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Igor B. Roninson

Researcher at University of South Carolina

Publications -  197
Citations -  26213

Igor B. Roninson is an academic researcher from University of South Carolina. The author has contributed to research in topics: Gene & Multiple drug resistance. The author has an hindex of 71, co-authored 186 publications receiving 24450 citations. Previous affiliations of Igor B. Roninson include Russian Academy of Sciences & University of Illinois at Chicago.

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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.
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Internal duplication and homology with bacterial transport proteins in the mdr1 (P-glycoprotein) gene from multidrug-resistant human cells

TL;DR: Results are consistent with a function for P-glycoprotein as an energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells.
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Expression and activity of P-glycoprotein, a multidrug efflux pump, in human hematopoietic stem cells

TL;DR: Staining of human bone marrow cells with fluorescent dyes is potentiated by P-gp inhibitors and inversely correlated with P- gp expression, finding implications for stem cell purification and bone marrow resistance to cancer chemotherapy.
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Growth retardation and increased apoptosis in mice with homozygous disruption of the akt1 gene

TL;DR: The disruption of the most ubiquitously expressed member of the akt family of genes, akt1, in the mouse is reported, resulting in viable but smaller mice and mice that are more susceptible to apoptosis induced by TNF, anti-Fas, UV irradiation, and serum withdrawal.
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If not apoptosis, then what? Treatment-induced senescence and mitotic catastrophe in tumor cells.

TL;DR: The senescent phenotype distinguishes tumor cells that survived drug exposure but lost the ability to form colonies from those that recover and proliferate after treatment, and should assist in improving the efficacy and decreasing side effects of cancer therapy.