scispace - formally typeset
J

John H. Kehrl

Researcher at National Institutes of Health

Publications -  228
Citations -  36680

John H. Kehrl is an academic researcher from National Institutes of Health. The author has contributed to research in topics: B cell & RGS Proteins. The author has an hindex of 83, co-authored 225 publications receiving 32876 citations. Previous affiliations of John H. Kehrl include Washington University in St. Louis.

Papers
More filters
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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.
Journal ArticleDOI

Transforming growth factor type beta: rapid induction of fibrosis and angiogenesis in vivo and stimulation of collagen formation in vitro.

TL;DR: Further data are obtained to support a role for TGF-beta as an intrinsic mediator of collagen formation: conditioned media obtained from activated human tonsillar T lymphocytes contain greatly elevated levels of T GF-beta compared tomedia obtained from unactivated lymphocytes.
Journal ArticleDOI

Production of transforming growth factor beta by human T lymphocytes and its potential role in the regulation of T cell growth.

TL;DR: TGF-beta may be an important antigen-nonspecific regulator of human T cell proliferation, and important in T cell interaction with other cell types whose cellular functions are modulated by TGF- beta.
Journal ArticleDOI

Activation of Autophagy by Inflammatory Signals Limits IL-1β Production by Targeting Ubiquitinated Inflammasomes for Destruction

TL;DR: It is shown that the induction of AIM2 or NLRP3 inflammasomes in macrophages triggered activation of the G protein RalB and autophagosome formation, which indicates that autophagy accompaniesinflammasome activation to temper inflammation by eliminating active inflammaomes.