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PLoS ONE, ISSN 1932-6203, 06/2014, Volume 9, Issue 6, p. e99835
Tissue hypoxia induces reprogramming of cell metabolism and may result in normal cell transformation and cancer progression. Hypoxia-inducible factor 1-alpha... 
RISK | PROMOTER POLYMORPHISMS | NF-KAPPA-B | TUMORS | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | Stomach Neoplasms - genetics | Toll-Like Receptor 2 - genetics | Hypoxia-Inducible Factor 1, alpha Subunit - genetics | Humans | Peptides - genetics | Stomach Neoplasms - metabolism | Toll-Like Receptor 2 - metabolism | Receptors, IgG - metabolism | Interferon Regulatory Factor-1 - genetics | Tissue Inhibitor of Metalloproteinase-1 - genetics | Tissue Inhibitor of Metalloproteinase-1 - metabolism | Genes, Regulator - genetics | Receptors, IgG - genetics | Peptides - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Genes, Regulator - physiology | Trefoil Factor-3 | Matrix Metalloproteinase 1 - metabolism | Gene Expression Regulation, Neoplastic - physiology | Gene Expression Regulation, Neoplastic - genetics | Interferon Regulatory Factor-1 - metabolism | Matrix Metalloproteinase 1 - genetics | Hypoxia-inducible factor 1 | Transformation | Transcription factors | Laboratories | Genes | Gene regulation | Science | Interferon regulatory factor 1 | Tissues | Tissue inhibitor of metalloproteinase 1 | Stomach cancer | Data bases | Proteins | Signal transduction | Biomedical materials | Cell growth | Rodents | Toll-like receptors | Bioindicators | Stat1 protein | Gastric cancer | Hypoxia-inducible factors | BRCA1 protein | Stat3 protein | Breast cancer | Metabolism | Gene expression | Studies | Fc receptors | Signaling | Medical prognosis | TLR2 protein | Biomarkers | Hypoxia | Cancer
Journal Article
Cell Reports, ISSN 2211-1247, 05/2017, Volume 19, Issue 6, pp. 1189 - 1201
Journal Article
SHOCK, ISSN 1073-2322, 02/2016, Volume 46, Issue 3, pp. 329 - 338
ABSTRACTPreviously, we demonstrated that pyroptosis in alveolar macrophages (AMs) plays an essential role in LPS-induced acute lung injury (ALI). However, the... 
Acute lung injury | pyroptosis | alveolar macrophage | interferon regulatory factor-1 | caspase-1 | GAMMA | SURGERY | APOPTOSIS | EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS | ENDOTOXEMIA | INDUCTION | RELEASE | OLIGODENDROCYTES | CELL-DEATH | INFLAMMATION | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | CRITICAL CARE MEDICINE | Pyroptosis - physiology | Lipopolysaccharides - toxicity | Interleukin-18 - blood | Macrophages, Alveolar - physiology | Male | Acute Lung Injury - blood | Pyroptosis - genetics | Interferon Regulatory Factor-1 - genetics | Interleukin-1beta - blood | Mice, Knockout | Animals | Acute Lung Injury - chemically induced | Acute Lung Injury - immunology | Acute Lung Injury - metabolism | Mice | Macrophages, Alveolar - metabolism | HMGB1 Protein - blood | Interferon Regulatory Factor-1 - metabolism | TLR-4 | quantitative PCR | AMs | alveolar macrophages | IRF-1 | HMGB1 | MyD88 | LPS | IFN | ASC | LDH | interferon regulatory factor 1 | myeloid differentiation factor 88 | NLRP3 | qPCR | pathogen-associated molecular pattern | ARDS | knockout | nod-like receptor protein 3 | BALF | Lactate dehydrogenase | Basic Science Aspects | interferon | apoptosis-associated speck-like protein containing a caspase activation and recruitment domain | PAMP | high-mobility group box 1 | adenosine triphosphate | acute respiratory distress syndrome | bronchoalveolar lavage fluid | lipopolysaccharide | wild-type | ATP | toll-like receptor 4 | ALI
Journal Article
Journal Article
Journal of Immunology, ISSN 0022-1767, 08/2010, Volume 185, Issue 4, pp. 2467 - 2481
Epidermal keratinocytes can counteract the detrimental effects of IFN-gamma by inducing the expression of suppressor of cytokine signaling (SOCS) 1, which... 
