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dc.contributor.authorCorallino, S
dc.contributor.authorIwai, LK
dc.contributor.authorPayne, LS
dc.contributor.authorHuang, PH
dc.contributor.authorSacco, F
dc.contributor.authorCesareni, G
dc.contributor.authorCastagnoli, L
dc.date.accessioned2018-07-19T11:35:53Z
dc.date.issued2016-09
dc.identifier.citationNew biotechnology, 2016, 33 (5 Pt A), pp. 524 - 536
dc.identifier.issn1871-6784
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/2096
dc.identifier.eissn1876-4347en_US
dc.identifier.doi10.1016/j.nbt.2015.08.002en_US
dc.description.abstractThe phosphatase SHP-2 plays an essential role in growth factor signaling and mutations in its locus is the cause of congenital and acquired pathologies. Mutations of SHP-2 are known to affect the activation of the RAS pathway. Gain-of-function mutations cause the Noonan syndrome, the most common non-chromosomal congenital disorder. In order to obtain a holistic picture of the intricate regulatory mechanisms underlying SHP-2 physiology and pathology, we set out to characterize perturbations of the cell phosphorylation profile caused by an altered localization of SHP-2. To describe the proteins whose activity may be directly or indirectly modulated by SHP-2 activity, we identified tyrosine peptides that are differentially phosphorylated in wild type SHP-2 cells and isogenic cells expressing a non-functional SHP-2 variant that cannot dephosphorylate the physiological substrates due to a defect in cellular localization upon growth factor stimulation. By an iTRAQ based strategy coupled to mass spectrometry, we have identified 63 phosphorylated tyrosine residues in 53 different proteins whose phosphorylation is affected by SHP-2 activity. Some of these confirm already established regulatory mechanisms while many others suggest new possible signaling routes that may contribute to the modulation of the ERK and p38 pathways by SHP-2. Interestingly many new proteins that we found to be regulated by SHP-2 activity are implicated in the formation and regulation of focal adhesions.
dc.formatPrint-Electronic
dc.format.extent524 - 536
dc.languageeng
dc.language.isoeng
dc.subjectNIH 3T3 Cells
dc.subjectAnimals
dc.subjectHumans
dc.subjectMice
dc.subjectPhosphotyrosine
dc.subjectProtein Array Analysis
dc.subjectProteomics
dc.subjectBiotechnology
dc.subjectMAP Kinase Signaling System
dc.subjectPhosphorylation
dc.subjectModels, Biological
dc.subjectMutant Proteins
dc.subjectMass Spectrometry
dc.subjectProtein Tyrosine Phosphatase, Non-Receptor Type 11
dc.subjectHEK293 Cells
dc.titleAlterations in the phosphoproteomic profile of cells expressing a non-functional form of the SHP2 phosphatase.
dc.typeJournal Article
dcterms.dateAccepted2015-08-14
rioxxterms.versionofrecord10.1016/j.nbt.2015.08.002
rioxxterms.licenseref.startdate2016-09en_US
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfNew biotechnology
pubs.issue5 Pt A
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/Protein Networks
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology/Molecular and Systems Oncology
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/Protein Networks
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology/Molecular and Systems Oncology
pubs.publication-statusPublished
pubs.volume33en_US
pubs.embargo.termsNot known
icr.researchteamProtein Networksen_US
icr.researchteamMolecular and Systems Oncologyen_US
dc.contributor.icrauthorIwai, Leoen
dc.contributor.icrauthorHuang, Paulen


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