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anti-Human RAD54L Antibodies:
anti-Mouse (Murine) RAD54L Antibodies:
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Human Monoclonal RAD54L Primary Antibody for CyTOF, FACS - ABIN257916
Srivastava, Modi, Tripathi, Mudgal, De, Sengupta: BLM helicase stimulates the ATPase and chromatin-remodeling activities of RAD54. in Journal of cell science 2009
Human Polyclonal RAD54L Primary Antibody for ICC, IF - ABIN4349162
Bai, Wang, Huo, Xie, Xie, Xu, Wang: Serine/Threonine Kinase CHEK1-Dependent Transcriptional Regulation of RAD54L Promotes Proliferation and Radio Resistance in Glioblastoma. in Translational oncology 2018
Data show that the RAD54 N-terminal domain (NTD) is responsible for initiation of branch migration (BM) through two coupled, but distinct steps; specific binding to Holliday junctions and RAD54 oligomerization.
Nap1 binds to RAD54.
TAF12 and NFYC are transcription factors that regulate the epigenome, whereas RAD54L plays a central role in DNA repair
support a model in which RAD54L and RAD54B counteract genome-destabilizing effects of direct binding of RAD51 to dsDNA in tumor cells
The RAD54L polymorphism (2290C/T) can be used as a genetic marker inside the consensus deletion region at 1p32 in human meningiomas.
Shortened telomeres in murine scid cells expressing mutant RAD54L coincide wirth reduction in recombination at telomeres.
hRad54, a Swi2/Snf2 protein, binds HJ-like structures with high specificity and promotes their bidirectional branch migration in an ATPase-dependent manner
Some immortal cells use the alternative lengthening of telomeres (ALT) pathway to maintain their telomeres instead of telomerase. This is the first genetic evidence that Rad54 is dispensable for the ALT pathway.
RAD54 is recruited by RAD51-ssDNA filament to the chromatin of the intact chromosome and it remodels that chromatin to facilitate accessibility for strand exchange
analysis of human rad54 protein interactions with branched DNA molecules
Rad54 protein causes dissociation of joint molecules by ATP-dependent branch-migration and therefore plays an important role in double strand DNA break repair.
germline mutations in RAD51, RAD51AP1, RAD51L1, RAD51L3, RAD52 and RAD54L are unlikely to be causal of an inherited predisposition to CLL.
Rad51 protein stimulates the branch migration activity of Rad54 protein.(
Rad54 structure suggests that SWI2/SNF2 proteins use a mechanism analogous to helicases to translocate on dsDNA
The protein encoded by this gene belongs to the DEAD-like helicase superfamily, and shares similarity with Saccharomyces cerevisiae Rad54, a protein known to be involved in the homologous recombination and repair of DNA. This protein has been shown to play a role in homologous recombination related repair of DNA double-strand breaks. The binding of this protein to double-strand DNA induces a DNA topological change, which is thought to facilitate homologous DNA paring, and stimulate DNA recombination. Alternative splicing results in multiple transcript variants encoding the same protein.
DNA repair and recombination protein RAD54-like
, RAD54 homolog
, putative recombination factor GdRad54
, RAD54-like protein
, RAD54-like (S. cerevisiae)