H
Hong-Tao Lu
Researcher at Yale University
Publications - 5
Citations - 2912
Hong-Tao Lu is an academic researcher from Yale University. The author has contributed to research in topics: MAP kinase kinase kinase & MAP2K7. The author has an hindex of 5, co-authored 5 publications receiving 2788 citations. Previous affiliations of Hong-Tao Lu include University of Massachusetts Medical School.
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Journal ArticleDOI
Carbon monoxide has anti-inflammatory effects involving the mitogen-activated protein kinase pathway
Leo E. Otterbein,Leo E. Otterbein,Fritz H. Bach,Jawed Alam,Miguel P. Soares,Hong-Tao Lu,Mark Allen Wysk,Roger J. Davis,Richard A. Flavell,Augustine M.K. Choi,Augustine M.K. Choi +10 more
TL;DR: It is demonstrated here that carbon monoxide, a by-product of heme catabolism by heme oxygenase, mediates potent anti-inflammatory effects and may have an important protective function in inflammatory disease states and thus has potential therapeutic uses.
Journal ArticleDOI
Defective IL-12 production in mitogen-activated protein (MAP) kinase kinase 3 (Mkk3)-deficient mice.
Hong-Tao Lu,Derek D. Yang,Mark Allen Wysk,Evelina Gatti,Ira Mellman,Roger J. Davis,Richard A. Flavell +6 more
TL;DR: It is concluded that the p38 MAP kinase, activated through MKK3, is required for the production of inflammatory cytokines by both antigen‐presenting cells and CD4+ T cells.
Journal ArticleDOI
Targeted disruption of the MKK4 gene causes embryonic death, inhibition of c-Jun NH2-terminal kinase activation, and defects in AP-1 transcriptional activity
Di Yang,Cathy Tournier,Mark Allen Wysk,Hong-Tao Lu,Hong-Tao Lu,Jie Xu,Roger J. Davis,Richard A. Flavell,Richard A. Flavell +8 more
TL;DR: Data establish that MKK4 is a JNK activator in vivo and demonstrate that Mkk4 is an essential component of the JNK signal transduction pathway.
Journal ArticleDOI
Requirement of mitogen-activated protein kinase kinase 3 (MKK3) for tumor necrosis factor-induced cytokine expression
TL;DR: It is reported that Mkk3 gene disruption caused a selective defect in the response of fibroblasts to the proinflammatory cytokine tumor necrosis factor, including reduced p38 MAP kinase activation and cytokine expression.
Journal ArticleDOI
Molecular basis of T-cell differentiation.
Richard A. Flavell,Baiyong Li,Chen Dong,Hong-Tao Lu,Derek D. Yang,Derek D. Yang,Hervé Enslen,Cathy Tournier,Alan J. Whitmarsh,Mark Allen Wysk,Dietrich Conze,Mercedes Rincon,Roger J. Davis +12 more
TL;DR: The laboratory has used reporter transgenic mice, selective hybridization techniques, and studies of cell signaling to show that a complex pattern of gene expression is reprogrammed as the decision is made to become either a Th1 or Th2 cell.