R
Richard A. Flavell
Researcher at Yale University
Publications - 1389
Citations - 223064
Richard A. Flavell is an academic researcher from Yale University. The author has contributed to research in topics: Immune system & T cell. The author has an hindex of 231, co-authored 1328 publications receiving 205119 citations. Previous affiliations of Richard A. Flavell include National Institute for Medical Research & University of Michigan.
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Journal ArticleDOI
JNK and PTEN cooperatively control the development of invasive adenocarcinoma of the prostate
Anette Hübner,David J. Mulholland,Claire L. Standen,Maria Karasarides,Julie Cavanagh-Kyros,Tamera Barrett,Hongbo Chi,Dale L. Greiner,Cathy Tournier,Charles L. Sawyers,Richard A. Flavell,Hong Wu,Roger J. Davis +12 more
TL;DR: It is demonstrated that the JNK and PTEN signaling pathways can cooperate to regulate the progression of prostate neoplasia to invasive adenocarcinoma.
Journal ArticleDOI
JNK Regulates Autocrine Expression of TGF-β1
TL;DR: Together, these data demonstrate that the JNK pathway may contribute to the regulation of autocrine TGF-β1-mediated biological responses in vivo and represents an unexpected form of cross-talk between two important signaling pathways.
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c-Jun NH2-Terminal Kinase 1 Plays a Critical Role in Intestinal Homeostasis and Tumor Suppression
Chang Tong,Zhinan Yin,Zibo Song,Ashley Dockendorff,Chuanshu Huang,John M. Mariadason,Richard A. Flavell,Roger J. Davis,Leonard H. Augenlicht,Wancai Yang +9 more
TL;DR: JNK1 plays a critical role in the regulation of homeostasis and in the suppression of tumor formation in the intestine, which was linked to the altered expression of p21(WAF1/cip1).
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The glycosyl phosphatidylinositol anchor is critical for Ly-6A/E-mediated T cell activation.
TL;DR: It is demonstrated that the GPI-anchor is critical to Ly-6A/E-mediated T cell activation, and the transmembrane anchored Ly- 6EDb antigen was unable to mediate T cellactivation.
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An intrinsic mechanism predisposes Foxp3-expressing regulatory T cells to Th2 conversion in vivo.
TL;DR: An intrinsic mechanism that imposes a Th2/Th1 imbalance and predisposes Foxp3-expressing cells to IL-4 production independent of STAT-6 signaling is identified.