COL8A1 1501 skeletal system development 6.98E-05 RBP4, MINPP1, PTGS2, LGALS3, FBN1, FGFRL1, TGFB3, POSTN, COL5A2, PAX1, ATP7A, FMN1, HOXA3, GNAQ, CTGF, COL12A1, PDGFRB, SHOX, WNT9A, PLEKHA1 1525 angiogenesis 7.82E-05 COL4A1, ACVRL1, NRP1, PDGFA, NLK, COL15A1, MYH9, ARHGAP24, HOXA3, CTGF, ITGA5, DLL4, VEGFA, COL8A1 43062 extracellular structure organization 1.43E-04 ATP7A, COL4A2, LGALS3, CTGF, LUM, COL12A1, POSTN, VWA1, COL5A2, B4GALT7, COL11A1, COL5A1, SNTA1 9653 anatomical structure morphogenesis 1.98E-04 RBP4, SHROOM1, NRP1, ACVRL1, GCLC, PDGFA, FGFRL1, TGFB3, PAX1, TIMP3, DAB2, FOXQ1, HOXA3, FLI1, HEY1, CTGF, TGM2, COL8A1, ERRFI1, COL4A1, MYO1E, NLK, ITGA1, COL15A1, ARHGAP24, MYH9, COL5A2, COL5A1, ATP7A, FMN1, GNAQ, ITGA5, ULK2, DLL4, VEGFA, PDGFRB, JAK2, WNT9A, SLC40A1, PLEKHA1 48008 platelet-derived growth factor receptor 3.87E-04 PDGFA, MYO1E, VEGFA, PDGFRB, JAK2, PLEKHA1 signaling pathway 30199 collagen fibril organization 1.25E-03 ATP7A, LUM, COL12A1, COL5A2, COL11A1, COL5A1 50730 regulation of peptidyl-tyrosine phosphorylation 3.53E-03 ITGA5, PDGFA, VEGFA, PDGFRB, JAK2, ERRFI1, THBS4 40012 regulation of locomotion 4.08E-03 PLD2, ACVRL1, PTGS2, PDGFA, F2RL1, FURIN, LAMA4, CXCR4, PTP4A1, DLL4, VEGFA, PDGFRB, JAK2, THBS4 30154 cell differentiation 4.08E-03 MEF2C, FRK, RBP4, CLCN2, NRP1, TIMP2, PAX1, ITGB1, PAQR5, DAB2, NDRG3, CTGF, GPSM1, LHX6, HTRA3, ZNF423, PLD2, ALDH6A1, COL4A1, LGALS3, MYO1E, ITGA1, COL15A1, RCAN1, ARHGAP24, MYH9, PPDPF, SCEL, ATP7A, GCM2, LAMA4, G6PD, RHCG, GNAQ, NEDD4, ULK2, DLL4, VEGFA, VAMP5, CAMK1, JAK2, PRDM1, WNT9A, SNTA1 48869 cellular developmental process 4.08E-03 MEF2C, FRK, RBP4, SHROOM1, CLCN2, NRP1, TIMP2, PAX1, ITGB1, PAQR5, DAB2, NDRG3, CTGF, GPSM1, LHX6, HTRA3, ZNF423, PLD2, ALDH6A1, COL4A1, LGALS3, MYO1E, ITGA1, COL15A1, RCAN1, ARHGAP24, MYH9, PPDPF, SCEL, ATP7A, GCM2, LAMA4, G6PD, RHCG, GNAQ, NEDD4, ULK2, DLL4, VEGFA, VAMP5, CAMK1, JAK2, PRDM1, WNT9A, SNTA1 GO ID GO category description FDR P-value Genes within GO category 35313 wound healing, spreading of epidermal cells 4.08E-03 ACVRL1, ITGA5, COL5A1 44319 wound healing, spreading of epithelial cells 4.08E-03 ACVRL1, ITGA5, COL5A1 7155 cell adhesion 4.08E-03 MTSS1, NRP1, PCDH20, FERMT2, PPFIA1, ITGA1, COL15A1, CD99, LMO7, POSTN, MYH9, CD151, ITGB1, COL5A1, ARVCF, ANXA9, ITGA5, CTGF, COL6A3, COL12A1, COL8A1, COL11A1, THBS4 22610 biological adhesion 4.08E-03 MTSS1, NRP1, PCDH20, FERMT2, PPFIA1, ITGA1, COL15A1, CD99, LMO7, POSTN, MYH9, CD151, ITGB1, COL5A1, ARVCF, ANXA9, ITGA5, CTGF, COL6A3, COL12A1, COL8A1, COL11A1, THBS4 51270 regulation of cellular component movement 4.29E-03 PLD2, LAMA4, NRP1, ACVRL1, PTGS2, PDGFA, DLL4, PTP4A1, F2RL1, VEGFA, PDGFRB, JAK2, FURIN, THBS4 30335 positive regulation of cell migration 4.29E-03 PLD2, PTGS2, PDGFA, PTP4A1, F2RL1, VEGFA, PDGFRB, JAK2, FURIN, THBS4 48646 anatomical structure formation involved in 4.41E-03 RBP4, COL4A1, ACVRL1, NRP1, PDGFA, NLK, COL15A1, ARHGAP24, MYH9, PAX1, ATP7A, HOXA3, morphogenesis