Cited by 244BRCA gene mutations in cancerCancer-related Molecular PathwaysDNA Repair Mechanisms

BRCA1 tumor suppression depends on BRCT phosphoprotein binding, but not its E3 ligase activity

Open access
Shakya, Reena, Reid, Latarsha J., Reczek, Colleen R., Cole, Francesca, Egli, Dieter, Lin, Chyuan-Sheng, deRooij, Dirk G., Hirsch, Steffen +6 more·2011·Science

Abstract

The properties of breast cancer susceptibility protein required for tumor suppression have been explored.

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Crossref · 10.1126/science.1209909

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  • Mice carrying a BRCA1 BRCT mutant defective in phosphoprotein recognition are prone to tumors, indicating that BRCT phosphoprotein recognition is required for BRCA1 tumor suppression.

    “Mice carrying a BRCT mutant of BRCA1 defective in recognition of phosphorylated proteins are prone to tumor development indicating that BRCT phosphoprotein recognition is required for BRCA1 tumor suppression (Shakya et al., 2011).”

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Authors
Shakya, R., Reid, L. J., Reczek, C. R., Cole, F., Egli, D., Lin, C.-S., deRooij, D. G., Hirsch, S., Ravi, K., Hicks, J. B., Szabolcs, M., Jasin, M., Baer, R., & Ludwig, T.
Affiliations
  • Columbia University (US)
  • Memorial Sloan Kettering Cancer Center (US)
  • New York Stem Cell Foundation (US)
  • Amsterdam University Medical Centers (NL)
  • Cold Spring Harbor Laboratory (US)
  • Herbert Irving Comprehensive Cancer Center (US)
Corresponding author
  • Shakya, Reena
  • Reid, Latarsha J.
  • Baer, Richard
  • Ludwig, Thomas
Venue
Science
Published
2011-10-28
Volume
334
Issue
6055
Pages
525-528
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W2000636252
Cited by
244
References
28
Citations by year
2026: 7 · 2025: 7 · 2024: 7 · 2023: 10 · 2022: 12 · 2021: 14 · 2020: 19 · 2019: 11 · 2018: 17 · 2017: 15 · 2016: 25 · 2015: 20 · 2014: 20 · 2013: 22 · 2012: 35
FWCI
15.74
Type
journal article
Language
en
Open access
Locations
  • Science (publishedVersion)
  • PubMed (publishedVersion)
  • Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
  • Data Archiving and Networked Services (DANS) (submittedVersion)
  • Pure Amsterdam UMC (submittedVersion)
Funders
  • National Cancer Institute (P01CA097403, R01CA137023, T32CA009503, F31CA132626)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (F32HD051392, R01HD040916)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › BRCA gene mutations in cancer
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Keywords
BRCA1, tumor suppression, BRCT domain, E3 ubiquitin ligase activity, germline mutations, hereditary breast cancer, ovarian cancer, genetically engineered mouse models, ubiquitination
MeSH terms
Animals, Cells, Cultured, Disease Models, Animal, Ligands, Mammary Neoplasms, Experimental, Pancreatic Neoplasms, Phosphoproteins, Protein Binding, BRCA1 Protein, Genes, BRCA1, Tumor Suppressor Proteins, Ubiquitin-Protein Ligases, Mutant Proteins, Basic-Leucine Zipper Transcription Factors, Mice, Embryonic Stem Cells, Protein Interaction Domains and Motifs, RING Finger Domains, Protein Multimerization

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