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Background: disease:Defects in RAD54B may be a cause of tumor formation. Homozygous mutations at highly conserved position of RAD54B were observed in human primary lymphoma and colon cancer. These findings suggest that some cancers arise through defects of the RAD54B function.,function:Involved in DNA repair and mitotic recombination. May play an active role in recombination processes in concert with other members of the RAD52 epistasis group.,similarity:Belongs to the SNF2/RAD54 helicase family.,similarity:Contains 1 helicase ATP-binding domain.,similarity:Contains 1 helicase C-terminal domain.,subunit:Interacts with RAD51 through the NH2-terminal domain. Immunoprecipitation experiments show that the interaction is constitutive and not induced by ionizing radiation. The interaction may be indirect.,tissue specificity:Abundantly expressed in testis and spleen. Relatively low levels observed in thymus, prostate, ovary and colon.,