Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 18, Issue 9, Pages -Publisher
MDPI
DOI: 10.3390/ijms18091886
Keywords
Breast Cancer 1 (BRCA1); Breast Cancer 2 (BRCA2); Partner and Localizer of BRCA2 (PALB2); Fanconi Anemia Group N protein (FANCN); cancer predisposition; deoxyribonucleic acid (DNA) damage response; DNA double strand break; Fanconi anemia; homologous recombination
Funding
- Fundacao de Amparo a Pesquisa do Rio de Janeiro (FAPERJ)
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
- Fundacao do Cancer
- IFRJ
- Florida Breast Cancer Foundation
- NIH [U54 CA163068, U01 CA116167]
- NATIONAL CANCER INSTITUTE [U54CA163068, U01CA116167] Funding Source: NIH RePORTER
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The deoxyribonucleic acid (DNA) damage response (DDR) is a major feature in the maintenance of genome integrity and in the suppression of tumorigenesis. PALB2 (Partner and Localizer of Breast Cancer 2 (BRCA2)) plays an important role in maintaining genome integrity through its role in the Fanconi anemia (FA) and homologous recombination (HR) DNA repair pathways. Since its identification as a BRCA2 interacting partner, PALB2 has emerged as a pivotal tumor suppressor protein associated to hereditary cancer susceptibility to breast and pancreatic cancers. In this review, we discuss how other DDR proteins (such as the kinases Ataxia Telangiectasia Mutated (ATM) and ATM- and Rad3-Related (ATR), mediators BRCA1 (Breast Cancer 1)/BRCA2 and effectors RAD51/DNA Polymerase (Pol) interact with PALB2 to orchestrate DNA repair. We also examine the involvement of PALB2 mutations in the predisposition to cancer and the role of PALB2 in stimulating error-free DNA repair through the FA/HR pathway.
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