ITGA5, CTGF, DLL4, VEGFA, TGM2, COL8A1 3013 circulatory system process 4.41E-03 GCLC, ACVRL1, FLI1, PTGS2, DLL4, MYL1, VEGFA, ITGA1, RCAN1, ATP1A1, GCGR 8015 blood circulation 4.41E-03 GCLC, ACVRL1, FLI1, PTGS2, DLL4, MYL1, VEGFA, ITGA1, RCAN1, ATP1A1, GCGR 30334 regulation of cell migration 4.82E-03 PLD2, LAMA4, ACVRL1, PTGS2, PDGFA, DLL4, PTP4A1, F2RL1, VEGFA, PDGFRB, JAK2, FURIN, THBS4 3008 system process 4.89E-03 IQCB1, SEPT5, RBP4, ACVRL1, GCLC, PTGS2, LUM, MYL1, NTAN1, GCGR, TIMP3, MYOT, HCRTR2, DAB2, FLI1, LMOD1, COL11A1, ITGA1, RCAN1, ATP1A1, SLC17A7, ITGA5, OTOF, DLL4, VEGFA, MYLK, SNTA1, ABCC6, CACNA1B 40017 positive regulation of locomotion 5.44E-03 PLD2, PTGS2, PDGFA, PTP4A1, F2RL1, VEGFA, PDGFRB, JAK2, FURIN, THBS4 51272 positive regulation of cellular component 6.25E-03 PLD2, PTGS2, PDGFA, PTP4A1, F2RL1, VEGFA, PDGFRB, JAK2, FURIN, THBS4 movement 21884 forebrain neuron development 6.68E-03 ATP7A, GNAQ, LHX6 48286 lung alveolus development 6.68E-03 ATP7A, PDGFA, VEGFA, TGFB3, ERRFI1 60541 respiratory system development 1.16E-02 ATP7A, RBP4, CLCN2, PDGFA, CTGF, VEGFA, FGFRL1, TGFB3, ERRFI1 9888 tissue development 1.16E-02 RBP4, MINPP1, COL4A1, NRP1, PTGS2, PDGFA, RCAN1, POSTN, COL5A2, TIMP3, COL5A1, SCEL, ATP7A, FOXQ1, HOXA3, RHCG, CTGF, VEGFA, TGM2, VAMP5, PDGFRB, JAK2, ERRFI1, SNTA1 60017 parathyroid gland development 1.16E-02 GCM2, HOXA3, PAX1 30001 metal ion transport 1.16E-02 TRPM4, SLC39A14, CACNA2D1, KCTD1, ATP1A1, ITPR2, SLC17A7, ATP7A, CTGF, MCOLN1, SLC4A4, SLC39A3, SLC40A1, SLC30A9, CACNA1B 6812 cation transport 1.31E-02 TRPM4, SLC39A14, CACNA2D1, KCTD1, ATP1A1, RHAG, ITPR2, SLC17A7, ATP7A, RHCG, CTGF, GO ID GO category description FDR P-value Genes within GO category MCOLN1, SLC4A4, SLC39A3, SLC40A1, SLC30A9, CACNA1B 43588 skin development 1.59E-02 ATP7A, PDGFA, COL5A2, ERRFI1, COL5A1 8544 epidermis development 1.93E-02 ATP7A, FOXQ1, PTGS2, PDGFA, CTGF, COL5A2, ERRFI1, COL5A1, SCEL 1974 blood vessel remodeling 2.36E-02 ATP7A, HOXA3, VEGFA, TGM2 30324 lung development 2.36E-02 ATP7A, RBP4, CLCN2, PDGFA, CTGF, VEGFA, TGFB3, ERRFI1 9887 organ morphogenesis 2.44E-02 RBP4, NRP1, PDGFA, FGFRL1, TGFB3, COL5A2, PAX1, COL5A1, ATP7A, FMN1, FOXQ1, HOXA3, FLI1, HEY1, CTGF, VEGFA, TGM2, PDGFRB,
Recommended publications
  • Gene Symbol Gene Description ACVR1B Activin a Receptor, Type IB
    Table S1. Kinase clones included in human kinase cDNA library for yeast two-hybrid screening Gene Symbol Gene Description ACVR1B activin A receptor, type IB ADCK2 aarF domain containing kinase 2 ADCK4 aarF domain containing kinase 4 AGK multiple substrate lipid kinase;MULK AK1 adenylate kinase 1 AK3 adenylate kinase 3 like 1 AK3L1 adenylate kinase 3 ALDH18A1 aldehyde dehydrogenase 18 family, member A1;ALDH18A1 ALK anaplastic lymphoma kinase (Ki-1) ALPK1 alpha-kinase 1 ALPK2 alpha-kinase 2 AMHR2 anti-Mullerian hormone receptor, type II ARAF v-raf murine sarcoma 3611 viral oncogene homolog 1 ARSG arylsulfatase