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dc.contributor.authorPaterson, H
dc.date.accessioned2018-06-05T10:42:06Z
dc.date.issued2001-04
dc.identifierhttp://jcs.biologists.org/cgi/reprint/114/7/1357
dc.identifier.citationJOURNAL OF CELL SCIENCE, 2001, 114 (7), pp. 1357 - 1366
dc.identifier.issn0021-9533
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/1709
dc.description.abstractAnalysis of R-Ras signalling pathways. R-Ras has a high degree of sequence homology to Ras and to other members of the Ras subfamily including Rap, TC21 and ill- Ras. Activated versions of Ras and TC21 are highly transforming in a variety of cell lines and mutated forms of both proteins have been found in human tumours, R-Ras interacts with many of the same proteins as Res and TC21, including c-Raf1, and call induce transformed foci, although this activity is weak compared to Ras and appears to be cell-type specific, Here, we have investigated R-Ras signalling pathways in a variety of cell types, We find that microinjection of activated R-Ras into quiescent fibroblasts stimulates cell cycle progression through G(1) phase and subsequent DNA synthesis. However, unlike Bas, R-Ras does not activate the ERK MAP kinase pathway nor does it activate the JNK or p38/Mpk2 MAP kinase pathways. microinjection of R-Ras into PC12 cells does not induce terminal differentiation, but instead causes extensive cell spreading, consistent with R-Ras having a role in integrin activation. Finally, in a macrophage cell line, R-Ras activates the alphaM beta (2) integrin ria the small GTPase Rapt, leading to phagocytosis of opsonized red blood cells, whereas Ras does not, These results indicate that R-Ras has an important role in the regulation of cell growth and adhesion, but that this is mediated through downstream signals distinct from those used by Ras.
dc.format.extent1357 - 1366
dc.subjectR-Ras; DNA synthesis; ERK MAP kinase; integrin NUCLEOTIDE DISSOCIATION STIMULATOR; GTPASE-ACTIVATING PROTEIN; H-RAS; PHOSPHATIDYLINOSITOL 3-KINASE; MONOCLONAL-ANTIBODIES; INTEGRIN ACTIVATION; REGULATED KINASE; PLASMA-MEMBRANE; CDC42 GTPASES; GROWTH-FACTOR
dc.titleAnalysis of R-Ras signalling pathways
dc.typeJournal Article
rioxxterms.licenseref.startdate2001-04en_US
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfJOURNAL OF CELL SCIENCE
pubs.issue7
pubs.notesNot known
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology/Oncogene
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology/Oncogene
pubs.volume114en_US
pubs.embargo.termsNot known
icr.researchteamOncogeneen_US
dc.contributor.icrauthorPaterson, Hughen


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