K
Kavita Shah
Researcher at Purdue University
Publications - 111
Citations - 7332
Kavita Shah is an academic researcher from Purdue University. The author has contributed to research in topics: Kinase & Neurodegeneration. The author has an hindex of 46, co-authored 107 publications receiving 6741 citations. Previous affiliations of Kavita Shah include University of California, San Francisco & Novartis Foundation.
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Journal ArticleDOI
Novel Genetic Tools Reveal Cdk5's Major Role in Golgi Fragmentation in Alzheimer's Disease
Kai-Hui Sun,Yolanda de Pablo,Fabien Vincent,Emmanuel O. Johnson,Angela K. Chavers,Kavita Shah +5 more
TL;DR: A major role of Cdk5 in Golgi fragmentation upon beta-amyloid and glutamate stimulation in differentiated neuronal cells and primary neurons was revealed and a crucial role ofCdk5 was further confirmed when Cdk4 activation alone resulted in robust Golgi disassembly.
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Novel bis(indolyl)hydrazide-hydrazones as potent cytotoxic agents.
TL;DR: A series of bis(indolyl) hydrazide-hydrazones 5a-n were synthesized and evaluated for their cytotoxicity against selected human cancer cell lines and the compound 5b with N-(p-chlorobenzyl) and bromo substituents was found to be the most potent against multiple cancer cell Lines.
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The Conserved NDR Kinase Orb6 Controls Polarized Cell Growth by Spatial Regulation of the Small GTPase Cdc42
TL;DR: It is shown that the fission yeast NDR homolog, Orb6 kinase, maintains polarized cell growth at the cell tips by spatially regulating the localization of Cdc42 GTPase, a key morphology regulator.
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c-Abl phosphorylates Dok1 to promote filopodia during cell spreading
Pamela J. Woodring,Jill Meisenhelder,Sam A. Johnson,Guo-Lei Zhou,Jeffrey Field,Kavita Shah,Friedhelm Bladt,Tony Pawson,Masaru Niki,Pier Paolo Pandolfi,Jean Y. J. Wang,Tony Hunter +11 more
TL;DR: The data suggest a novel pathway by which c-Abl transduces signals to the actin cytoskeleton through phosphorylating Dok1 Y361 and recruiting Nck, indicating that they function in the same signaling pathway.
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Deregulated Cdk5 triggers aberrant activation of cell cycle kinases and phosphatases inducing neuronal death
TL;DR: Inhibition of Cdk5 confers the highest neuroprotection against A&bgr;1-42 toxicity, whereas inhibition of Cdc25 isoforms was partially neuroprotective, further emphasizing a decisive role of C DK5 deregulation in cell-cycle-driven AD neuronal death.