2010 - Fellow of the American Association for the Advancement of Science (AAAS)
His primary areas of study are Molecular biology, Signal transduction, Chemokine, Immunology and Gene expression. His Molecular biology study combines topics from a wide range of disciplines, such as Tumor necrosis factor alpha, NFKB1, Interferon gamma, Regulation of gene expression and Transcription. His Signal transduction research is multidisciplinary, relying on both I-Kappa-B Kinase, Cancer research and Neutrophilia.
His Chemokine research is multidisciplinary, incorporating elements of Messenger RNA, In situ hybridization and Cell biology. His work on Immune system and Cytokine as part of general Immunology study is frequently linked to Encephalomyelitis, bridging the gap between disciplines. His Gene expression study incorporates themes from Complementary DNA, Open reading frame, Nucleic acid sequence and Homology.
His primary areas of investigation include Molecular biology, Gene expression, Cell biology, Chemokine and Messenger RNA. The Molecular biology study combines topics in areas such as Lipopolysaccharide and Transcription, Gene, MRNA stabilization. His research on Gene expression also deals with topics like
His Cell biology research focuses on subjects like Chemokine receptor, which are linked to CXCL10. His work investigates the relationship between Chemokine and topics such as Cell type that intersect with problems in In situ hybridization. His studies deal with areas such as Proinflammatory cytokine and CXCL1 as well as Messenger RNA.
Thomas A. Hamilton focuses on Cell biology, Cancer research, Inflammation, Chemokine and Pathology. His Cell biology study focuses on Signal transducing adaptor protein in particular. His work carried out in the field of Signal transducing adaptor protein brings together such families of science as Messenger RNA, Untranslated region and Stem cell.
His work deals with themes such as CXCL1, Macrophage and Immunotherapy, which intersect with Cancer research. His studies in Inflammation integrate themes in fields like Amyotrophic lateral sclerosis and Neuron. His Chemokine research includes elements of Proinflammatory cytokine, Translation, P-bodies and MRNA stabilization.
His primary areas of investigation include Cell biology, Carcinogenesis, Population, Wound healing and Signal transducing adaptor protein. The various areas that Thomas A. Hamilton examines in his Cell biology study include P-bodies, Messenger RNA, Untranslated region, MRNA stabilization and Proinflammatory cytokine. His Proinflammatory cytokine study often links to related topics such as Chemokine.
His work on CXC chemokine receptors as part of general Chemokine research is frequently linked to Myeloid-derived Suppressor Cell, bridging the gap between disciplines. The concepts of his Carcinogenesis study are interwoven with issues in Progenitor cell, Cancer research, Colitis and Epidermis. His work in Progenitor cell addresses issues such as Pathology, which are connected to fields such as CXCL5.
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TLR4, but not TLR2, mediates IFN-beta-induced STAT1alpha/beta-dependent gene expression in macrophages.
Vladimir Toshchakov;Bryan W Jones;Pin-Yu Perera;Karen Thomas.
Nature Immunology (2002)
Astrocyte expression of mRNA encoding cytokines IP-10 and JE/MCP-1 in experimental autoimmune encephalomyelitis.
R M Ransohoff;T A Hamilton;M Tani;M H Stoler.
The FASEB Journal (1993)
The adaptor Act1 is required for interleukin 17–dependent signaling associated with autoimmune and inflammatory disease
Youcun Qian;Caini Liu;Justin Hartupee;Cengiz Zubeyir Altuntas.
Nature Immunology (2007)
Synergy between Interferon-γ and Tumor Necrosis Factor-α in Transcriptional Activation Is Mediated by Cooperation between Signal Transducer and Activator of Transcription 1 and Nuclear Factor κB
Yoshihiro Ohmori;Robert D. Schreiber;Thomas A. Hamilton.
Journal of Biological Chemistry (1997)
IL-17 enhances chemokine gene expression through mRNA stabilization
Justin Hartupee;Caini Liu;Michael Novotny;Xiaoxia Li.
Journal of Immunology (2007)
Cooperative interaction between interferon (IFN) stimulus response element and kappa B sequence motifs controls IFN gamma- and lipopolysaccharide-stimulated transcription from the murine IP-10 promoter.
Yoshihiro Ohmori;Thomas A Hamilton.
Journal of Biological Chemistry (1993)
Requirement for STAT1 in LPS-induced gene expression in macrophages.
Yoshihiro Ohmori;Thomas A. Hamilton.
Journal of Leukocyte Biology (2001)
Treatment with IL-17 prolongs the half-life of chemokine CXCL1 mRNA via the adaptor TRAF5 and the splicing-regulatory factor SF2 (ASF).
Dongxu Sun;Michael Novotny;Katarzyna Bulek;Caini Liu.
Nature Immunology (2011)
T-Cells Infiltrating Renal Cell Carcinoma Display a Poor Proliferative Response Even Though They Can Produce Interleukin 2 and Express Interleukin 2 Receptors
Jeannine P. Alexander;Seiji Kudoh;Kathryn A. Melsop;Thomas A. Hamilton.
Cancer Research (1993)
Monokine Induced by IFN-γ Is a Dominant Factor Directing T Cells into Murine Cardiac Allografts During Acute Rejection
Masayoshi Miura;Ken Morita;Hirohito Kobayashi;Thomas A. Hamilton.
Journal of Immunology (2001)
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