G;ARSG AURKB aurora kinase B AURKC aurora kinase C BCKDK branched chain alpha-ketoacid dehydrogenase kinase BMPR1A bone morphogenetic protein receptor, type IA BMPR2 bone morphogenetic protein receptor, type II (serine/threonine kinase) BRAF v-raf murine sarcoma viral oncogene homolog B1 BRD3 bromodomain containing 3 BRD4 bromodomain containing 4 BTK Bruton agammaglobulinemia tyrosine kinase BUB1 BUB1 budding uninhibited by benzimidazoles 1 homolog (yeast) BUB1B BUB1 budding uninhibited by benzimidazoles 1 homolog beta (yeast) C9orf98 chromosome 9 open reading frame 98;C9orf98 CABC1 chaperone, ABC1 activity of bc1 complex like (S. pombe) CALM1 calmodulin 1 (phosphorylase kinase, delta) CALM2 calmodulin 2 (phosphorylase kinase, delta) CALM3 calmodulin 3 (phosphorylase kinase, delta) CAMK1 calcium/calmodulin-dependent protein kinase I CAMK2A calcium/calmodulin-dependent protein kinase (CaM kinase) II alpha CAMK2B calcium/calmodulin-dependent
    [Show full text]
  • Precision Medicine for Human Cancers with Notch Signaling Dysregulation (Review)
    INTERNATIONAL JOURNAL OF MOleCular meDICine 45: 279-297, 2020 Precision medicine for human cancers with Notch signaling dysregulation (Review) MASUKO KATOH1 and MASARU KATOH2 1M & M PrecMed, Tokyo 113-0033; 2Department of Omics Network, National Cancer Center, Tokyo 104-0045, Japan Received September 16, 2019; Accepted November 20, 2019 DOI: 10.3892/ijmm.2019.4418 Abstract. NOTCH1, NOTCH2, NOTCH3 and NOTCH4 are conjugate (ADC) Rova-T, and DLL3-targeting chimeric antigen transmembrane receptors that transduce juxtacrine signals of receptor‑modified T cells (CAR‑Ts), AMG 119, are promising the delta-like canonical Notch ligand (DLL)1, DLL3, DLL4, anti-cancer therapeutics, as are other ADCs or CAR-Ts targeting jagged canonical Notch ligand (JAG)1 and JAG2. Canonical tumor necrosis factor receptor superfamily member 17, Notch signaling activates the transcription of BMI1 proto-onco- CD19, CD22, CD30, CD79B, CD205, Claudin 18.2, fibro- gene polycomb ring finger, cyclin D1, CD44, cyclin dependent blast growth factor receptor (FGFR)2, FGFR3, receptor-type kinase inhibitor 1A, hes family bHLH transcription factor 1, tyrosine-protein kinase FLT3, HER2, hepatocyte growth factor hes related family bHLH transcription factor with YRPW receptor, NECTIN4, inactive tyrosine-protein kinase 7, inac- motif 1, MYC, NOTCH3, RE1 silencing transcription factor and tive tyrosine-protein kinase transmembrane receptor ROR1 transcription factor 7 in a cellular context-dependent manner, and tumor-associated calcium signal transducer 2. ADCs and while non-canonical Notch signaling activates NF-κB and Rac CAR-Ts could alter the therapeutic framework for refractory family small GTPase 1. Notch signaling is aberrantly activated cancers, especially diffuse-type gastric cancer, ovarian cancer in breast cancer, non-small-cell lung cancer and hematological and pancreatic cancer with peritoneal dissemination.
