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Inbal Simcha
Researcher at Weizmann Institute of Science
Publications - 13
Citations - 4175
Inbal Simcha is an academic researcher from Weizmann Institute of Science. The author has contributed to research in topics: Beta-catenin & Cadherin. The author has an hindex of 12, co-authored 13 publications receiving 4054 citations.
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Journal ArticleDOI
The cyclin D1 gene is a target of the beta-catenin/LEF-1 pathway
Michael Shtutman,Jacob Zhurinsky,Inbal Simcha,Chris Albanese,Mark D'Amico,Richard G. Pestell,Avri Ben-Ze'ev +6 more
TL;DR: Increased beta-catenin levels may promote neoplastic conversion by triggering cyclin D1 gene expression and, consequently, uncontrolled progression into the cell cycle through a LEF-1 binding site in the cyclinD1 promoter.
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Autoregulation of E-cadherin expression by cadherin–cadherin interactions: the roles of β-catenin signaling, Slug, and MAPK
Maralice Conacci-Sorrell,Inbal Simcha,Tamar Ben-Yedidia,Janna Blechman,Pierre Savagner,Avri Ben-Ze'ev +5 more
TL;DR: This autoregulation of E-cadherin by cell–cell adhesion involving Slug, β-catenin and ERK could be important in tumorigenesis.
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Differential Nuclear Translocation and Transactivation Potential of β-Catenin and Plakoglobin
Inbal Simcha,Michael Shtutman,Daniela Salomon,Jacob Zhurinsky,Einat Sadot,Benjamin Geiger,Avri Ben-Ze'ev +6 more
TL;DR: The results indicate that plakoglobin and β-catenin differ in their nuclear translocation and complexing with LEF-1 and vinculin, and LEF–1–dependent transactivation is preferentially driven by β- catenin; and the cytoplasmic partners of β-Catenin, cadherin and α-catanin, can sequester it to the cy toplasm and inhibit its transcriptional activity.
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Excess beta-catenin promotes accumulation of transcriptionally active p53.
Alexander Damalas,Avri Ben-Ze'ev,Inbal Simcha,Michael Shtutman,Juan Fernando Martinez Leal,Jacob Zhurinsky,Benjamin Geiger,Moshe Oren +7 more
TL;DR: It is reported here that overexpression of β‐catenin results in accumulation of p53, apparently through interference with its proteolytic degradation, and is accompanied by augmented transcriptional activity of p 53 in the affected cells.
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Inhibition of β-catenin-mediated transactivation by cadherin derivatives
TL;DR: Results indicate that β-catenin binding to the cadherin cytoplasmic tail either in the membrane, or in the nucleus, can inhibit β- catenin degradation and efficiently block its transactivation capacity.