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Kotb Abdelmohsen

Researcher at National Institutes of Health

Publications -  163
Citations -  21231

Kotb Abdelmohsen is an academic researcher from National Institutes of Health. The author has contributed to research in topics: RNA-binding protein & Gene silencing. The author has an hindex of 63, co-authored 145 publications receiving 17825 citations. Previous affiliations of Kotb Abdelmohsen include Catalan Institution for Research and Advanced Studies & University of Maryland, Baltimore.

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Journal ArticleDOI

LncRNA OIP5-AS1/cyrano suppresses GAK expression to control mitosis

TL;DR: Findings indicate that the abnormal mitoses seen after silencing OIP5-AS1 were caused by an untimely rise in GAK levels and suggest that OIP4-AS2 suppresses cell proliferation at least in part by reducing GAK Levels.
Book ChapterDOI

Analysis of Circular RNAs Using the Web Tool CircInteractome.

TL;DR: A web tool is designed to explore potential interactions of circRNAs with RBPs, design specific divergent primers to detect circ RNAs, study tissue- and cell-specificcircRNAs, identify gene-specific circRNas, explore potential miRNAs interacting with circRNA, and design specific siRNAs to silence circRN as.
Journal ArticleDOI

Methods for analysis of circular RNAs.

TL;DR: The challenges of analyzing circRNAs are discussed, alternative approaches for studying this unique class of transcripts are proposed, and resources and molecular methods currently utilized to quantify circ RNAs are reviewed.
Journal ArticleDOI

Induction of VEGFA mRNA translation by CoCl2 mediated by HuR.

TL;DR: It is proposed that under hypoxia-like conditions, HuR enhances VEGFA mRNA translation, and exposure to CoCl2 increases the interaction of HuR with V EGFA mRNA and promoted the colocalization ofHuR and the distal part of the VEG FA 3′-untranslated region (UTR) in the cytoplasm.
Journal ArticleDOI

RNA binding protein HuR regulates the expression of ABCA1

TL;DR: HuR is identified as a novel posttranscriptional regulator of ABCA1 expression and cellular cholesterol homeostasis, thereby opening new avenues for increasing cholesterol efflux from atherosclerotic foam macrophages and raising circulating HDL cholesterol levels.