    [Show full text]
  • Multifactorial Erβ and NOTCH1 Control of Squamous Differentiation and Cancer
    Multifactorial ERβ and NOTCH1 control of squamous differentiation and cancer Yang Sui Brooks, … , Karine Lefort, G. Paolo Dotto J Clin Invest. 2014;124(5):2260-2276. https://doi.org/10.1172/JCI72718. Research Article Oncology Downmodulation or loss-of-function mutations of the gene encoding NOTCH1 are associated with dysfunctional squamous cell differentiation and development of squamous cell carcinoma (SCC) in skin and internal organs. While NOTCH1 receptor activation has been well characterized, little is known about how NOTCH1 gene transcription is regulated. Using bioinformatics and functional screening approaches, we identified several regulators of the NOTCH1 gene in keratinocytes, with the transcription factors DLX5 and EGR3 and estrogen receptor β (ERβ) directly controlling its expression in differentiation. DLX5 and ERG3 are required for RNA polymerase II (PolII) recruitment to the NOTCH1 locus, while ERβ controls NOTCH1 transcription through RNA PolII pause release. Expression of several identified NOTCH1 regulators, including ERβ, is frequently compromised in skin, head and neck, and lung SCCs and SCC-derived cell lines. Furthermore, a keratinocyte ERβ–dependent program of gene expression is subverted in SCCs from various body sites, and there are consistent differences in mutation and gene-expression signatures of head and neck and lung SCCs in female versus male patients. Experimentally increased ERβ expression or treatment with ERβ agonists inhibited proliferation of SCC cells and promoted NOTCH1 expression and squamous differentiation both in vitro and in mouse xenotransplants. Our data identify a link between transcriptional control of NOTCH1 expression and the estrogen response in keratinocytes, with implications for differentiation therapy of squamous cancer. Find the latest version: https://jci.me/72718/pdf Research article Multifactorial ERβ and NOTCH1 control of squamous differentiation and cancer Yang Sui Brooks,1,2 Paola Ostano,3 Seung-Hee Jo,1,2 Jun Dai,1,2 Spiro Getsios,4 Piotr Dziunycz,5 Günther F.L.
