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Gene Review

RAD51D  -  RAD51 paralog D

Homo sapiens

Synonyms: BROVCA4, DNA repair protein RAD51 homolog 4, HsTRAD, R51H3, RAD51 homolog D, ...
 
 
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Disease relevance of RAD51L3

  • The variant E233G of the RAD51D gene could be a low-penetrance allele in high-risk breast cancer families without BRCA1/2 mutations [1].
  • The self-reliant system for alternative care of diabetes mellitus patients--experience macrobiotic management in Trad Province [2].
  • Eight different inactivating germline mutations in the RAD51D gene were found to be associated with significantly (6 fold) increased risk of ovarian cancer [3].
 

High impact information on RAD51L3

  • Telomere maintenance requires the RAD51D recombination/repair protein [4].
  • It associates with RAD51D and ablating its expression reduces the number of RAD51 foci [5].
  • These findings support a crucial role for mammalian RAD51D in normal development, recombination, and maintaining mammalian genome stability [6].
  • We show that the RAD51L3-XRCC2 complex stimulates BLM to disrupt synthetic 4-way junctions that model the Holliday junction [7].
  • RESULTS: TRAD induced selective E1A and E1B expression in human cancer cells, but not in normal cells such as human fibroblasts [8].
 

Biological context of RAD51L3

 

Anatomical context of RAD51L3

  • Ectopic expression of wild-type human RAD51D or mutants having a non-functional A or B motif was used to test for complementation of a rad51d knockout hamster CHO cell line [13].
  • TRAD replicated efficiently and induced marked cell killing in a panel of human cancer cell lines, whereas replication as well as cytotoxicity was highly attenuated in normal human fibroblasts lacking telomerase activity [8].
 

Other interactions of RAD51L3

  • Functional interaction between the Bloom's syndrome helicase and the RAD51 paralog, RAD51L3 (RAD51D) [7].
  • By using purified proteins, we demonstrate that the interaction between RAD51L3 and XRCC2 is direct [9].
  • HR also plays a role in the maintenance of eukaryotic telomeres; cells defective in the recombinational repair proteins RAD51D or RAD54 exhibit telomere shortening and end-to-end chromosome fusions [14].
 

Analytical, diagnostic and therapeutic context of RAD51L3

 

References

  1. The variant E233G of the RAD51D gene could be a low-penetrance allele in high-risk breast cancer families without BRCA1/2 mutations. Rodríguez-López, R., Osorio, A., Ribas, G., Pollán, M., Sánchez-Pulido, L., de la Hoya, M., Ruibal, A., Zamora, P., Arias, J.I., Salazar, R., Vega, A., Martínez, J.I., Esteban-Cardeñosa, E., Alonso, C., Letón, R., Urioste Azcorra, M., Miner, C., Armengod, M.E., Carracedo, A., González-Sarmiento, R., Caldés, T., Díez, O., Benítez, J. Int. J. Cancer (2004) [Pubmed]
  2. The self-reliant system for alternative care of diabetes mellitus patients--experience macrobiotic management in Trad Province. Bhumisawasdi, J., Vanna, O., Surinpang, N. Journal of the Medical Association of Thailand = Chotmaihet thangphaet (2006) [Pubmed]
  3. Germline mutations in RAD51D confer susceptibility to ovarian cancer. Loveday, C., Turnbull, C., Ramsay, E., Hughes, D., Ruark, E., Frankum, J.R., Bowden, G., Kalmyrzaev, B., Warren-Perry, M., Snape, K., Adlard, J.W., Barwell, J., Berg, J., Brady, A.F., Brewer, C., Brice, G., Chapman, C., Cook, J., Davidson, R., Donaldson, A., Douglas, F., Greenhalgh, L., Henderson, A., Izatt, L., Kumar, A., Lalloo, F., Miedzybrodzka, Z., Morrison, P.J., Paterson, J., Porteous, M., Rogers, M.T., Shanley, S., Walker, L., Eccles, D., Evans, D.G., Renwick, A., Seal, S., Lord, C.J., Ashworth, A., Reis-Filho, J.S., Antoniou, A.C., Rahman, N. Nat. Genet. (2011) [Pubmed]
  4. Telomere maintenance requires the RAD51D recombination/repair protein. Tarsounas, M., Muñoz, P., Claas, A., Smiraldo, P.G., Pittman, D.L., Blasco, M.A., West, S.C. Cell (2004) [Pubmed]
  5. Sws1 is a conserved regulator of homologous recombination in eukaryotic cells. Martín, V., Chahwan, C., Gao, H., Blais, V., Wohlschlegel, J., Yates, J.R., McGowan, C.H., Russell, P. EMBO J. (2006) [Pubmed]
  6. Extensive chromosomal instability in Rad51d-deficient mouse cells. Smiraldo, P.G., Gruver, A.M., Osborn, J.C., Pittman, D.L. Cancer Res. (2005) [Pubmed]
  7. Functional interaction between the Bloom's syndrome helicase and the RAD51 paralog, RAD51L3 (RAD51D). Braybrooke, J.P., Li, J.L., Wu, L., Caple, F., Benson, F.E., Hickson, I.D. J. Biol. Chem. (2003) [Pubmed]
  8. Telomerase-specific replication-selective virotherapy for human cancer. Kawashima, T., Kagawa, S., Kobayashi, N., Shirakiya, Y., Umeoka, T., Teraishi, F., Taki, M., Kyo, S., Tanaka, N., Fujiwara, T. Clin. Cancer Res. (2004) [Pubmed]
  9. The RAD51 family member, RAD51L3, is a DNA-stimulated ATPase that forms a complex with XRCC2. Braybrooke, J.P., Spink, K.G., Thacker, J., Hickson, I.D. J. Biol. Chem. (2000) [Pubmed]
  10. Identification, characterization, and genetic mapping of Rad51d, a new mouse and human RAD51/RecA-related gene. Pittman, D.L., Weinberg, L.R., Schimenti, J.C. Genomics (1998) [Pubmed]
  11. Multiple alternative transcripts of the human homologue of the mouse TRAD/R51H3/RAD51D gene, a member of the rec A/RAD51 gene family. Kawabata, M., Saeki, K. Biochem. Biophys. Res. Commun. (1999) [Pubmed]
  12. Differential roles of XRCC2 in homologous recombinational repair of stalled replication forks. Liu, N., Lim, C.S. J. Cell. Biochem. (2005) [Pubmed]
  13. Disparate requirements for the Walker A and B ATPase motifs of human RAD51D in homologous recombination. Wiese, C., Hinz, J.M., Tebbs, R.S., Nham, P.B., Urbin, S.S., Collins, D.W., Thompson, L.H., Schild, D. Nucleic Acids Res. (2006) [Pubmed]
  14. Recombination at mammalian telomeres: an alternative mechanism for telomere protection and elongation. Tarsounas, M., West, S.C. Cell Cycle (2005) [Pubmed]
 
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