scispace - formally typeset
S

Srinivasa Subramaniam

Researcher at Scripps Research Institute

Publications -  56
Citations -  7720

Srinivasa Subramaniam is an academic researcher from Scripps Research Institute. The author has contributed to research in topics: Huntingtin & PI3K/AKT/mTOR pathway. The author has an hindex of 27, co-authored 51 publications receiving 6984 citations. Previous affiliations of Srinivasa Subramaniam include Johns Hopkins University & Johns Hopkins University School of Medicine.

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

Rhes, a striatal specific protein, mediates mutant-huntingtin cytotoxicity.

TL;DR: The small guanine nucleotide–binding protein Rhes, which is localized very selectively to the striatum, binds physiologically to mHtt, and Rhes-mHtt interactions can account for the localized neuropathology of HD.
Journal ArticleDOI

ERK and cell death: ERK1/2 in neuronal death.

TL;DR: Recent evidence for a role of ERK1/2 in neuronal death is summarized and the mechanisms involved in ERK 1/2 mediating neuronal death are discussed.
Journal ArticleDOI

ERK activation promotes neuronal degeneration predominantly through plasma membrane damage and independently of caspase-3.

TL;DR: The data identify ERK as an important executor of neuronal damage involving a caspase-3–independent mechanism, allowing the distinction between plasma membrane (PM)–, DNA-, and PM/DNA-damaged populations.
Journal ArticleDOI

Growth differentiation factor-15 prevents low potassium-induced cell death of cerebellar granule neurons by differential regulation of Akt and ERK pathways.

TL;DR: The data suggest that GDF-15 prevents apoptosis in CGN by activating Akt and inhibiting endogenously active ERK, and it is shown that G DF-15 prevented generation of reactive oxygen species, a known activator of ERK.