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FLASH GENE

Symbol

RAD51D

contributors: mct - updated : 08-09-2016

HGNC name	RAD51-like 3 (S. cerevisiae)
HGNC id	9823

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains	N-terminal domain (AAs 1-83), which consists of four short helices flanked by long N- and C-terminal tails, is required for the ssDNA-specific binding function of human Rad51D
	a two ATP binding domains

HOMOLOGY

interspecies

homolog to yeast S.cerevisiae RAD51, D

intraspecies

paralog to RAD51

Homologene

FAMILY

RAD51 gene family

CATEGORY

DNA associated

SUBCELLULAR LOCALIZATION	intracellular
	intracellular,nucleus,chromatin/chromosome,telomere
text	to the telomere of the meiotic and somatic cells

basic FUNCTION	likely involved in double strand break repair, recombination and telomere maintenance
	required for homologous recombination and disruption of Holliday junctions with bloom syndrome protein (BLM)
	RAD51B, RAD51C, RAD51D, XRCC2 and XRCC3, play an essential role in the DNA repair reactions through homologous recombination
	RAD51B, RAD51C, RAD51D, XRCC2 and XRCC3 are key enzymes for DNA double-strand break repair
	RAD51B, RAD51C, RAD51D, XRCC2, XRCC3 sequentially orchestrate clinically relevant transactions at replication forks, cooperatively promoting fork remodeling and restart

CELLULAR PROCESS

nucleotide, repair, recombination

PHYSIOLOGICAL PROCESS

PATHWAY

metabolism

signaling

pathway in cells for the repair of severe DNA damage such as double-strand breaks

a component

member of the BCDX2 protein complex—comprising RAD51B, RAD51C, RAD51D, and XRCC2—which is thought to have several functions in HR, including stabilization of RAD51 nucleoprotein filaments

INTERACTION

DNA

RNA

small molecule

protein	XRCC2 (protection against DNA damaging)
	HELQ is associated with the RAD51 paralogs RAD51B/C/D and XRCC2, and with the DNA damage-responsive kinase ATR

cell & other

REGULATION

ASSOCIATED DISORDERS

corresponding disease(s)

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function tumoral somatic mutation       mutations are more likely to be found in families with two or more ovarian cancers, or in probands with first-degree relatives with ovarian cancer tumoral germinal mutation       germinal deleterious variants in the RAD51 paralogs to breast and ovarian cancers

Susceptibility

to ovarian cancer

Variant & Polymorphism other	RAD51D mutations confer a sixfold increased risk of ovarian cancer

Candidate gene
Marker
Therapy target
	System Type Disorder Pubmed cancer reproductive ovary cells deficient in RAD51D are sensitive to treatment with a PARP inhibitor, suggesting a possible therapeutic approach for cancers arising in RAD51D mutation carriers

ANIMAL & CELL MODELS