RAD54B: Difference between revisions

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(Added a section on implications of RAD54B defect in cancer.)
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==Interactions==
==Interactions==
RAD54B has been shown to [[Protein-protein interaction|interact]] with [[RAD51]].<ref name=pmid10851248 />
RAD54B has been shown to [[Protein-protein interaction|interact]] with [[RAD51]].<ref name=pmid10851248 />
==Cancer==
The ''RAD54B'' [[gene]] is somatically [[Mutation|mutated]] or deleted in numerous types of cancer including [[colorectal cancer]] (~3.3%), [[breast cancer]] (~3.4%), and [[lung cancer]] (~2.6%).<ref name="pmid27902462">{{cite journal |vauthors=McAndrew EN, Lepage CC, McManus KJ |title=The synthetic lethal killing of RAD54B-deficient colorectal cancer cells by PARP1 inhibition is enhanced with SOD1 inhibition |journal=Oncotarget |volume=7 |issue=52 |pages=87417–87430 |date=December 2016 |pmid=27902462 |pmc=5349998 |doi=10.18632/oncotarget.13654 |url=}}</ref>  In North America, these three cancers alone account for about 20,500 individuals diagnosed annually with ''RAD54B'' defective cancer.  In a pre-clinical study, colon cancer cells defective in ''RAD54B'' were determined to be selectively killed by inhibitors of the [[DNA repair]] protein [[PARP1]].<ref name="pmid27902462" />  [[PARP inhibitor|Inhibitors of PARP1]] likely impede alternative DNA repair responses that might otherwise compensate for loss of the ''RAD54B'' pathway in cancer cells.  Thus ''RAD54B''-deficient cancer cells treated with a PARP1 inhibitor are apparently more vulnerable to killing by [[DNA damage (naturally occurring)|naturally occurring DNA damages]] than non-cancerous cells without a RAD54 defect (see article [[Synthetic lethality]]).


==References==
==References==

Revision as of 20:30, 23 February 2018

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Identifiers
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External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez
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DNA repair and recombination protein RAD54B is a protein that in humans is encoded by the RAD54B gene.[1][2][3]

The protein encoded by this gene belongs to the DEAD-like helicase superfamily. It shares similarity with Saccharomyces cerevisiae RAD54 and RDH54, both of which are involved in homologous recombination and repair of DNA. This protein binds to double-stranded DNA, and displays ATPase activity in the presence of DNA. This gene is highly expressed in testis and spleen, which suggests active roles in meiotic and mitotic recombination. Homozygous mutations of this gene were observed in primary lymphoma and colon cancer.[3]

Interactions

RAD54B has been shown to interact with RAD51.[2]

Cancer

The RAD54B gene is somatically mutated or deleted in numerous types of cancer including colorectal cancer (~3.3%), breast cancer (~3.4%), and lung cancer (~2.6%).[4] In North America, these three cancers alone account for about 20,500 individuals diagnosed annually with RAD54B defective cancer. In a pre-clinical study, colon cancer cells defective in RAD54B were determined to be selectively killed by inhibitors of the DNA repair protein PARP1.[4] Inhibitors of PARP1 likely impede alternative DNA repair responses that might otherwise compensate for loss of the RAD54B pathway in cancer cells. Thus RAD54B-deficient cancer cells treated with a PARP1 inhibitor are apparently more vulnerable to killing by naturally occurring DNA damages than non-cancerous cells without a RAD54 defect (see article Synthetic lethality).

References

  1. Hiramoto T, Nakanishi T, Sumiyoshi T, Fukuda T, Matsuura S, Tauchi H, Komatsu K, Shibasaki Y, Inui H, Watatani M, Yasutomi M, Sumii K, Kajiyama G, Kamada N, Miyagawa K, Kamiya K (Jun 1999). "Mutations of a novel human RAD54 homologue, RAD54B, in primary cancer". Oncogene. 18 (22): 3422–6. doi:10.1038/sj.onc.1202691. PMID 10362364.
  2. 2.0 2.1 Tanaka K, Hiramoto T, Fukuda T, Miyagawa K (Sep 2000). "A novel human rad54 homologue, Rad54B, associates with Rad51". J Biol Chem. 275 (34): 26316–21. doi:10.1074/jbc.M910306199. PMID 10851248.
  3. 3.0 3.1 "Entrez Gene: RAD54B RAD54 homolog B (S. cerevisiae)".
  4. 4.0 4.1 McAndrew EN, Lepage CC, McManus KJ (December 2016). "The synthetic lethal killing of RAD54B-deficient colorectal cancer cells by PARP1 inhibition is enhanced with SOD1 inhibition". Oncotarget. 7 (52): 87417–87430. doi:10.18632/oncotarget.13654. PMC 5349998. PMID 27902462.

Further reading