ATRX Antibodies

Transcriptional regulator ATRX (ATRX)

Facilitates DNA replication in multiple mobile environments and is necessary for efficient replication of a subset of genomic loci. May help stabilizing G-rich regions into routine chromatin structures by remodeling G4 DNA and integrating H3.

3- containing nucleosomes. Catalytic component of the chromatin remodeling complex ATRX:DAXX that has ATP-dependent DNA translocase activity and catalyzes the replication-independent deposition of histone H3.

Gene Information

Human
Gene Name:	ATRX
Uniprot:	P46100
Entrez:	546

Family

Belongs to:
SNF2/RAD54 helicase family

Alternative Names

alpha thalassemia/mental retardation syndrome X-linked (RAD54 (S. cerevisiae)homolog); alpha thalassemia/mental retardation syndrome X-linked (RAD54 homolog, S.cerevisiae); alpha thalassemia/mental retardation syndrome X-linked; ATP-dependent helicase ATRX; ATR2; DNA dependent ATPase and helicase; EC 3.6.1; EC 3.6.4.12; helicase 2, X-linked; Juberg-Marsidi syndrome; MGC2094; MRXHF1; RAD54 homolog; RAD54L; SFM1; SHS; transcriptional regulator ATRX; XH2RAD54; X-linked helicase II; X-linked nuclear protein; XNPZNF-HX; Zinc finger helicase; Znf-HX

Molecular Weight

Mass (kDA):
282.586 kDA

Genomic Context

Human
Location:	Xq21.1
Sequence:	X; NC_000023.11 (77504878..77786235, complement)

Tissue Specificity

Ubiquitous.

Subcellular Localizations

Nucleus. Chromosome, telomere. Nucleus, PML body. Associated with pericentromeric heterochromatin during interphase and mitosis, probably by interacting with CBX5/HP1 alpha. Colocalizes with histone H3.3, DAXX, HIRA and ASF1A at PML-nuclear bodies. Colocalizes with cohesin (SMC1 and SMC3) and MECP2 at the maternal H19 ICR (By similarity).

Diseases

• Alpha-thalassemia
• Alpha-thalassemia/mental Retardation Syndrome, Nondeletion Type, X-linked
• Thalassemia
• Neoplasms
• Leukemia
• Severe Mental Retardation
• Malignant Neoplasms
• Dysmyelopoietic Syndromes
• Acute Promyelocytic Leukemia
• Congenital Anomaly Of Face

• Cytomegalovirus Infections
• Hereditary Diseases
• Pancreatic Neoplasm
• Neuroendocrine Tumors
• Urogenital Abnormalities

Interacting Proteins

• CBX5
• DAXX
• EZH2
• Mecp2
• RAD50

Pathways

• Chromatin Remodeling
• Methylation
• Localization
• Dna Methylation
• Pathogenesis
• Mitosis
• Cell Cycle
• Meiosis
• Brain Development
• Metaphase
• Sex Determination
• Atp-dependent Chromatin Remodeling
• Sex Differentiation

• Spermatogenesis
• Interphase
• Regulation Of Gene Expression
• Cell Death
• Cell Proliferation
• S Phase
• Chromosome Segregation

PTMs

• Methylation
• Phosphorylation
• Sumoylation

• Deacetylation
• Cleavage
• Amidation

• Acetylation

Research Areas

• Cancer
• Checkpoint signaling
• DNA Double Strand Break Repair
• DNA Repair

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/ATRX

Boster Bio - Best Uses Of The ATRX Marker

In 1993, Steven Boster developed his first product which earned him the moniker "he who converts science to the lavatory". His innovations spanned the scope of immunohistochemistry, he developed hundreds of primary antibodies, and he was soon one of the largest catalog antibody companies in China. In the late 90s, Boster had also created his own ELISA platform, PicoKine(tm). This platform uses proprietary trade secrets to provide sensitive ELISA kits, reagents and kits.

Gene infographics

Boster Bio's gene infographics offer brief information on each gene, rather than the lengthy manual. In addition to covering all mouse and human genes that can be accessed using the website's search bar. You can also select one specific gene to conduct further research. If you're a nerd or a novice, the infographics about genes on Boster Bio can aid in understanding the human genome in greater detail.

Predicting gene expression

ATRX is an mRNA that is variable in its levels of expression. The median expression of the marker is the highest and can be used to predict gene expression in various types of cancer cells. The results from the ATRX test are available on CGGA. We will discuss the methods and applications of the ATRX marker to determine gene expression. A case study is presented based on the analysis and interpretation of gene expression data from a single patient.

