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Kun Jiang

Researcher at University of South Florida

Publications -  51
Citations -  1944

Kun Jiang is an academic researcher from University of South Florida. The author has contributed to research in topics: Pancreatic cancer & Medicine. The author has an hindex of 15, co-authored 47 publications receiving 1746 citations. Previous affiliations of Kun Jiang include Los Alamos National Laboratory & Emory University.

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Pivotal role of phosphoinositide-3 kinase in regulation of cytotoxicity in natural killer cells.

TL;DR: It is shown that inhibition of phosphoinositide-3 kinase (PI3K) in NK cells blocks p21-activated kinase 1 (PAK1), MAPK Kinase (MEK) and ERK activation by target cell ligation, interferes with perforin and granzyme B movement toward target cells and suppresses NK cytotoxicity.
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The phosphoinositide 3-OH kinase/AKT2 pathway as a critical target for farnesyltransferase inhibitor-induced apoptosis

TL;DR: It is demonstrated that FTI-277 inhibits phosphatidylinositol 3-OH kinase (PI 3-kinase)/AKT2-mediated growth factor- and adhesion-dependent survival pathways and induces apoptosis in human cancer cells that overexpress AKT2.
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Cooperative regulation of Mcl-1 by Janus kinase/stat and phosphatidylinositol 3-kinase contribute to granulocyte-macrophage colony-stimulating factor-delayed apoptosis in human neutrophils

TL;DR: It is found that suboptimal doses of AG-490 and wortmannin had an additive effect on delayed apoptosis and Mcl-1 expression, which suggests that cooperative regulation of M cl-1 by the Janus kinase/STAT and PI 3-kinase pathways contribute to GM-CSF-delayed apoptosis.
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Akt Mediates Ras Downregulation of RhoB, a Suppressor of Transformation, Invasion, and Metastasis

TL;DR: In this article, the authors demonstrate that Ras downregulates RhoB expression by a phosphatidylinositol 3-kinase (PI3K)- and Akt- but not Mek-dependent mechanism.
Journal Article

A View to a Kill: Signals Triggering Cytotoxicity

TL;DR: A view to a kill is provided, bringing together a unifying concept for a common signal pathway that dictates lytic function through a specific Syk/Zap70 --> PI3K --> Rac --> PAK --> MEK --> ERK signal cascade triggered by target cell recognition.