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Manoj B. Menon

Researcher at Hannover Medical School

Publications -  50
Citations -  11108

Manoj B. Menon is an academic researcher from Hannover Medical School. The author has contributed to research in topics: Medicine & Protein kinase A. The author has an hindex of 22, co-authored 38 publications receiving 9485 citations. Previous affiliations of Manoj B. Menon include Tufts University.

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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

Beclin 1 Phosphorylation - at the Center of Autophagy Regulation.

TL;DR: Several pieces of evidence indicate that the phosphorylation and ubiquitination of BECN1 at an array of residues fine-tune the responses to diverse autophagy modulating stimuli and helps in maintaining the balance between pro-survivalautophagy and pro-apoptotic responses.
Journal ArticleDOI

MAPKAP kinases MK2 and MK3 in inflammation: complex regulation of TNF biosynthesis via expression and phosphorylation of tristetraprolin.

TL;DR: It is demonstrated that MK2/3 also contribute to the de novo synthesis of TTP, and a model is proposed, which demonstrates how this new function of transcriptional activation of T TP by MK 2/3 cooperates with the role of MK2 /3 in post-transcriptional gene expression to limit the inflammatory response.