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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 126 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
ATRX mutation was identified in 2/5 (40%) cases with mosaic staining while one case showed DAXX (show DAXX Antibodies) mutation. All these cases were characterized by distinctly separate immune-negative and positive/intermixed foci.
ATRX deficiency was mutually exclusive with LOH. Conversely, ATRX-proficient tumours immunoreactive for R132H-mutant isocitrate dehydrogenase 1 (IDH1 (show IDH1 Antibodies)) showed a high rate (85%) of LOH.
Nuclear ATRX loss, either complete or heterogeneous, is encountered in a considerable number of high-grade sarcomas with non-specific genetic alterations.
data suggest that the presence of ATRX at telomeres may have a central role in suppressing deleterious DNA secondary structures that form at transcribed telomeric repeats, and this may account for the increased DNA damage, stalling of replication and homology-directed repair previously observed upon loss of ATRX function
Both primary Alternative lengthening of telomeres(ALT) -positive and ATRX/DAXX (show DAXX Antibodies)-negative PanNETs are independently associated with aggressive clinicopathologic behavior and displayed reduced recurrence-free survival. In contrast, ALT activation and loss of ATRX/DAXX (show DAXX Antibodies) are both associated with better overall survival in patients with metastases
Whole-exome sequencing has identified recurrent mutations in the genes DAXX (show DAXX Antibodies) and ATRX, which correlate with loss of protein expression and alternative lengthening of telomeres (ALT).ALT and DAXX (show DAXX Antibodies)/ATRX loss in PanNETs was associated with shorter disease-free survival (DFS (show FST Antibodies)) and disease-specific survival (DSS (show NR0B1 Antibodies)) and likely plays a significant role in driving metastatic disease
The results of this study support an important role for ATRX loss and acquisition of ALT in the biology of NF1 (show NF1 Antibodies)-associated gliomas, particularly diffuse and high-grade tumors developing in adults.
We propose that mutations in alpha thalassemia-mental retardation syndrome X-linked (ATRX)/death-domain associated protein (DAXX (show DAXX Antibodies)) prime alternative lengthening of telomeres activation by disrupting telomeric heterochromatin.
Structural and biochemical characterization of DAXX (show DAXX Antibodies)-ATRX interaction.
Structural basis for DAXX (show DAXX Antibodies) interaction with ATRX.
PML (show PML Antibodies) protein organizes heterochromatin domains where it regulates histone H3.3 (show H3F3A Antibodies) deposition by ATRX and DAXX (show DAXX Antibodies).
Gene expression changes in the Atrx-null retina indicate defective synaptic structure and neuronal circuitry, suggest excitotoxic mechanisms of neurodegeneration, and demonstrate that common targets of ATRX in the forebrain and retina may contribute to similar neuropathological processes underlying cognitive impairment and visual dysfunction in ATR-X syndrome.
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.
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.
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
, HP1 alpha-interacting protein
, alpha thalassemia/mental retardation syndrome (X-linked)
, heterochromatin protein 2
, alpha thalassemia/mental retardation syndrome X-linked homolog
, helicase II
, alpha thalassemia/mental retardation syndrome X-linked (RAD54 homolog)