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Jeffrey C. Rathmell

Researcher at Vanderbilt University Medical Center

Publications -  254
Citations -  35713

Jeffrey C. Rathmell is an academic researcher from Vanderbilt University Medical Center. The author has contributed to research in topics: T cell & Immune system. The author has an hindex of 76, co-authored 211 publications receiving 28092 citations. Previous affiliations of Jeffrey C. Rathmell include Durham University & University Hospital Regensburg.

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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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A guide to immunometabolism for immunologists

Luke A. J. O'Neill, +2 more
- 01 Sep 2016 - 
TL;DR: A brief refresher course on six of the major metabolic pathways involved in immunometabolism is provided, giving specific examples of how precise changes in the metabolites of these pathways shape the immune cell response.
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Cutting Edge: Distinct Glycolytic and Lipid Oxidative Metabolic Programs Are Essential for Effector and Regulatory CD4+ T Cell Subsets

Ryan D. Michalek, +8 more
- 15 Mar 2011 - 
TL;DR: Teff and Treg were selectively increased in Glut1 transgenic mice and reliant on glucose metabolism, whereas Treg had activated AMP-activated protein kinase and were dependent on lipid oxidation.
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The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues.

Tullia Lindsten, +20 more
- 01 Dec 2000 - 
TL;DR: Bax and Bak have overlapping roles in the regulation of apoptosis during mammalian development and tissue homeostasis and are found to be developmentally normal and reproductively fit.
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The CD28 signaling pathway regulates glucose metabolism.

Kenneth A. Frauwirth, +8 more
- 01 Jun 2002 - 
TL;DR: It is shown that CD28 costimulation functions to increase glycolytic flux, allowing T cells to anticipate energetic and biosynthetic needs associated with a sustained response.