ATRX Antibody [B2B21] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat, Monkey

Usage Information

Dilution
WB1:1000 IP1:100 IHC1:150 - 1:600

Application
WB, IP, IHC

Reactivity
Human, Mouse, Rat, Monkey

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
280 kDa

Positive Control	Mouse colon; Human colon carcinoma; Human esophageal carcinoma; Human parathyroid; Human prostate carcinoma; Human gastric carcinoma; Human uterus ; SH-SY5Y cells; LN-18 cells; SK-N-MC cells; MOLT-4 cells; NIH/3T3 cells; H-4-II-E cells; COS-7 cells
Negative Control	Saos-2 cells; U-2-02 cells

Datasheet & SDS

Biological Description

Specificity
ATRX Antibody [B2B21] detects endogenous levels of total ATRX protein.

Clone
B2B21

Synonym(s)
Transcriptional regulator ATRX; ATP-dependent helicase ATRX; X-linked helicase II; X-linked nuclear protein (XNP); Znf-HX; ATRX; RAD54L; XH2

Background
ATRX, or alpha-thalassemia/mental retardation syndrome X-linked, is a SWI/SNF family chromatin remodeler and ATPase/helicase that partners with DAXX to deposit the histone variant H3.3 at heterochromatic regions such as telomeres, pericentromeres, and ribosomal DNA repeats, as well as at euchromatic regulatory elements, thereby ensuring genomic stability, replication fidelity, and precise control of gene expression. ATRX features an N-terminal ADD domain that binds H3K9 trimethylation through a plant homeodomain finger, a central SNF2-like helicase core with seven motifs for ATP hydrolysis and DNA translocation, a C-terminal SWI/SNF ATPase domain, and zinc fingers including those that recognize G-quadruplex DNA; key residues enable specific deposition of H3.3 without nucleosome assembly activity. The primary function of ATRX involves binding G-quadruplex structures, putative quadruplex sequences, and CpG islands to maintain chromatin accessibility at active promoters and enhancers, increasing marks such as H3K4 trimethylation and H3K27 acetylation and promoting transcription factor occupancy by factors like RUNX3 and GATA1. ATRX deposits H3.3 to facilitate replication-coupled repair and elongation, indicated by H3K36 trimethylation, represses telomeric RNA, and coordinates sister chromatid cohesion and meiosis through stochastic single-cell effects at alpha-globin and zinc finger gene loci. ATRX supports S-phase progression through MRN complex recruitment and replication fork restart, enables homologous recombination repair subpathways, and contributes to developmental gene silencing, while its loss results in heterogeneous chromatin closure, replication stress, and alternative lengthening of telomeres in cancer cells. ATRX mutations cause ATR-X syndrome, characterized by intellectual disability and alpha-thalassemia due to globin dysregulation, and ATRX loss in cancers such as pancreatic neuroendocrine tumors and glioblastomas enables telomerase-independent survival.

Background

ATRX, or alpha-thalassemia/mental retardation syndrome X-linked, is a SWI/SNF family chromatin remodeler and ATPase/helicase that partners with DAXX to deposit the histone variant H3.3 at heterochromatic regions such as telomeres, pericentromeres, and ribosomal DNA repeats, as well as at euchromatic regulatory elements, thereby ensuring genomic stability, replication fidelity, and precise control of gene expression. ATRX features an N-terminal ADD domain that binds H3K9 trimethylation through a plant homeodomain finger, a central SNF2-like helicase core with seven motifs for ATP hydrolysis and DNA translocation, a C-terminal SWI/SNF ATPase domain, and zinc fingers including those that recognize G-quadruplex DNA; key residues enable specific deposition of H3.3 without nucleosome assembly activity. The primary function of ATRX involves binding G-quadruplex structures, putative quadruplex sequences, and CpG islands to maintain chromatin accessibility at active promoters and enhancers, increasing marks such as H3K4 trimethylation and H3K27 acetylation and promoting transcription factor occupancy by factors like RUNX3 and GATA1. ATRX deposits H3.3 to facilitate replication-coupled repair and elongation, indicated by H3K36 trimethylation, represses telomeric RNA, and coordinates sister chromatid cohesion and meiosis through stochastic single-cell effects at alpha-globin and zinc finger gene loci. ATRX supports S-phase progression through MRN complex recruitment and replication fork restart, enables homologous recombination repair subpathways, and contributes to developmental gene silencing, while its loss results in heterogeneous chromatin closure, replication stress, and alternative lengthening of telomeres in cancer cells. ATRX mutations cause ATR-X syndrome, characterized by intellectual disability and alpha-thalassemia due to globin dysregulation, and ATRX loss in cancers such as pancreatic neuroendocrine tumors and glioblastomas enables telomerase-independent survival.

References
https://pubmed.ncbi.nlm.nih.gov/21653732/ https://pubmed.ncbi.nlm.nih.gov/37190157/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%