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Ratna K. Vadlamudi

Researcher at University of Texas at Austin

Publications -  240
Citations -  13012

Ratna K. Vadlamudi is an academic researcher from University of Texas at Austin. The author has contributed to research in topics: Estrogen receptor & Cancer. The author has an hindex of 60, co-authored 195 publications receiving 11457 citations. Previous affiliations of Ratna K. Vadlamudi include University of Texas System & University of Texas at San Antonio.

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Transcriptional repression of oestrogen receptor by metastasis-associated protein 1 corepressor

TL;DR: Results identify ER-mediated transcription as a nuclear target of MTA1 and indicate that HDAC complexes associated with the MTA1 corepressor may mediate ER transcriptional repression by HRG.
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Cloning and Expression of a Receptor for an Insecticidal Toxin of Bacillus thuringiensis

TL;DR: Cl cloning and expression of a cDNA that encodes a receptor (BT-R1) of the tobacco hornworm Manduca sexta for an insecticidal toxin of B. thuringiensis subsp.
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Filamin is essential in actin cytoskeletal assembly mediated by p21-activated kinase 1

TL;DR: The results indicate that FLNa may be essential for Pak1-induced cytoskeletal reorganization and that the two-way regulatory interaction between Pak1 and FLNa might contribute to the local stimulation of Pak1 activity and its targets in cytoskeleton structures.
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p62, a Phosphotyrosine-independent Ligand of the SH2 Domain of p56lck, Belongs to a New Class of Ubiquitin-binding Proteins

TL;DR: Results suggest that p 62 belongs to a new class of ubiquitin-binding proteins and that p62 affects signal transduction at least partly through ubiquitination-mediated protein degradation.
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Heregulin regulates cytoskeletal reorganization and cell migration through the p21-activated kinase-1 via phosphatidylinositol-3 kinase.

TL;DR: A role of PI-3 kinase/PAK1-dependent reorganization of the cortical actin cytoskeleton in HRG-mediated increased cell migration is suggested, and these changes may have significant consequences leading to enhanced invasion by breast cancer cells.