ATR Antibody (YA7579)
(Synonyms: FRP1, ATR, Serine/threonine-protein kinase ATR, Ataxia telangiectasia and Rad3-related protein, FRAP-related protein 1)
Based on 1 Customer Validation
ATR Antibody (YA7579) is a Rabbit-derived and non-conjugated IgG, Kappa monoclonal antibody, targeting to ATR.
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, ICC/IF, IP, ELISA
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Reactivity :
Human, Mouse, Rat
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Formulation:
Supplied in PBS (pH7.4) containing 50% glycerol, 0.05% Proclin 300, 0.05%BSA
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Conjugation:
Non-conjugated
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Applications
| Application |
WB
WB: Western Blot
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ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
ELISA
ELISA: Enzyme Linked Immunosorbent Assay
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IP
IP: Immunoprecipitation
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|---|---|---|---|---|
| Dilution Ratio | 1:1000-1:5000 | 1:200-1:1000 | 1:5000-1:20000 | 1:50-1:200 |
Product Details
ATR Antibody (YA7579) is a Rabbit-derived and non-conjugated IgG, Kappa monoclonal antibody, targeting to ATR.
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Host Rabbit
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Clonality Monoclonal,Recombinant
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Species ReactivityHuman, Mouse, Rat
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Observed Molecular WeightObserved band size: 301 kDa
Note: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 301 kDa
The exact sequence is proprietary to MCE.
Endogenous
Protein A affinity purified
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS (pH7.4) containing 50% glycerol, 0.05% Proclin 300, 0.05%BSA
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Concentration
Batch-dependent, Please check the COA for the concentration of each lot. Check Lot Concentration
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
Ataxia telangiectasia mutated (ATM) encodes a serine/threonine protein kinase that coordinates cellular signaling after DNA double-strand breaks, oxidative stress, and cell-cycle checkpoint activation[1]. Mechanistically, ATM and ATR (ATM-Rad3-related) act as proximal DNA damage response kinases, but ATM is central to double-strand-break signaling, whereas ATR leads a parallel cascade activated by replication stress[2][3]. In disease contexts, ATM mutation causes ataxia-telangiectasia, a multisystem disorder involving neurodegeneration, immunodeficiency, radiosensitivity, cancer susceptibility, and genetic instability[4][5]. Compared with ATR, ATM deficiency creates experimental dependence on ATR in some cancer models, supporting ATR inhibition as a synthetic-lethal strategy in ATM-deficient prostate cancer and colorectal xenograft models[6][7]. For research applications, ATM inhibitors such as KU-55933 help interrogate ATM-dependent DNA damage signaling and have reduced HSV-1 replication and stromal keratitis severity in experimental corneal models[8].
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Subcellular Localization
Nucleus,Chromosome,Nucleus envelope
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Expression
Tissue_Specificity: Ubiquitous, with highest expression in testis|Isoform 2 is found in pancreas, placenta and liver but not in heart, testis and ovary -
Isoforms & Post-Translational Modification
Q13535 has three isomers: Q13535-1: 301367 Da (predicted); Q13535-2: 294219 Da (predicted); Q13535-3: 297479 Da (predicted).
Phosphorylated (PubMed:21144835) -
Subunit
Forms a heterodimer with ATRIP, forming the ATR-ATRIP complex (PubMed:11721054, PubMed:12791985, PubMed:14729973, PubMed:15758953, PubMed:21777809)
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SwissProt ID
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Synonyms
FRP1, ATR, Serine/threonine-protein kinase ATR, Ataxia telangiectasia and Rad3-related protein, FRAP-related protein 1
Documentation
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Data Sheet (260 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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User Guide for Antibodies (1077 KB)
References
[1]. Amirifar P, et al. Ataxia-telangiectasia: A review of clinical features and molecular pathology. Pediatr Allergy Immunol. 2019 May;30(3):277-288. [Content Brief]
[2]. Mu JJ, et al. A proteomic analysis of ataxia telangiectasia-mutated (ATM)/ATM-Rad3-related (ATR) substrates identifies the ubiquitin-proteasome system as a regulator for DNA damage checkpoints. J Biol Chem. 2007 Jun 15;282(24):17330-4. [Content Brief]
[3]. Balmus G, et al. Disease severity in a mouse model of ataxia telangiectasia is modulated by the DNA damage checkpoint gene Hus1. Hum Mol Genet. 2012 Aug 1;21(15):3408-20. [Content Brief]
[4]. Meyn MS. Ataxia-telangiectasia, et al. Ataxia-telangiectasia, cancer and the pathobiology of the ATM gene. Clin Genet. 1999 May;55(5):289-304. [Content Brief]
[5]. Putti S, et al. ATM Kinase Dead: From Ataxia Telangiectasia Syndrome to Cancer. Cancers (Basel). 2021 Nov 1;13(21):5498. [Content Brief]
[6]. Gulliver C, et al. Ataxia-telangiectasia mutated and ataxia telangiectasia and Rad3-related kinases as therapeutic targets and stratification indicators for prostate cancer. Int J Biochem Cell Biol. 2022 Jun;147:106230. [Content Brief]
[7]. Shao J, et al. Design, Synthesis, and Biological Evaluation of Potent and Selective Inhibitors of Ataxia Telangiectasia Mutated and Rad3-Related (ATR) Kinase for the Efficient Treatment of Cancer. Molecules. 2023 Jun 2;28(11):4521. [Content Brief]
[8]. Alekseev O, et al. Inhibition of ataxia telangiectasia mutated (ATM) kinase suppresses herpes simplex virus type 1 (HSV-1) keratitis. Invest Ophthalmol Vis Sci. 2014 Feb 3;55(2):706-15. [Content Brief]
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