    [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]
  • 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]
  • PGC-1A Protects from Notch-Induced Kidney Fibrosis Development
    BASIC RESEARCH www.jasn.org PGC-1a Protects from Notch-Induced Kidney Fibrosis Development † ‡ ‡ Seung Hyeok Han,* Mei-yan Wu, § Bo Young Nam, Jung Tak Park,* Tae-Hyun Yoo,* ‡ † † † † Shin-Wook Kang,* Jihwan Park, Frank Chinga, Szu-Yuan Li, and Katalin Susztak *Department of Internal Medicine, Institute of Kidney Disease Research, Yonsei University College of Medicine, Seoul, Korea; †Renal Electrolyte and Hypertension Division, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania; ‡Severance Biomedical Science Institute, Brain Korea 21 PLUS, Yonsei University College of Medicine, Seoul, Korea; and §Department of Nephrology, The First Hospital of Jilin University, Changchun, China ABSTRACT Kidney fibrosis is the histologic manifestation of CKD. Sustained activation of developmental pathways, such as Notch, in tubule epithelial cells has been shown to have a key role in fibrosis development. The molecular mechanism of Notch-induced fibrosis, however, remains poorly understood. Here, we show that, that expression of peroxisomal proliferation g-coactivator (PGC-1a) and fatty acid oxidation-related genes are lower in mice expressing active Notch1 in tubular epithelial cells (Pax8-rtTA/ICN1) compared to littermate controls. Chromatin immunoprecipitation assays revealed that the Notch target gene Hes1 directly binds to the regulatory region of PGC-1a. Compared with Pax8-rtTA/ICN1 transgenic animals, Pax8-rtTA/ICN1/Ppargc1a transgenic mice showed improvement of renal structural alterations (on his- tology) and molecular defect (expression of profibrotic genes). Overexpression of PGC-1a restored mi- tochondrial content and reversed the fatty acid oxidation defect induced by Notch overexpression in vitro in tubule cells. Furthermore, compared with Pax8-rtTA/ICN1 mice, Pax8-rtTA/ICN1/Ppargc1a mice exhibited improvement in renal fatty acid oxidation gene expression and apoptosis.
    [Show full text]
  • The NOTCH4-HEY1 Pathway Induces Epithelial Mesenchymal Transition in Head and Neck Squamous Cell Carcinoma
    Author Manuscript Published OnlineFirst on November 16, 2017; DOI: 10.1158/1078-0432.CCR-17-1366 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. The NOTCH4-HEY1 pathway induces epithelial mesenchymal transition in head and neck squamous cell carcinoma Authors: Takahito Fukusumi1, Theresa W Guo2, Akihiro Sakai1, Mizuo Ando1, Shuling Ren1, Sunny Haft1, Chao Liu1, Panomwat Amornphimoltham1, J. Silvio Gutkind1, Joseph A Califano1 1 Moores Cancer Center, University of California San Diego, 3855 Health Science Drive, MC 0803 La Jolla, California 92093, U.S.A. 2 Department of Otolaryngology-Head and Neck Surgery, Johns Hopkins Medical Institutions, 1550 Orleans Street, Baltimore, Maryland 21231, U.S.A. Running Title: NOTCH4-HEY1 induces EMT in HNSCC Key Words: Head and neck squamous cell carcinoma, TCGA, NOTCH4, HEY1, EMT Financial Support This study was supported by National Institute of Dental and Craniofacial Research (NIDCR, number: R01DE023347). J.A.Califano received this grant. Correspondence: Joseph A. Califano, MD, Department of Otolaryngology - Head and Neck Surgery, University of California San Diego, 3855 Health Science Drive, MC 0803 La Jolla, California 92093, U.S.A. Phone: 619-543-7895; E-mail; [email protected] Disclosure of Potential Conflict of Interest The authors declare no potential conflicts of interest. 1 Downloaded from clincancerres.aacrjournals.org on October 1, 2021. © 2017 American Association for Cancer Research. Author Manuscript Published OnlineFirst on November 16, 2017; DOI: 10.1158/1078-0432.CCR-17-1366 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. ABSTRACT Background: Recently, several comprehensive genomic analyses demonstrated NOTCH1 and NOTCH3 mutations in head and neck squamous cell carcinoma (HNSCC) in approximately 20% of cases.
