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The protein encoded by ATRX contains an ATPase/helicase domain, and thus it belongs to the SWI/SNF family of chromatin remodeling proteins. Additionally we are shipping ATRX Antibodies (126) and ATRX Proteins (4) and many more products for this protein.
The results suggest that ATRX is required to limit replication stress during cellular proliferation, whereas upregulation of PARP-1 (show PARP1 ELISA Kits) activity functions as a compensatory mechanism to protect stalled forks, limiting genomic damage, and facilitating late-born neuron production.
Distinct histological and molecular characteristics of adult diffuse gliomas with and without ATRX immunoreactivity indicate the utility of ATRX immunohistochemistry in diagnostic practice.
ATRX loss can be reliable for the pathogenesis of neuroendocrine pancreatic neoplasms.
Mutation in ATRX gene is associated with cancer more frequently in males.
Nek1 (show NEK1 ELISA Kits) phosphorylates Rad54 and regulates Rad51 (show RAD51 ELISA Kits) removal to orchestrate homologous recombination and replication fork stability.
Results suggest that cell cycle progression and proliferation of HeLa cells can be tightly controlled by the abundance of RAD51 (show RAD51 ELISA Kits) and RAD54 proteins, which are essential for the rapid response to postreplicative stress and DNA damage stress.
ATRX interacts with ZNF274 (show ZNF274 ELISA Kits), TRIM28 (show TRIM28 ELISA Kits) and SETDB1 (show SETDB1 ELISA Kits) and binds to the 3' exons of zinc finger genes that present an atypical H3K9me3/H3K36me3 chromatin signature. Depletion of ATRX or ZNF274 (show ZNF274 ELISA Kits) leads to decreased H3K9me3 levels at zinc finger genes and other atypical chromatin regions.
somatic mutations in the ATRX gene have been observed as recurrent alterations in both osteosarcoma and brain tumors. However, it is unclear if there is any association between osteosarcoma and germline ATRX mutations, specifically in patients with constitutional ATR-X syndrome.
AMab-6 sensitively detects ATRX in Western blot and immunohistochemical analyses, indicating that AMab-6 could become the standard marker to determine the ATRX mutation status of gliomas in immunohistochemical analyses
our study describes a novel missense mutation of the ATRX gene helicase domain, carried by three affected males of the two generations of the same family and segregated with intellectual deficiency, dysmorphism and behaviour disorder without alpha-thalassaemia and with non-skewed X-chromosome inactivation
Our study highlights the importance of the cooperation between Rad54 (show RAD54L ELISA Kits) and Mus81 (show MUS81 ELISA Kits) for mediating DNA DSB repair and restraining chromosome missegregation.
The long noncoding RNA, TERRA (show DMRT2 ELISA Kits) can bind both in cis (show 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. TERRA (show DMRT2 ELISA Kits) and ATRX share hundreds of target genes and are functionally antagonistic at these loci: whereas TERRA (show DMRT2 ELISA Kits) activates, ATRX represses gene expression.
The changes of ATRX 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 mutation is associated with increased mutation rate at the single-nucleotide variant (SNV) level.
Daxx (show DAXX ELISA Kits) and Atrx safeguard the genome by silencing repetitive elements when DNA methylation (show HELLS ELISA Kits) levels are low.
A direct role of Atrx 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 promotes the incorporation of histone H3.3 (show 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; ATRX functions as a high-affinity RNA-binding protein that directly interacts with RepA/Xist RNA to promote loading of PRC2 in vivo. Without ATRX, PRC2 cannot load onto Xist RNA nor spread in cis (show CISH ELISA Kits) along the X chromosome.
The protein encoded by this gene contains an ATPase/helicase domain, and thus it belongs to the SWI/SNF family of chromatin remodeling proteins. The mutations of this gene are associated with an X-linked mental retardation (XLMR) syndrome most often accompanied by alpha-thalassemia (ATRX) syndrome. These mutations have been shown to cause diverse changes in the pattern of DNA methylation, which may provide a link between chromatin remodeling, DNA methylation, and gene expression in developmental processes. This protein is found to undergo cell cycle-dependent phosphorylation, which regulates its nuclear matrix and chromatin association, and suggests its involvement in the gene regulation at interphase and chromosomal segregation in mitosis. Multiple alternatively spliced transcript variants encoding distinct isoforms have been reported.
ATP-dependent helicase ATRX
, DNA dependent ATPase and helicase
, X-linked helicase II
, X-linked nuclear protein
, Zinc finger helicase
, alpha thalassemia/mental retardation syndrome X-linked (RAD54 homolog, S. cerevisiae)
, helicase 2, X-linked
, transcriptional regulator ATRX
, alpha thalassemia/mental retardation syndrome X-linked homolog
, helicase II
, HP1 alpha-interacting protein
, alpha thalassemia/mental retardation syndrome (X-linked)
, heterochromatin protein 2
, DNA repair and recombination protein RAD54-like
, RAD54 homolog