TRANSCRIPTION FACTORS | ATOPIC-DERMATITIS | INTERFERON-GAMMA | CYTOKINE SIGNALING-1 | CHEMOKINE PRODUCTION | GENE-EXPRESSION | FUNCTIONAL-ANALYSIS | TUMOR-SUPPRESSOR | IMMUNOLOGY | NUCLEAR-LOCALIZATION SIGNAL | T-LYMPHOCYTES | Luciferases - metabolism | Humans | Suppressor of Cytokine Signaling 1 Protein | Immunoblotting | Sp1 Transcription Factor - metabolism | Promoter Regions, Genetic - genetics | Luciferases - genetics | DNA-Binding Proteins - metabolism | Psoriasis - genetics | Transfection | Chromatin Immunoprecipitation | Psoriasis - pathology | Time Factors | Kruppel-Like Transcription Factors - metabolism | Protein Binding - drug effects | Psoriasis - metabolism | Repressor Proteins - metabolism | Proto-Oncogene Proteins - metabolism | Cells, Cultured | Repressor Proteins - genetics | Suppressor of Cytokine Signaling Proteins - genetics | Proto-Oncogene Proteins - genetics | Binding Sites - genetics | DNA-Binding Proteins - genetics | Reverse Transcriptase Polymerase Chain Reaction | Interferon Regulatory Factor-1 - genetics | Gene Expression Regulation - drug effects | Keratinocytes - pathology | Keratinocytes - drug effects | Sp1 Transcription Factor - genetics | Keratinocytes - metabolism | Suppressor of Cytokine Signaling Proteins - metabolism | Kruppel-Like Transcription Factors - genetics | Interferon Regulatory Factor-1 - metabolism | Interferon-gamma - pharmacology
Journal Article
Oncotarget, ISSN 1949-2553, 2015, Volume 6, Issue 31, pp. 31479 - 31492
Purpose: Antiangiogenic therapy is commonly being used for the treatment of glioblastoma. However, the benefits of angiogenesis inhibitors are typically... 
Autophagy | Antiangiogenesis | IRF1 | Bevacizumab | autophagy | PLUS IRINOTECAN | CANCER CELLS | INDUCED APOPTOSIS | PROGNOSIS | TEMOZOLOMIDE | CELL BIOLOGY | GLIOBLASTOMA | INHIBITION | THERAPY | PATHWAY | bevacizumab | RESISTANCE | antiangiogenesis
Journal Article
Biochemical and Biophysical Research Communications, ISSN 0006-291X, 06/2014, Volume 448, Issue 3, pp. 323 - 328
Pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) is considered to be the major one contributing to the process of development of... 
Matrix metalloproteinase 13 (MMP-13) | Tumor necrosis factor-alpha (TNF-α) | Osteoarthritis (OA) | Glatiramer acetate (GA) | Collagen II | Interferon regulatory factor-1 (IRF-1) | TRANSCRIPTION FACTORS | PATHWAYS | CELLS | CHONDROCYTES | Tumor necrosis factor-alpha (TNF-alpha) | IRF FAMILY | BIOCHEMISTRY & MOLECULAR BIOLOGY | INDUCTION | CARTILAGE | BIOPHYSICS | DISEASE | OSTEOARTHRITIS | EXPRESSION | Tumor Necrosis Factor-alpha - metabolism | Humans | Interferon Regulatory Factor-1 - antagonists & inhibitors | Glatiramer Acetate | RNA, Messenger - metabolism | Matrix Metalloproteinase 13 - biosynthesis | Gene Knockdown Techniques | Collagen Type II - metabolism | Chondrocytes - drug effects | Proteolysis - drug effects | STAT1 Transcription Factor - metabolism | Enzyme Induction - drug effects | Immunosuppressive Agents - pharmacology | Chondrocytes - metabolism | Nitric Oxide - biosynthesis | Matrix Metalloproteinase 13 - genetics | RNA, Messenger - genetics | Osteoarthritis, Knee - etiology | STAT1 Transcription Factor - genetics | STAT1 Transcription Factor - antagonists & inhibitors | Interferon Regulatory Factor-1 - genetics | Peptides - pharmacology | Up-Regulation - drug effects | Nitric Oxide Synthase Type II - genetics | Interferon Regulatory Factor-1 - metabolism | Osteoarthritis, Knee - drug therapy | Osteoarthritis, Knee - metabolism | Nitric Oxide Synthase Type II - metabolism | Biological response modifiers | Collagen | Interferon
Journal Article
Journal Article