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AtRAD51C and SWI (show SMARCA1 Proteins) may function at distinct stages of meiosis.
AtRAD51C is essential for normal meiosis and is probably required for homologous synapsis.[AtRAD51C]
Crossing of RAD51C mutant with wild-type plants showed defective male and female gametogeneses as evidenced by lack of seed production. Furthermore, meiosis was severely disturbed in the mutant.
a critical synergy between Rad51c and Trp53 (show TP53 Proteins) in tumour progression and provide a predictable in vivo model system for studying mechanisms of Rad51c-mediated carcinogenesis
These results imply that adequate expression of Rad51C in mammalian cells is essential for maintaining genomic stability and sister chromatid cohesion to prevent malignant transformation.
the RAD51C-XRCC3-associated Holliday junction resolvase complex associates with crossovers and may play an essential role in the resolution of recombination intermediates prior to chromosome segregation
RAD51C has a late role in meiotic recombination.
Rad51c mutation in DH-cis (show CISH Proteins) mice promoted the development of tumors of specialized sebaceous glands and suppressed tumors characteristic of Trp53 (show TP53 Proteins) mutation. In addition, DH-cis (show CISH Proteins) females developed tumors significantly earlier than any other group.
DNA replication licensing factor MCM2 (show MCM2 Proteins) and DNA mismatch repair (MMR (show MRC1 Proteins)) protein MSH2 (show MSH2 Proteins) were confirmed to be present in co-precipitations with MmRAD51C.
Germline RAD51C mutation was found in patients with hereditary and sporadic gastric cancer.
individuals with mutations in RAD51C that are exposed to estrogen would be more susceptible to accumulation of DNA damage, leading to cancer progression.
Overexpression of RAD51C is associated with resistance to cisplatin and radiation in non-small cell lung cancer.
RAD51C mutations were identified in 0.5 % of Danish families.
RAD51C mutation is not associated with high-risk patients from Serbian hereditary breast/ovarian cancer.
a mutation analysis in 171 high-risk BRCA1 and BRCA2 (show BRCA2 Proteins) negative ovarian cancer patients, to evaluate the frequency of hereditary RAD51C and RAD51D (show RAD51D Proteins) variants in Czech population, is reported.
Novel Rad51C splice variants occur in colorectal tumors and cells: Variant 1 without exon-7, Variant 2 without exon 6 and 7 , or Variant 3 without exon 7 and 8. They are associated with FANCD2 foci positive colorectal tumors and microsatellite stability.
conclude that the woman has two potential disease-causing mutations and that predictive testing of family members should include both the RAD51C and BRCA2 (show BRCA2 Proteins) mutation
RAD51C and RAD51D (show RAD51D Proteins) are moderate ovarian cancer susceptibility genes.
RAD51C mutation is associated with breast and ovarian cancer.
This gene is a member of the RAD51 family of related genes, which encode strand-transfer proteins thought to be involved in recombinational repair of damaged DNA and in meiotic recombination. This gene product interacts with two other DNA repair proteins, encoded by RAD51B and XRCC3, but not with itself. The protein copurifies with XRCC3 protein in a complex, reflecting their endogenous association and suggesting a cooperative role during recombinational repair. This gene is one of four localized to a region of chromosome 17q23 where amplification occurs frequently in breast tumors. Overexpression of the four genes during amplification has been observed and suggests a possible role in tumor progression. Alternative splicing has been observed for this gene and two variants encoding different isoforms have been identified.
Rad51 homolog c
, RAD51 homolog C
, RAD51 homolog C (S. cerevisiae)
, DNA repair protein RAD51 homolog 3
, Rad51 DNA recombinase 3
, RAD51C protein
, RAD51-like protein 2
, yeast RAD51 homolog 3