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AtRAD51C and SWI (zeige SMARCA1 ELISA Kits) 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.
Similar to other BC models, Rad51c/p53 double-mutant mouse mammary tumors also rev (zeige TP53 ELISA Kits)eal a propensity for genomic instability, but lack the focal amplification of the Met locus or distinct mutational signatures reported for other HR genes
a critical synergy between Rad51c and Trp53 (zeige TP53 ELISA Kits) 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 (zeige CISH ELISA Kits) mice promoted the development of tumors of specialized sebaceous glands and suppressed tumors characteristic of Trp53 (zeige TP53 ELISA Kits) mutation. In addition, DH-cis (zeige CISH ELISA Kits) females developed tumors significantly earlier than any other group.
DNA replication licensing factor MCM2 (zeige MCM2 ELISA Kits) and DNA mismatch repair (MMR (zeige MRC1 ELISA Kits)) protein MSH2 (zeige MSH2 ELISA Kits) were confirmed to be present in co-precipitations with MmRAD51C.
Here we report yet another example of a rare RAD51C missense change (p.Arg312Trp) that impairs protein function.
Using the human mammary epithelial cell line MCF10A, we show that deletion of TP53 (zeige TP53 ELISA Kits) can rescue RAD51C-deficient cells from radiation-induced cellular senescence, whereas it exacerbates their centrosome amplification and nuclear abnormalities
Results identified a chromosomal translocation between Rad51C and Ataxin-7 (zeige ATXN7 ELISA Kits) in colorectal tumors. The in-frame fusion transcript results in a fusion protein with molecular weight of 110 KDa. In vitro 5-Azacytidine treatment of colorectal tumor cells showed expression of the fusion gene is regulated by promoter methylation.
Germline mutation in RAD51C gene is associated with neoadjuvant therapy response in triple negative breast patients.
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 (zeige BRCA2 ELISA Kits) negative ovarian cancer patients, to evaluate the frequency of hereditary RAD51C and RAD51D (zeige RAD51D ELISA Kits) variants in Czech population, is reported.
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