mTORC1 and mTORC2 Converge on the Arp2/3 Complex to Promote Kras

Autor:	Yamin, Zhao, Benjamin, Schoeps, Dianbo, Yao, Zhiheng, Zhang, Kathleen, Schuck, Vivien, Tissen, Carsten, Jäger, Anna Melissa, Schlitter, Rob, van der Kammen, Christina, Ludwig, Jan G, D'Haese, Susanne, Raulefs, Nadja, Maeritz, Shanshan, Shen, Xiaoping, Zou, Achim, Krüger, Jörg, Kleeff, Christoph W, Michalski, Helmut, Friess, Metello, Innocenti, Bo, Kong
Rok vydání:	2020
Předmět:	Mice Knockout Metaplasia Pancreatic Ducts Acinar Cells Mechanistic Target of Rapamycin Complex 2 Regulatory-Associated Protein of mTOR Mechanistic Target of Rapamycin Complex 1 Actin-Related Protein 2-3 Complex Gene Expression Regulation Neoplastic Mice Inbred C57BL Pancreatic Neoplasms Proto-Oncogene Proteins p21(ras) Disease Models Animal Cell Transformation Neoplastic Rapamycin-Insensitive Companion of mTOR Protein Mutation Animals Humans Carcinoma Pancreatic Ductal Signal Transduction
Zdroj:	Gastroenterology. 160(5)
ISSN:	1528-0012
Popis:	Oncogenic KrasA mouse model of inflammation-accelerated KrasWe found that mTORC1 and mTORC2 are markedly activated in human and mouse ADM lesions, and cooperate to promote KrasHere, we show that mTORC1 and mTORC2 attain a dual, yet nonredundant regulatory role in ADM and early pancreatic carcinogenesis by promoting Arp2/3 complex function. The role of Arp2/3 complex as a common effector of mTORC1 and mTORC2 fills the gap between oncogenic signals and actin dynamics underlying PDAC initiation.
Databáze:	OpenAIRE
Externí odkaz:	https://explore.openaire.eu/search/publication?articleId=pmid________::4560c9a27e846ea57221b61a92f95f35 https://pubmed.ncbi.nlm.nih.gov/33388318 Zobrazit plný text záznamu