The ATRX protein is believed to have a sequence that it will begin at mRNA Exon 2911. It's comprised of 2288 amino acids, and an kDa of 260. There are several alternative transcripts for splicing with the longest codifying three-protein transcripts with the same length. Exons 6 and 7, respectively, are both incorporated into the longest transcript. The first methionine is encoded in nucleotide 946, and the predicted protein size is 2288 amino acids and 260 kDa.

An analysis of the ATRX gene structure has revealed that the protein is part of the SNF2 family. The extended sequence reveals that ATRX is a new member of the SNF2 family. The flanking regions of ATRX are in contradiction to previous studies and suggests it is more closely related to the RAD54 gene family rather than the SNF2 group. ATRX is a great candidate for predicting genes by microarrays that use the cDNA.

To predict the expression of genes using the ATRX marker A complete replica of the ATRX cDNA sequence was obtained. The cDNA sequence is 10 448 nucleotides long , and consists of two transcripts that are alternative. The newly acquired sequence was searched for mouse and human ESTs in databases. The results were not significant. These genes are important in both cancer and disease, but they also have many biological functions.

The ATRX altered mRNA expression pattern has the potential to predict astrocytic cancers. Combining mutations in IDH or Ki-67 and the ATRX gene expression pattern can help subclassify astrocytic cancers. This new approach may aid doctors and researchers to determine the best treatment options for cancer patients. For example, for the case of breast cancer, it may aid in predicting the results of a clinical study.

Predicting IDh2/2 mutation

838 samples were analyzed for IDh2/2 mutation analysis. 345 of these samples carried an IDh2/2 mutation. The canonical IDh2 mutation p.R132H was found in 305 samples, while three other samples showed IDH2 mutations p.R172K or p.R172M. Of the remaining nine samples, one contained an IDH2 p.R172W mutation.

The study also examined a subset IDh2/2 mutant tumors with an ATRX mutation. The study found that loss of ATRX changes was significantly connected to an H3F3A p.G34R mutation and only seven patients with IDh2/2 tumors had the K27M mutation. These results suggest that ATRX could be linked to midline gliomas.

Although ATRX interacts with H3.3 It binds many other histones, including histone H3.3. H3.3 is essential to maintain genomic stability. The loss of ATRX hinders tankyrase 1 from resolving telomere-sister cohesion. While it isn't a direct cause of an IDh2/2 mutation, it is one of the most accurate indicators to predict the condition.

Despite the latest advances in molecular test technology, there is still a lot to be learned. A high rate of survival following chemotherapy are linked to IDH mutations in tumors. The TP53 gene is also implicated in IDH mutations. The mutations of IDH and TP53 are also associated with a higher risk of recurrence. Although the results of this study are encouraging, the retrospective nature of the study can make it difficult to determine the prognostic value of these mutations. Prospective studies are required to determine the most effective treatment for this molecular subgroup.

The most frequent reason for cancer-related IDh2 tumors with mutations is the IDh2/2 mutation. IDH mutations are often associated with high levels in histone methylation and a number of CpG islands, which could be a sign of an early stage of tumorigenesis. IDH mutations can be used to determine early glioma formation, but they are not diagnostic tools by themselves.

It has been established that IDH mutations in tumors can identify distinct subsets of patients. These mutations can also be associated with various disease characteristics. These tumors are typically younger, have more frontal lobe involvement and a higher risk of non-enhancing components and have better outcomes than other. The tumours that are found to be suspicious should be discovered early so that they are treated properly.

Predicting MGMT

One method for predicting MGMT is by determining the methylation status of the ATRX marker in tumors. The ATRX gene exhibits a comparatively homogeneous pattern and is highly expressed in gynecologic cancers. The ATRX gene is involved with heterochromatin modifications and preserves the integrity of the genome. It was recently identified as a biomarker of MGMT.

The ATRX gene has a distinctive binding pocket that contains two regions that are sensitive to di-/tri-methylated Lys4 and unmodified Lys9. The ATRX/DAXXX family plays an essential role in maintaining the stability of the genome. It also interacts with MeCP2 and homochromatin protein 1 proteins. It has been proven that the ATRX gene can assist in the formation of heterochromatin in the intracisternal A particle retrotransposons.

IDH mutations are closely connected to the ATRX gene. It has been shown that ATRX mutations can subclassify the glioma patients into groups that have higher survival rates. Doctors can use ATRX status to help them make clinical decisions. The ATRX gene could be a clue to future treatment options for MGMT.

Kaplan-Meier survival rates for 103 patients suffering from MGMT have been calculated. In addition to Kaplan Meier survival estimates, MGMT promoter methylation is related to the TERT promoter mutation. ATRX expression in tumors with both methylation and IDH mutations is a sign of poor outcomes in these patients. In addition, the gene could be a biomarker to detect the glioma.