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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.
Similar to other BC models, Rad51c/p53 double-mutant mouse mammary tumors also rev (show TP53 Proteins)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 (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 and DNA mismatch repair (MMR) protein MSH2 were confirmed to be present in co-precipitations with MmRAD51C.
results increase our knowledge about the RAD51C and RAD51D mutation spectrum and support the notion that these genes should be included in the gene panel testing performed on patients with hereditary breast and ovarian cancer syndrome
The authors assessed whether RAD51C promoter hypermethylation like mutation was associated with increased survival or increased sensitivity to platinum chemotherapy. However the results showed that neither outcomes were met
novel splice-site mutations affect the last nucleotide of exon 2 (c.404G>C, c.404G>T) and disrupt proper RAD51C pre-mRNA processing.
We showed that the mutation frequency of RAD51C in Japanese familial breast cancer cases was similar to that in Western countries and that the prevalence of deleterious mutation of PALB2 was possibly lower. Furthermore, our results suggested that BRIP1 mutation frequency in Japan might differ from that in Western countries
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 (show TP53 Proteins) 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 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.
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