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Mouse Anti-ATR Recombinant Antibody (1E9) (CBMAB-A4129-YC)

Provided herein is a Mouse monoclonal antibody against Human ATR Serine/Threonine Kinase. The antibody can be used for immunoassay techniques, such as ELISA, IHC.
See all ATR antibodies
Published Data
Fig.1 Microphotograph of ATR and pCHEK1 negative and positive breast cancer tissue.
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Fig.2 Western blot analysis in chinese hamster (CH) cells (CHO9, EM-C11, EM-C12).
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Fig.3 Western blotting analysis for PTEN, ATR expression in breast cancer cell lines.
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Summary

Host Animal
Mouse
Specificity
Human
Clone
1E9
Antibody Isotype
IgG1, κ
Application
ELISA, IHC

Basic Information

Immunogen
Recombinant corresponding to human ATR, NP_001175, aa 2545-2645 with GST tag.
Specificity
Human
Antibody Isotype
IgG1, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.
ApplicationNote
IHC3 µg/ml

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
PBS, pH 7.4
Preservative
None
Concentration
Batch dependent
Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
ataxia telangiectasia and Rad3 related
Introduction
ATR is a serine/threonine kinase and DNA damage sensor, activating cell cycle checkpoint signaling upon DNA stress. The encoded protein can phosphorylate and activate several proteins involved in the inhibition of DNA replication and mitosis, and can prom
Entrez Gene ID
545
UniProt ID
Q13535
Alternative Names
ATR Serine/Threonine Kinase; Ataxia Telangiectasia And Rad3-Related Protein; EC 2.7.11.1; FRP1; MEC1, Mitosis Entry Checkpoint 1, Homolog (S. Cerevisiae); MEC1, Mitosis Entry Checkpoint 1, Homolog; Ataxia Telangiectasia And Rad3 Related; Serine/Threonine-
Function
Serine/threonine protein kinase which activates checkpoint signaling upon genotoxic stresses such as ionizing radiation (IR), ultraviolet light (UV), or DNA replication stalling, thereby acting as a DNA damage sensor. Recognizes the substrate consensus sequence [ST]-Q. Phosphorylates BRCA1, CHEK1, MCM2, RAD17, RPA2, SMC1 and p53/TP53, which collectively inhibit DNA replication and mitosis and promote DNA repair, recombination and apoptosis. Phosphorylates 'Ser-139' of histone variant H2AX at sites of DNA damage, thereby regulating DNA damage response mechanism. Required for FANCD2 ubiquitination. Critical for maintenance of fragile site stability and efficient regulation of centrosome duplication. Positively regulates the restart of stalled replication forks following activation by the KHDC3L-OOEP scaffold complex (By similarity).
Biological Process
Cellular response to DNA damage stimulus Source: UniProtKB
Cellular response to gamma radiation Source: BHF-UCL
Cellular response to UV Source: BHF-UCL
DNA damage checkpoint Source: UniProtKB
DNA repair Source: ProtInc
DNA replication Source: Reactome
Establishment of protein-containing complex localization to telomere Source: BHF-UCL
Establishment of RNA localization to telomere Source: BHF-UCL
Interstrand cross-link repair Source: Reactome
Multicellular organism development Source: ProtInc
Negative regulation of DNA replication Source: UniProtKB
Peptidyl-serine phosphorylation Source: BHF-UCL
Positive regulation of DNA damage response, signal transduction by p53 class mediator Source: BHF-UCL
Positive regulation of telomerase catalytic core complex assembly Source: BHF-UCL
Positive regulation of telomere maintenance via telomerase Source: BHF-UCL
Protein autophosphorylation Source: BHF-UCL
Protein localization to chromosome, telomeric region Source: BHF-UCL
Regulation of cellular response to heat Source: Reactome
Regulation of signal transduction by p53 class mediator Source: Reactome
Replication fork processing Source: UniProtKB
Replicative senescence Source: BHF-UCL
Response to drug Source: Ensembl
Telomere maintenance Source: GO_Central
Cellular Location
Nucleus; Chromosome. Depending on the cell type, it can also be found in PML nuclear bodies. Recruited to chromatin during S-phase. Redistributes to discrete nuclear foci upon DNA damage, hypoxia or replication fork stalling.
Involvement in disease
Seckel syndrome 1 (SCKL1): A rare autosomal recessive disorder characterized by proportionate dwarfism of prenatal onset associated with low birth weight, growth retardation, severe microcephaly with a bird-headed like appearance, and mental retardation.
Cutaneous telangiectasia and cancer syndrome, familial (FCTCS): A disease characterized by cutaneous telangiectases in infancy with patchy alopecia over areas of affected skin, thinning of the lateral eyebrows, and mild dental and nail anomalies. Affected individuals are at increased risk of developing oropharyngeal cancer, and other malignancies have been reported as well.
PTM
Phosphorylated; autophosphorylates in vitro.

Mustafa, A. H. M., & Krämer, O. H. (2021). Novel insight into mechanisms for ATR activation by chromatin structures. Archives of Toxicology, 1-2.

Yang, J., Wang, J., Liang, Y., Wang, J., Hsu, J., Liu, G., ... & Chen, Y. (2021). ATR and BRCA2 simultaneous mutation in a ccRCC with sarcomatoid differentiation and extensive metastases: a case report. Urology.

Guo, J., Zhang, L., Lian, L., Hao, M., Chen, S., & Hong, Y. (2020). CircATP2B4 promotes hypoxia-induced proliferation and migration of pulmonary arterial smooth muscle cells via the miR-223/ATR axis. Life Sciences, 262, 118420.

Fuller, M., Mozer, B., & Van Pevenage, P. (2020). Non-ionizing electromagnetic field impact on ATR expression in Tetrahymena thermophila.

Brunner, A. M. (2019). Ceralasertib. ATR kinase inhibitor, Treatment of cancer. DRUGS OF THE FUTURE, 44(10), 767-777.

Corcoles-Saez, I., Dong, K., & Cha, R. S. (2019). Versatility of the Mec1 ATM/ATR signaling network in mediating resistance to replication, genotoxic, and proteotoxic stresses. Current genetics, 65(3), 657-661.

Rozpędek, W., Pytel, D., Nowak-Zduńczyk, A., Lewko, D., Wojtczak, R., Diehl, J. A., & Majsterek, I. (2019). Breaking the DNA damage response via serine/threonine kinase inhibitors to improve cancer treatment. Current medicinal chemistry, 26(8), 1425-1445.

Saito, Y. D., Li, Z., Lustberg, M., Grenade, C., & Wesolowski, R. (2018). Remarkable response to a novel ATR inhibitor in a patient with poorly differentiated neuroendocrine carcinoma. Cancer treatment and research communications, 16, 9-12.

Jones, S. E., Fleuren, E. D., Frankum, J., Konde, A., Williamson, C. T., Krastev, D. B., ... & Lord, C. J. (2017). ATR is a therapeutic target in synovial sarcoma. Cancer research, 77(24), 7014-7026.

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For research use only. Not intended for any clinical use.

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