T
Thomas A. Hamilton
Researcher at Cleveland Clinic
Publications - 172
Citations - 16700
Thomas A. Hamilton is an academic researcher from Cleveland Clinic. The author has contributed to research in topics: Gene expression & Chemokine. The author has an hindex of 68, co-authored 171 publications receiving 15964 citations. Previous affiliations of Thomas A. Hamilton include Yeungnam University & Research Triangle Park.
Papers
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Journal ArticleDOI
The Cell Biology of Macrophage Activation
Journal ArticleDOI
TLR4, but not TLR2, mediates IFN-beta-induced STAT1alpha/beta-dependent gene expression in macrophages.
Vladimir Y. Toshchakov,Bryan W. Jones,Pin-Yu Perera,Karen Thomas,M. Joshua Cody,Shuling Zhang,Bryan R.G. Williams,Jennifer Major,Thomas A. Hamilton,Matthew J. Fenton,Stefanie N. Vogel +10 more
TL;DR: These findings provide the first mechanistic basis for differential patterns of gene expression activated by TLR4 and TLR2 agonists.
Journal ArticleDOI
The adaptor Act1 is required for interleukin 17–dependent signaling associated with autoimmune and inflammatory disease
Youcun Qian,Caini Liu,Justin Hartupee,Cengiz Z. Altuntas,Muhammet F. Gulen,Daniel Jane-wit,Jianhua Xiao,Yi Lu,Natalia Giltiay,Jinbo Liu,Tomasz Kordula,Qi-Wei Zhang,Bruce A. Vallance,Shadi Swaidani,Mark A. Aronica,Vincent K. Tuohy,Thomas A. Hamilton,Xiaoxia Li +17 more
TL;DR: The data show that Act1 is essential in IL-17-dependent signaling in autoimmune and inflammatory disease and was associated with much less inflammatory disease in vivo in both autoimmune encephalomyelitis and dextran sodium sulfate–induced colitis.
Journal ArticleDOI
Astrocyte expression of mRNA encoding cytokines IP-10 and JE/MCP-1 in experimental autoimmune encephalomyelitis.
Richard M. Ransohoff,Thomas A. Hamilton,Marie Tani,Mark H. Stoler,H E Shick,Jennifer Major,Melinda L. Estes,D M Thomas,Vincent K. Tuohy +8 more
TL;DR: In situ hybridizations showed, unexpectedly, that astrocytes were the major source of mRNAs encoding IP‐10 and JE/MCP‐1, which implicateAstrocyte‐derived cytokines as potential chemoattractants for inflammatory cells during EAE.
Journal ArticleDOI
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
TL;DR: In this paper, the authors demonstrate that a portion of this cooperativity is mediated by synergism between two distinct transcription factors: signal transducer and activator of transcription 1 (STAT1) and nuclear factor kappaB (NF-kappaB), which is most likely mediated by their independent interaction with one or more components of the basal transcription complex.