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Gary L. Firestone

Researcher at University of California, Berkeley

Publications -  157
Citations -  12851

Gary L. Firestone is an academic researcher from University of California, Berkeley. The author has contributed to research in topics: Glycoprotein & Glucocorticoid. The author has an hindex of 59, co-authored 157 publications receiving 12311 citations. Previous affiliations of Gary L. Firestone include University of California, San Francisco.

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Epithelial sodium channel regulated by aldosterone-induced protein sgk.

TL;DR: Sgk (serum and glucocorticoid-regulated kinase), a member of the serine-threonine kinase family, is identified as an aldosterone-induced regulator of ENaC activity, suggesting that sgk plays a central role in ald testosterone regulation of Na+ absorption and thus in the control of extracellular fluid volume, blood pressure, and sodium homeostasis.
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Sequence-specific binding of glucocorticoid receptor to MTV DNA at sites within and upstream of the transcribed region.

TL;DR: Five regions of MTV DNA that are bound specifically by purified receptor are mapped and compared, suggesting that receptor affinity for upstream and internal regions may differ by less than one order of magnitude.
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Characterization of sgk, a novel member of the serine/threonine protein kinase gene family which is transcriptionally induced by glucocorticoids and serum.

TL;DR: This is the first report of a presumed serine/threonine protein kinase that is highly regulated at the transcriptional level by glucocorticoid hormones and suggests a novel interplay between glucoc Corticoid receptor signalling and aprotein kinase of the second messenger family.
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Serum and glucocorticoid-inducible kinase (SGK) is a target of the PI 3-kinase-stimulated signaling pathway

TL;DR: Evidence is presented that SGK is a component of the phosphoinositide 3 (PI 3)‐kinase signaling pathway and that hyperphosphorylation of endogenous SGK, and promoted translocation to the nucleus could be inhibited by wortmannin, but not by rapamycin.
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Estrogen Receptor β Inhibits Human Breast Cancer Cell Proliferation and Tumor Formation by Causing a G2 Cell Cycle Arrest

TL;DR: It is demonstrated that ERβ-selective estrogens may lack breast cancer promoting properties exhibited by estrogens in hormone replacement regimens and may be useful for chemoprevention of breast cancer.