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Kim A. Heidenreich

Researcher at Anschutz Medical Campus

Publications -  56
Citations -  11783

Kim A. Heidenreich is an academic researcher from Anschutz Medical Campus. The author has contributed to research in topics: Insulin receptor & Insulin. The author has an hindex of 36, co-authored 56 publications receiving 10666 citations. Previous affiliations of Kim A. Heidenreich include University of Colorado Denver & University of California, San Diego.

Papers
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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes

Daniel J. Klionsky, +235 more
- 16 Feb 2008 - 
TL;DR: A set of guidelines for the selection and interpretation of the methods that can be used by investigators who are attempting to examine macroautophagy and related processes, as well as by reviewers who need to provide realistic and reasonable critiques of papers that investigate these processes are presented.
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Akt/protein kinase B up-regulates Bcl-2 expression through cAMP-response element-binding protein.

Subbiah Pugazhenthi, +8 more
- 14 Apr 2000 - 
TL;DR: Data indicate that regulation of Bcl-2 expression by IGF-I involves a signaling cascade mediated by PI 3-kinase/PDK1/Akt/CREB, and the observation that enhanced CREB activity by Akt signaling leads to increased B cl-2 promoter activity and cell survival.
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Apoptosis Induced by Withdrawal of Trophic Factors Is Mediated by p38 Mitogen-activated Protein Kinase

Jennifer L. Kummer, +2 more
- 15 Aug 1997 - 
TL;DR: The hypothesis that insulin promotes cell survival, at least in part, by inhibiting the p38 pathway is supported, and the role of p38 in cellular apoptosis is supported.
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FoxO1 regulates multiple metabolic pathways in the liver: effects on gluconeogenic, glycolytic, and lipogenic gene expression

Wenwei Zhang, +26 more
- 14 Apr 2006 - 
TL;DR: Results indicate that FoxO proteins promote hepatic glucose production through multiple mechanisms and contribute to the regulation of other metabolic pathways important in the adaptation to fasting and feeding in the liver, including glycolysis, the pentose phosphate shunt, and lipogenic and sterol synthetic pathways.