Enhancement of RAD51 recombinase activity by the tumor suppressor PALB2
Copyright policy )Enhancement of RAD51 recombinase activity by the tumor suppressor PALB2
Homologous recombination mediated by RAD51 recombinase helps eliminate chromosomal lesions, such as DNA double-strand breaks induced by radiation or arising from injured DNA replication forks. The tumor suppressors BRCA2 and PALB2 act together to deliver RAD51 to chromosomal lesions to initiate repair. Here we document a new function of PALB2: to enhance RAD51's ability to form the D loop. We show that PALB2 binds DNA and physically interacts with RAD51. Notably, although PALB2 alone stimulates D-loop formation, it has a cooperative effect with RAD51AP1, an enhancer of RAD51. This stimulation stems from the ability of PALB2 to function with RAD51 and RAD51AP1 to assemble the synaptic complex. Our results demonstrate the multifaceted role of PALB2 in chromosome damage repair. Because PALB2 mutations can cause cancer or Fanconi anemia, our findings shed light on the mechanism of tumor suppression in humans.
- Lawrence Berkeley National Laboratory United States
- University of Virginia United States
- Yale University United States
- Queensland University of Technology Australia
- School of Medicine Yale University United States
DNA, Neoplasm - metabolism, DNA Repair, Recombinant Fusion Proteins, DNA-Binding Proteins - chemistry - physiology, Breast Neoplasms, 612, Neoplasm - metabolism, Chromosomes, Article, Neoplasms, Radiations, Nuclear Proteins - chemistry - genetics - physiology, Protein Interaction Mapping, Humans, Tumor Suppressor Proteins - chemistry - genetics - physiology, BRCA2 Protein, Recombination, Genetic, Tumor Suppressor Proteins, 59, Nuclear Proteins, RNA-Binding Proteins, DNA, Dna, DNA, Neoplasm, Breast Neoplasms - metabolism, Mammary Glands, Recombination, Dna Replication, Peptide Fragments, Neoplasm Proteins, DNA-Binding Proteins, Multiprotein Complexes, Stimulation, Female, Rad51 Recombinase, Apoptosis Regulatory Proteins, Fanconi Anemia Complementation Group N Protein, Repair, Mutations, Protein Binding
DNA, Neoplasm - metabolism, DNA Repair, Recombinant Fusion Proteins, DNA-Binding Proteins - chemistry - physiology, Breast Neoplasms, 612, Neoplasm - metabolism, Chromosomes, Article, Neoplasms, Radiations, Nuclear Proteins - chemistry - genetics - physiology, Protein Interaction Mapping, Humans, Tumor Suppressor Proteins - chemistry - genetics - physiology, BRCA2 Protein, Recombination, Genetic, Tumor Suppressor Proteins, 59, Nuclear Proteins, RNA-Binding Proteins, DNA, Dna, DNA, Neoplasm, Breast Neoplasms - metabolism, Mammary Glands, Recombination, Dna Replication, Peptide Fragments, Neoplasm Proteins, DNA-Binding Proteins, Multiprotein Complexes, Stimulation, Female, Rad51 Recombinase, Apoptosis Regulatory Proteins, Fanconi Anemia Complementation Group N Protein, Repair, Mutations, Protein Binding
citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).150 popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.Top 1% influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).Top 10% impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.Top 10%
Citations provided by BIP!Popularity provided by BIP!