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Article

Embryonic arrest at midgestation and disruption of Notch signaling produced by the absence of both epsin 1 and epsin 2 in mice.

Proceedings of the National Academy of Sciences of the United States of America - 18 Aug 2009

Chen Hong, Ko Genevieve, Zatti Alessandra, Di Giacomo Giuseppina, Liu Lijuan, Raiteri Elisabetta, Perucco Ezio, Collesi Chiara, Min Wang, Zeiss Caroline, De Camilli Pietro, Cremona Ottavio

Abstract excerpt

Epsins are endocytic adaptors with putative functions in general aspects of clathrin-mediated endocytosis as well as in the internalization of specific membrane proteins. We have now tested the role of the ubiquitously expressed epsin genes, Epn1 and Epn2, by a genetic approach in mice. While either gene is dispensable for life, their combined inactivation results in embryonic lethality at E9.5-E10, i.e., at the...

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Share to Adaptor Proteins, Vesicular Transport
Share to Clathrin

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Endocytosis

Share to Fibroblasts

Share to Gene Expression Regulation, Developmental

Share to Mice, Knockout

Share to Receptors, Notch

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Identifiers

PMID: 19666558
DOI: 10.1073/pnas.0907008106
PMCID: PMC2728981

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