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dc.contributor.authorHervieu, A
dc.contributor.authorKermorgant, S
dc.date.accessioned2021-04-09T15:32:36Z
dc.date.available2021-04-09T15:32:36Z
dc.date.issued2020-08-18
dc.identifier.issn2372-3556
dc.identifier.urihttps://qmro.qmul.ac.uk/xmlui/handle/123456789/71155
dc.description.abstractWe reported that RAC1 is a master regulator of cell migration and anchorage-independent growth, downstream of the oncogenic Receptor Tyrosine Kinase (RTK) MET. RAC1 growth-promoting role is guanosine triphosphatase (GTPase)- and phosphatidylinositol 3-kinase (PI3K)-independent but promotes mammalian target of rapamycin (mTOR) signaling through triggering its plasma membrane localization.en_US
dc.format.extent1803029 - ?
dc.languageeng
dc.relation.ispartofMol Cell Oncol
dc.subjectMETen_US
dc.subjectPI3Ken_US
dc.subjectRAC1en_US
dc.subjectmTORen_US
dc.titleUnconventional role of RAC1 in MET-driven anchorage-independent tumor growth.en_US
dc.typeArticleen_US
dc.identifier.doi10.1080/23723556.2020.1803029
pubs.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/33235904en_US
pubs.issue6en_US
pubs.notesNot knownen_US
pubs.publication-statusPublished onlineen_US
pubs.volume7en_US
qmul.funderUnravelling c-Met signalling from autophagic endomembranes::Medical Research Councilen_US


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