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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 Proteins (4) and many more products for this protein.
Showing 10 out of 127 products:
Human Polyclonal ATRX Primary Antibody for IHC, IHC (p) - ABIN4282398
Heaphy, de Wilde, Jiao, Klein, Edil, Shi, Bettegowda, Rodriguez, Eberhart, Hebbar, Offerhaus, McLendon, Rasheed, He, Yan, Bigner, Oba-Shinjo, Marie, Riggins, Kinzler, Vogelstein, Hruban, Maitra et al.: Altered telomeres in tumors with ATRX and DAXX mutations. ... in Science (New York, N.Y.) 2011
Show all 16 Pubmed References
Human Polyclonal ATRX Primary Antibody for ICC, IF - ABIN442805
Wille, Maurer, Piatti, Whittle, Rieder, Singewald, Lusser: Impaired Contextual Fear Extinction Learning is Associated with Aberrant Regulation of CHD-Type Chromatin Remodeling Factors. in Frontiers in behavioral neuroscience 2015
Show all 2 Pubmed References
Structural and biochemical characterization of DAXX (show DAXX Antibodies)-ATRX interaction.
Structural basis for DAXX (show DAXX Antibodies) interaction with ATRX.
Review of research progress of TERT (show TERT Antibodies)-mediated and ATRX-mediated telomere maintenance and neuroblastoma (show ARHGEF16 Antibodies), especially high-risk tumors
This study demonstrated the ATRX loss in glioneuronal tumors with neuropil-like islands.
6 cases of diffuse glioma that presented a diagnostic challenge due to conflicting IDH1 (show IDH1 Antibodies)/IDH2 (show IDH2 Antibodies), ATRX, and 1p/19q results.
The chromatin remodeling enzyme ATRX is a regulator of therapy induced senescence and drives cells into this state via multiple mechanisms.
The present study explored the structural consequences influenced by two observed mutations V194I and C220R on ADD domain of ATRX protein by applying all atom molecular dynamics (MD) simulation.
Study demonstrate that the retention of ATRX expression in all oligodendroglial tumor nuclei strongly supports the diagnosis of oligodendroglioma. Conversely, its loss in tumor astrocytic nuclei favors the diagnosis of astrocytoma.
Given the high frequency of ATRX and DAXX (show DAXX Antibodies) mutations in cancer, these chromatin regulators likely play a key role in pathogenesis [review]
Data suggest that identification of IDH1 (show IDH1 Antibodies)-R132H and ATRX loss status in the primary-recurrent gliomas may aid in treatment strategy selection, therapeutic trial design, and clinical prognosis evaluation.
mosaic loss of ATRX expression in the central nervous system leads to endocrine defects and decreased body size and has a negative impact on learning and memory.
The results suggest that ATRX is required to limit replication stress during cellular proliferation, whereas upregulation of PARP-1 (show PARP1 Antibodies) 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 (show RAD54L Antibodies) and Mus81 (show MUS81 Antibodies) for mediating DNA DSB repair and restraining chromosome missegregation.
The long noncoding RNA, TERRA (show DMRT2 Antibodies) can bind both in cis (show CISH Antibodies) 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 Antibodies) and ATRX share hundreds of target genes and are functionally antagonistic at these loci: whereas TERRA (show DMRT2 Antibodies) 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 Antibodies) and Atrx safeguard the genome by silencing repetitive elements when DNA methylation (show HELLS Antibodies) 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 Antibodies) at particular transcribed genes and facilitates transcriptional elongation through G-rich sequences.
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