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The results suggest that ATRX (zeige ATRX ELISA Kits) is required to limit replication stress during cellular proliferation, whereas upregulation of PARP-1 (zeige PARP1 ELISA Kits) activity functions as a compensatory mechanism to protect stalled forks, limiting genomic damage, and facilitating late-born neuron production.
Our study highlights the importance of the cooperation between Rad54 and Mus81 (zeige MUS81 ELISA Kits) for mediating DNA DSB repair and restraining chromosome missegregation.
The long noncoding RNA, TERRA (zeige DMRT2 ELISA Kits) can bind both in cis (zeige CISH ELISA Kits) to telomeres and in trans to genic targets; a large network of interacting proteins was defined, including epigenetic factors, telomeric proteins, and the RNA helicase, ATRX (zeige ATRX ELISA Kits). TERRA (zeige DMRT2 ELISA Kits) and ATRX (zeige ATRX ELISA Kits) share hundreds of target genes and are functionally antagonistic at these loci: whereas TERRA (zeige DMRT2 ELISA Kits) activates, ATRX (zeige ATRX ELISA Kits) represses gene expression.
The changes of ATRX (zeige ATRX ELISA Kits) distribution occur and partially correlate with the main stages of zygotic genome activation during mouse early development, butthese changes seem to be determined by other processes of structural and functional rearrangements of blastomere nuclei.
ATRX (zeige ATRX ELISA Kits) mutation is associated with increased mutation rate at the single-nucleotide variant (SNV) level.
Daxx (zeige DAXX ELISA Kits) and Atrx (zeige ATRX ELISA Kits) safeguard the genome by silencing repetitive elements when DNA methylation (zeige HELLS ELISA Kits) levels are low.
A direct role of Atrx (zeige ATRX ELISA Kits) in the establishment and robust maintenance of heterochromatin is demonstrated.
We propose a model whereby ATRX-dependent deposition of H3.3 into heterochromatin is normally required to maintain the memory of silencing at imprinted loci.
ATRX (zeige ATRX ELISA Kits) promotes the incorporation of histone H3.3 (zeige H3F3A ELISA Kits) at particular transcribed genes and facilitates transcriptional elongation through G-rich sequences.
Using X chromosome inactivation as a model, study applied an unbiased proteomics approach to isolate Xist and PRC2 regulators and identified ATRX (zeige ATRX ELISA Kits); ATRX (zeige ATRX ELISA Kits) functions as a high-affinity RNA-binding protein that directly interacts with RepA/Xist RNA to promote loading of PRC2 in vivo. Without ATRX (zeige ATRX ELISA Kits), PRC2 cannot load onto Xist RNA nor spread in cis (zeige CISH ELISA Kits) along the X chromosome.
Nap1 (zeige IL8 ELISA Kits) binds to RAD54 (zeige ATRX ELISA Kits).
TAF12 (zeige TAF12 ELISA Kits) and NFYC (zeige NFYC ELISA Kits) are transcription factors that regulate the epigenome, whereas RAD54L (zeige ATRX ELISA Kits) plays a central role in DNA repair
support a model in which RAD54L (zeige ATRX ELISA Kits) and RAD54B (zeige RAD54B ELISA Kits) counteract genome-destabilizing effects of direct binding of RAD51 (zeige RAD51 ELISA Kits) to dsDNA in tumor cells
The RAD54L (zeige ATRX ELISA Kits) 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 (zeige PRKDC ELISA Kits) cells expressing mutant RAD54L (zeige ATRX ELISA Kits) coincide wirth reduction in recombination at telomeres.
hRad54, a Swi2/Snf2 (zeige SMARCA2 ELISA Kits) protein, binds HJ-like structures with high specificity and promotes their bidirectional branch migration in an ATPase (zeige DNAH8 ELISA Kits)-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 (zeige ATRX ELISA Kits) is recruited by RAD51 (zeige RAD51 ELISA Kits)-ssDNA filament to the chromatin of the intact chromosome and it remodels that chromatin to facilitate accessibility for strand exchange
analysis of human rad54 (zeige ATRX ELISA Kits) protein interactions with branched DNA molecules
Rad54 (zeige ATRX ELISA Kits) protein causes dissociation of joint molecules by ATP-dependent branch-migration and therefore plays an important role in double strand DNA break repair.
Rad54 structure suggests that SWI2/SNF2 (zeige SMARCA4 ELISA Kits) 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.
, RAD54-like protein
, RAD54-like (S. cerevisiae)
, ATP-dependent helicase ATRX
, HP1 alpha-interacting protein
, X-linked nuclear protein
, alpha thalassemia/mental retardation syndrome (X-linked)
, heterochromatin protein 2
, transcriptional regulator ATRX
, DNA repair and recombination protein RAD54-like
, RAD54 homolog
, putative recombination factor GdRad54