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Ronit Sagi-Eisenberg

Researcher at Tel Aviv University

Publications -  69
Citations -  6937

Ronit Sagi-Eisenberg is an academic researcher from Tel Aviv University. The author has contributed to research in topics: Exocytosis & Mast cell. The author has an hindex of 23, co-authored 65 publications receiving 6247 citations.

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Basic secretagogues activate protein tyrosine phosphorylation and release of arachidonic acid in mast cells via a novel protein kinase C and phosphatidylinositol 3-kinase-dependent mechanism.

TL;DR: It is shown that compound 48/80 (c48/80), a synthetic member of the class of basic secretagogues, stimulates protein tyrosine phosphorylation of a number of as yet unidentified cellular substrates, suggesting that basic secretagogue induce protein tyrose phosphorylated as part of their parallel multiple signaling pathways which are presumably mediated by more than one G‐protein.
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Metabolic alterations in the tumor microenvironment and their role in oncogenesis.

TL;DR: The association between the reprogramming of glucose metabolism in the TME and oncogenic signaling and its reflection in the non-canonical functions of metabolic enzymes is discussed and special emphasis is given in this regard to lysophosphatidic acid (LPA) and adenosine, two powerful metabolites, the concentrations of which rise in theTME due to altered metabolism of the tumor and its surrounding cells.
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Mast Cells Are Directly Activated by Cancer Cell-Derived Extracellular Vesicles by a CD73- and Adenosine-Dependent Mechanism.

TL;DR: Exposure of MCs to EVs derived from pancreatic cancer cells or non–small cell lung carcinoma results in MC activation, evident by the increased phosphorylation of the ERK1/2 MAP kinases, and activation by EVs upregulates expression of angiogenic and tissue remodeling genes.
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Down-regulation of the A3 adenosine receptor in human mast cells upregulates mediators of angiogenesis and remodeling.

TL;DR: The human mast cell A3R is identified as regulator of tissue remodeling gene expression in human mast cells and a heretofore-unrecognized mode of feedback regulation that is exerted by this receptor is demonstrated.
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Anaphylactic Degranulation of Mast Cells: Focus on Compound Exocytosis

TL;DR: The possible reasons for the mast cell to utilize compound exocytosis during anaphylaxis, the conflicting evidence in different mast cell models, and the open questions in the field which remain to be answered are discussed.