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Mohamed Rahmani

Researcher at University of Sharjah

Publications -  84
Citations -  11459

Mohamed Rahmani is an academic researcher from University of Sharjah. The author has contributed to research in topics: Apoptosis & Protein kinase B. The author has an hindex of 45, co-authored 81 publications receiving 10595 citations. Previous affiliations of Mohamed Rahmani include Khalifa University & VCU Medical Center.

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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.
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The proteasome inhibitor bortezomib interacts synergistically with histone deacetylase inhibitors to induce apoptosis in Bcr/Abl+ cells sensitive and resistant to STI571.

Chunrong Yu, +5 more
- 15 Nov 2003 - 
TL;DR: Findings raise the possibility that combined proteasome/histone deacetylase inhibition may represent a novel strategy in leukemia, including apoptosis-resistant Bcr/Abl+ hematologic malignancies.
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Apoptosis Induced by the Kinase Inhibitor BAY 43-9006 in Human Leukemia Cells Involves Down-regulation of Mcl-1 through Inhibition of Translation

Mohamed Rahmani, +4 more
- 21 Oct 2005 - 
TL;DR: It is demonstrated that BAY 43-9006 mediates cell death in human leukemia cells, at least in part, through down-regulation of Mcl-1 via inhibition of translation.
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A selective sphingosine kinase 1 inhibitor integrates multiple molecular therapeutic targets in human leukemia

Steven W. Paugh, +10 more
- 15 Aug 2008 - 
TL;DR: SK1-I potently induced apoptosis in leukemic blasts isolated from patients with acute myelogenous leukemia but was relatively sparing of normal peripheral blood mononuclear leukocytes, and markedly reduced growth of AML xenograft tumors.
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A Bcr/Abl-independent, Lyn-dependent Form of Imatinib Mesylate (STI-571) Resistance Is Associated with Altered Expression of Bcl-2

Yun Dai, +4 more
- 13 Aug 2004 - 
TL;DR: Findings indicate that activation of Lyn in leukemia cells displaying a Bcr/Abl-independent form of imatinib mesylate resistance plays a functional role in Bcl-2 up-regulation and provide a theoretical basis for the development of therapeutic strategies targeting B cl-2 in such a setting.