    [Show full text]
  • Transcriptomic Analysis of Native Versus Cultured Human and Mouse Dorsal Root Ganglia Focused on Pharmacological Targets Short
    bioRxiv preprint doi: https://doi.org/10.1101/766865; this version posted September 12, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-ND 4.0 International license. Transcriptomic analysis of native versus cultured human and mouse dorsal root ganglia focused on pharmacological targets Short title: Comparative transcriptomics of acutely dissected versus cultured DRGs Andi Wangzhou1, Lisa A. McIlvried2, Candler Paige1, Paulino Barragan-Iglesias1, Carolyn A. Guzman1, Gregory Dussor1, Pradipta R. Ray1,#, Robert W. Gereau IV2, # and Theodore J. Price1, # 1The University of Texas at Dallas, School of Behavioral and Brain Sciences and Center for Advanced Pain Studies, 800 W Campbell Rd. Richardson, TX, 75080, USA 2Washington University Pain Center and Department of Anesthesiology, Washington University School of Medicine # corresponding authors [email protected], [email protected] and [email protected] Funding: NIH grants T32DA007261 (LM); NS065926 and NS102161 (TJP); NS106953 and NS042595 (RWG). The authors declare no conflicts of interest Author Contributions Conceived of the Project: PRR, RWG IV and TJP Performed Experiments: AW, LAM, CP, PB-I Supervised Experiments: GD, RWG IV, TJP Analyzed Data: AW, LAM, CP, CAG, PRR Supervised Bioinformatics Analysis: PRR Drew Figures: AW, PRR Wrote and Edited Manuscript: AW, LAM, CP, GD, PRR, RWG IV, TJP All authors approved the final version of the manuscript. 1 bioRxiv preprint doi: https://doi.org/10.1101/766865; this version posted September 12, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.
    [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]
  • Advancing a Clinically Relevant Perspective of the Clonal Nature of Cancer
    Advancing a clinically relevant perspective of the clonal nature of cancer Christian Ruiza,b, Elizabeth Lenkiewicza, Lisa Eversa, Tara Holleya, Alex Robesona, Jeffrey Kieferc, Michael J. Demeurea,d, Michael A. Hollingsworthe, Michael Shenf, Donna Prunkardf, Peter S. Rabinovitchf, Tobias Zellwegerg, Spyro Moussesc, Jeffrey M. Trenta,h, John D. Carpteni, Lukas Bubendorfb, Daniel Von Hoffa,d, and Michael T. Barretta,1 aClinical Translational Research Division, Translational Genomics Research Institute, Scottsdale, AZ 85259; bInstitute for Pathology, University Hospital Basel, University of Basel, 4031 Basel, Switzerland; cGenetic Basis of Human Disease, Translational Genomics Research Institute, Phoenix, AZ 85004; dVirginia G. Piper Cancer Center, Scottsdale Healthcare, Scottsdale, AZ 85258; eEppley Institute for Research in Cancer and Allied Diseases, Nebraska Medical Center, Omaha, NE 68198; fDepartment of Pathology, University of Washington, Seattle, WA 98105; gDivision of Urology, St. Claraspital and University of Basel, 4058 Basel, Switzerland; hVan Andel Research Institute, Grand Rapids, MI 49503; and iIntegrated Cancer Genomics Division, Translational Genomics Research Institute, Phoenix, AZ 85004 Edited* by George F. Vande Woude, Van Andel Research Institute, Grand Rapids, MI, and approved June 10, 2011 (received for review March 11, 2011) Cancers frequently arise as a result of an acquired genomic insta- on the basis of morphology alone (8). Thus, the application of bility and the subsequent clonal evolution of neoplastic cells with purification methods such as laser capture microdissection does variable patterns of genetic aberrations. Thus, the presence and not resolve the complexities of many samples. A second approach behaviors of distinct clonal populations in each patient’s tumor is to passage tumor biopsies in tissue culture or in xenografts (4, 9– may underlie multiple clinical phenotypes in cancers.
