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Query author contributions in Reactome

Reactome depends on collaboration between our curation team and outside experts to assemble and peer-review its pathway modules. The integration of ORCID within Reactome enables us to meet a key challenge with authoring, curating and reviewing biological information by incentivizing and crediting the external experts that contribute their expertise and time to the Reactome curation process. More information is available at ORCID and Reactome.

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Details on Person Park, Morag

Class:IdPerson:3108186
_displayNamePark, Morag
_timestamp2013-02-10 17:22:14
created[InstanceEdit:3108223] May, B, 2013-02-10
firstnameMorag
initialM
surnamePark
(author)[LiteratureReference:3108205] Pc2-mediated sumoylation of Smad-interacting protein 1 attenuates transcriptional repression of E-cadherin
[LiteratureReference:5218661] Crk associates with a multimolecular Paxillin/GIT2/beta-PIX complex and promotes Rac-dependent relocalization of Paxillin to focal contacts
[LiteratureReference:6807007] Hepatocyte growth factor receptor tyrosine kinase met is a substrate of the receptor protein-tyrosine phosphatase DEP-1
[LiteratureReference:6807026] Regulation of the Met receptor-tyrosine kinase by the protein-tyrosine phosphatase 1B and T-cell phosphatase
[LiteratureReference:8874699] A conserved DpYR motif in the juxtamembrane domain of the Met receptor family forms an atypical c-Cbl/Cbl-b tyrosine kinase binding domain binding site required for suppression of oncogenic activation
[LiteratureReference:8875182] Met/Hepatocyte growth factor receptor ubiquitination suppresses transformation and is required for Hrs phosphorylation
[LiteratureReference:8875502] Distinct recruitment of Eps15 via Its coiled-coil domain is required for efficient down-regulation of the met receptor tyrosine kinase
[LiteratureReference:8875550] Crk synergizes with epidermal growth factor for epithelial invasion and morphogenesis and is required for the met morphogenic program
[LiteratureReference:8875559] Crk adapter proteins promote an epithelial-mesenchymal-like transition and are required for HGF-mediated cell spreading and breakdown of epithelial adherens junctions
[LiteratureReference:8875664] GGA3 functions as a switch to promote Met receptor recycling, essential for sustained ERK and cell migration
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No pathways have been reviewed or authored by Park, Morag (3108186)