dc.contributor.author | Ryan, CJ | |
dc.contributor.author | Kennedy, S | |
dc.contributor.author | Bajrami, I | |
dc.contributor.author | Matallanas, D | |
dc.contributor.author | Lord, CJ | |
dc.date.accessioned | 2018-02-15T15:10:46Z | |
dc.date.issued | 2017-10-25 | |
dc.identifier.citation | Cell systems, 2017, 5 (4), pp. 399 - 409.e5 | |
dc.identifier.issn | 2405-4712 | |
dc.identifier.uri | https://repository.icr.ac.uk/handle/internal/1131 | |
dc.identifier.eissn | 2405-4720 | |
dc.identifier.doi | 10.1016/j.cels.2017.09.011 | |
dc.description.abstract | Protein complexes are responsible for the bulk of activities within the cell, but how their behavior and abundance varies across tumors remains poorly understood. By combining proteomic profiles of breast tumors with a large-scale protein-protein interaction network, we have identified a set of 285 high-confidence protein complexes whose subunits have highly correlated protein abundance across tumor samples. We used this set to identify complexes that are reproducibly under- or overexpressed in specific breast cancer subtypes. We found that mutation or deletion of one subunit of a co-regulated complex was often associated with a collateral reduction in protein expression of additional complex members. This collateral loss phenomenon was typically evident from proteomic, but not transcriptomic, profiles, suggesting post-transcriptional control. Mutation of the tumor suppressor E-cadherin (CDH1) was associated with a collateral loss of members of the adherens junction complex, an effect we validated using an engineered model of E-cadherin loss. | |
dc.format | Print-Electronic | |
dc.format.extent | 399 - 409.e5 | |
dc.language | eng | |
dc.language.iso | eng | |
dc.publisher | CELL PRESS | |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0 | |
dc.subject | Cell Line, Tumor | |
dc.subject | Humans | |
dc.subject | Breast Neoplasms | |
dc.subject | Cadherins | |
dc.subject | Proteome | |
dc.subject | Proteomics | |
dc.subject | Gene Expression Regulation, Neoplastic | |
dc.subject | RNA Processing, Post-Transcriptional | |
dc.subject | Mutation | |
dc.subject | Genes, Tumor Suppressor | |
dc.subject | Female | |
dc.subject | Protein Interaction Maps | |
dc.subject | MCF-7 Cells | |
dc.title | A Compendium of Co-regulated Protein Complexes in Breast Cancer Reveals Collateral Loss Events. | |
dc.type | Journal Article | |
dcterms.dateAccepted | 2017-09-18 | |
rioxxterms.versionofrecord | 10.1016/j.cels.2017.09.011 | |
rioxxterms.licenseref.uri | https://creativecommons.org/licenses/by/4.0 | |
rioxxterms.licenseref.startdate | 2017-10-11 | |
rioxxterms.type | Journal Article/Review | |
dc.relation.isPartOf | Cell systems | |
pubs.issue | 4 | |
pubs.notes | Not 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/Breast Cancer Research | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Breast Cancer Research/Gene Function | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Molecular Pathology | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Molecular Pathology/Gene Function | |
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/Breast Cancer Research | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Breast Cancer Research/Gene Function | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Molecular Pathology | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Molecular Pathology/Gene Function | |
pubs.publication-status | Published | |
pubs.volume | 5 | |
pubs.embargo.terms | Not known | |
icr.researchteam | Gene Function | |
dc.contributor.icrauthor | Lord, Christopher | |