    [Show full text]
  • Loss of Tgfb Receptor Type 2 Expression Impairs Estrogen Response and Confers Tamoxifen Resistance Susann Busch1, Andrew H
    Cancer Tumor and Stem Cell Biology Research Loss of TGFb Receptor Type 2 Expression Impairs Estrogen Response and Confers Tamoxifen Resistance Susann Busch1, Andrew H. Sims2, Olle Sta l3,Ma rten Ferno€4, and Goran€ Landberg1,5 Abstract One third of the patients with estrogen receptor a (ERa)- tamoxifen resistance. Functional investigations confirmed that positive breast cancer who are treated with the antiestrogen cell cycle or apoptosis responses to estrogen or tamoxifen in tamoxifen will either not respond to initial therapy or will ERa-positive breast cancer cells were impaired by TGFBR2 develop drug resistance. Endocrine response involves crosstalk silencing, as was ERa phosphorylation, tamoxifen-induced between ERa and TGFb signaling, such that tamoxifen non- transcriptional activation of TGFb, and upregulation of the responsiveness or resistance in breast cancer might involve multidrug resistance protein ABCG2. Acquisition of low aberrant TGFb signaling. In this study, we analyzed TGFb TGFBR2 expression as a contributing factor to endocrine resis- receptor type 2 (TGFBR2) expression and correlated it with tance was validated prospectively in a tamoxifen-resistant cell ERa status and phosphorylation in a cohort of 564 patients line generated by long-term drug treatment. Collectively, our who had been randomized to tamoxifen or no-adjuvant treat- results established a central contribution of TGFb signaling in ment for invasive breast carcinoma. We also evaluated an endocrineresistanceinbreastcancerandofferedevidencethat additional four independent genetic datasets in invasive breast TGFBR2 can serve as an independent biomarker to predict cancer. In all the cohorts we analyzed, we documented an treatment outcomes in ERa-positive forms of this disease. association of low TGFBR2 protein and mRNA expression with Cancer Res; 75(7); 1457–69.
    [Show full text]
  • Profiling Data
    Compound Name DiscoveRx Gene Symbol Entrez Gene Percent Compound Symbol Control Concentration (nM) JNK-IN-8 AAK1 AAK1 69 1000 JNK-IN-8 ABL1(E255K)-phosphorylated ABL1 100 1000 JNK-IN-8 ABL1(F317I)-nonphosphorylated ABL1 87 1000 JNK-IN-8 ABL1(F317I)-phosphorylated ABL1 100 1000 JNK-IN-8 ABL1(F317L)-nonphosphorylated ABL1 65 1000 JNK-IN-8 ABL1(F317L)-phosphorylated ABL1 61 1000 JNK-IN-8 ABL1(H396P)-nonphosphorylated ABL1 42 1000 JNK-IN-8 ABL1(H396P)-phosphorylated ABL1 60 1000 JNK-IN-8 ABL1(M351T)-phosphorylated ABL1 81 1000 JNK-IN-8 ABL1(Q252H)-nonphosphorylated ABL1 100 1000 JNK-IN-8 ABL1(Q252H)-phosphorylated ABL1 56 1000 JNK-IN-8 ABL1(T315I)-nonphosphorylated ABL1 100 1000 JNK-IN-8 ABL1(T315I)-phosphorylated ABL1 92 1000 JNK-IN-8 ABL1(Y253F)-phosphorylated ABL1 71 1000 JNK-IN-8 ABL1-nonphosphorylated ABL1 97 1000 JNK-IN-8 ABL1-phosphorylated ABL1 100 1000 JNK-IN-8 ABL2 ABL2 97 1000 JNK-IN-8 ACVR1 ACVR1 100 1000 JNK-IN-8 ACVR1B ACVR1B 88 1000 JNK-IN-8 ACVR2A ACVR2A 100 1000 JNK-IN-8 ACVR2B ACVR2B 100 1000 JNK-IN-8 ACVRL1 ACVRL1 96 1000 JNK-IN-8 ADCK3 CABC1 100 1000 JNK-IN-8 ADCK4 ADCK4 93 1000 JNK-IN-8 AKT1 AKT1 100 1000 JNK-IN-8 AKT2 AKT2 100 1000 JNK-IN-8 AKT3 AKT3 100 1000 JNK-IN-8 ALK ALK 85 1000 JNK-IN-8 AMPK-alpha1 PRKAA1 100 1000 JNK-IN-8 AMPK-alpha2 PRKAA2 84 1000 JNK-IN-8 ANKK1 ANKK1 75 1000 JNK-IN-8 ARK5 NUAK1 100 1000 JNK-IN-8 ASK1 MAP3K5 100 1000 JNK-IN-8 ASK2 MAP3K6 93 1000 JNK-IN-8 AURKA AURKA 100 1000 JNK-IN-8 AURKA AURKA 84 1000 JNK-IN-8 AURKB AURKB 83 1000 JNK-IN-8 AURKB AURKB 96 1000 JNK-IN-8 AURKC AURKC 95 1000 JNK-IN-8
    [Show full text]