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Carl G. Maki

Researcher at Rush University Medical Center

Publications -  69
Citations -  8653

Carl G. Maki is an academic researcher from Rush University Medical Center. The author has contributed to research in topics: Cell cycle & Cancer cell. The author has an hindex of 28, co-authored 61 publications receiving 8022 citations. Previous affiliations of Carl G. Maki include Stanford University & University of Chicago.

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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 Article

In Vivo Ubiquitination and Proteasome-mediated Degradation of p53

TL;DR: In this study, inhibitors of the 26S proteasome have been used to further explore the role of ubiquitin proteolysis in regulating p53 turnover and indicate that ubiquitIn-p53 conjugates were detected in untreated as well as gamma-irradiated cells, indicating that Ubiquitin-dependent proteolytic plays a role in the normal turnover of p53.
Journal ArticleDOI

The MDM2 RING-finger domain is required to promote p53 nuclear export

TL;DR: The results indicate that MDM2-mediated ubiquitination, or other activities associated with the RING-finger domain, can stimulate the export of p53 to the cytoplasm through the activity of the p53 NES.
Journal ArticleDOI

Ubiquitination of p53 and p21 is differentially affected by ionizing and UV radiation.

TL;DR: It is demonstrated that UV and gamma radiation have different effects on ubiquitinated p53 and suggested that the UV-induced stabilization of p53 results from a loss of p 53 ubiquitination, and that the radiation effects on p53 are specific.
Journal Article

Hypoxia Induces p53 Accumulation through MDM2 Down-Regulation and Inhibition of E6-mediated Degradation

TL;DR: Results suggest that the hypoxic induction of p53 is attributable to the down-regulation of MDM2 protein levels and uncoupling of p 53 from its interaction with the E6/E6AP complex.