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Rati Fotedar

Researcher at Sanford-Burnham Institute for Medical Research

Publications -  39
Citations -  6601

Rati Fotedar is an academic researcher from Sanford-Burnham Institute for Medical Research. The author has contributed to research in topics: Cell cycle & DNA damage. The author has an hindex of 24, co-authored 39 publications receiving 5640 citations. Previous affiliations of Rati Fotedar include Discovery Institute & La Jolla Institute for Allergy and Immunology.

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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.
Book ChapterDOI

Cell cycle control of DNA replication

TL;DR: The association of PCNA, a replication protein, with cdk-cyclins during G-1 to S phase transition and with cdK-cyclin inhibitors, adds an interesting complexity to regulation of DNA replication.
Journal ArticleDOI

UV Irradiation Triggers Ubiquitin-Dependent Degradation of p21WAF1 to Promote DNA Repair

TL;DR: It is shown that p21protein is degraded after irradiation of a variety of cell types with low but not high doses of UV, providing novel insight into regulation of p21 protein and its role in the cellular response to DNA damage.
Journal ArticleDOI

Regulation of p21WAF1/CIP1 Stability by WISp39, a Hsp90 Binding TPR Protein

TL;DR: The results demonstrate the importance of posttranslational stabilization of p21 protein by WISp39 in regulating cellular p21 activity and suggest that WIS p39 recruits Hsp90 to regulate p21protein stability.
Journal ArticleDOI

Cell cycle regulated phosphorylation of RPA-32 occurs within the replication initiation complex.

TL;DR: The cell cycle‐dependent phosphorylation of RPA‐32 may be regulated by its binding to single‐stranded origin DNA during replication initiation, specifically within the replication initiation complex.