Y
Yinon Ben-Neriah
Researcher at Hebrew University of Jerusalem
Publications - 139
Citations - 21396
Yinon Ben-Neriah is an academic researcher from Hebrew University of Jerusalem. The author has contributed to research in topics: Ubiquitin & Cancer. The author has an hindex of 58, co-authored 138 publications receiving 20011 citations. Previous affiliations of Yinon Ben-Neriah include Technion – Israel Institute of Technology & AMIT.
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Journal ArticleDOI
Phosphorylation meets ubiquitination: the control of NF-[kappa]B activity.
Michael Karin,Yinon Ben-Neriah +1 more
TL;DR: Recent progress has been made in understanding the details of the signaling pathways that regulate NF-kappaB activity, particularly those responding to the proinflammatory cytokines tumor necrosis factor-alpha and interleukin-1.
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NF-κB functions as a tumour promoter in inflammation-associated cancer
Eli Pikarsky,Rinnat M. Porat,Ilan Stein,Rinat Abramovitch,Sharon Amit,Shafika Kasem,Elena Gutkovich-Pyest,Simcha Urieli-Shoval,Eithan Galun,Yinon Ben-Neriah +9 more
TL;DR: It is shown that the inflammatory process triggers hepatocyte NF-κB through upregulation of tumour-necrosis factor-α (TNFα) in adjacent endothelial and inflammatory cells, and is therefore a potential target for cancer prevention in chronic inflammatory diseases.
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Inflammation meets cancer, with NF-κB as the matchmaker
Yinon Ben-Neriah,Michael Karin +1 more
TL;DR: Although it seems to fulfill a distinctly tumor-promoting role in many types of cancer, NF-κB has a confounding role in certain tumors.
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Rapid proteolysis of I kappa B-alpha is necessary for activation of transcription factor NF-kappa B.
Thomas Henkel,Thomas Machleidt,Irit Alkalay,Martin Krönke,Yinon Ben-Neriah,Patrick A. Baeuerle +5 more
TL;DR: It is reported that IκB-α (formerly MAD-3)11 is degraded in cells after stimulation with phorbol ester, interleukin-1, lipopolysaccharide and tumour necrosis factor-α, an event coincident with the appearance of active NF-κB.
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The chronic myelogenous leukemia-specific P210 protein is the product of the bcr/abl hybrid gene.
TL;DR: By analogy to the gag/abl fusion protein of Abelson murine leukemia virus, the replacement of amino terminal c-abl sequences by bcr sequences in P210 may create a transforming protein involved in CML.