J
Jin-Chen Yu
Researcher at National Institutes of Health
Publications - 15
Citations - 2579
Jin-Chen Yu is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Platelet-derived growth factor receptor & Growth factor receptor. The author has an hindex of 13, co-authored 15 publications receiving 2542 citations.
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Journal ArticleDOI
The small GTP-binding proteins Rac1 and Cdc42regulate the activity of the JNK/SAPK signaling pathway
Omar A. Coso,Mario Chiariello,Jin-Chen Yu,Hidemi Teramoto,Piero Crespo,Ningzhi Xu,Toru Miki,J. Silvio Gutkind +7 more
TL;DR: It is shown that in COS-7 cells, activated Ras effectively stimulates MAPK but poorly induces JNK activity, which strongly support a critical role for Rac1 and Cdc42 in controlling the JNK signaling pathway.
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An insert of seven amino acids confers functional differences between smooth muscle myosins from the intestines and vasculature.
TL;DR: It is found that intestinal, but not vascular, MHC mRNA contains an insert of 21 nucleotides, encoding 7 amino acids, in a region near the ATP binding site in the myosin head, suggesting that the 7-amino acid MHC insert is responsible for the different enzymatic activities of vascular and intestinal myosins.
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Tyrosine mutations within the alpha platelet-derived growth factor receptor kinase insert domain abrogate receptor-associated phosphatidylinositol-3 kinase activity without affecting mitogenic or chemotactic signal transduction.
Jin-Chen Yu,M. A. Heidaran,J. H. Pierce,J. S. Gutkind,D. Lombardi,Marco Ruggiero,Stuart A. Aaronson +6 more
TL;DR: It is concluded that alpha PDGF receptor-associated PI-3 kinase activity is not required for either of these major PDGF signalling functions.
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Role of alpha beta receptor heterodimer formation in beta platelet-derived growth factor (PDGF) receptor activation by PDGF-AB.
M. A. Heidaran,Jacalyn H. Pierce,Jin-Chen Yu,D. Lombardi,Artrip J,Timothy P. Fleming,A. Thomason,Stuart A. Aaronson +7 more
TL;DR: Findings argue that initial PDGF-AB interaction with the alpha PDGFR induces conformational changes in the ligand or receptor that facilitates efficient recruitment of betaPDGFR by this PDGF isoform.
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Characterization of a Protein Kinase C-δ (PKC-δ) ATP Binding Mutant AN INACTIVE ENZYME THAT COMPETITIVELY INHIBITS WILD TYPE PKC-δ ENZYMATIC ACTIVITY
TL;DR: Exposure of PKC-δWT transfectants to TPA induced 32D monocytic differentiation, the 32D/PKC- δK376R transfectantes were resistant to Tpa-induced differentiation, suggesting that expression of active PKC -δ is required to mediate 32DMonocytic differentiated differentiation in response to T PA stimulation.