A1106
Anti-ATM antibody,Mouse monoclonal
clone MAT3-4G10/8, purified from hybridoma cell culture
別名:
Anti-Ataxia-Telangiectasia Mutated
製品名
Anti-ATM antibody,Mouse monoclonal, clone MAT3-4G10/8, purified from hybridoma cell culture
biological source
mouse
recombinant
expressed in mouse cell line
conjugate
unconjugated
antibody form
purified from hybridoma cell culture
antibody product type
primary antibodies
clone
MAT3-4G10/8, monoclonal
form
PBS solution
mol wt
antigen ~300 kDa
species reactivity
human, mouse
packaging
antibody small pack of 25 μL
concentration
~2 mg/mL
technique(s)
immunoprecipitation (IP): suitable
indirect ELISA: suitable
western blot: 0.1-0.2 μg/mL using HEK-293T total cel extract
isotype
IgG1
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Quality Level
Gene Information
human ... ATM(472)
mouse ... Atm(11920)
Application
Monoclonal Anti-ATM antibody can be used in immunoblotting , ELISA and immunoprecipitation.
Biochem/physiol Actions
Anti-Ataxia-Telangiectasia Mutated (ATM) is responsible for the activation and stabilization of p53 in response to double-strand break (DSB). ATM phosphorylates p53 directly on Ser15 and concomitantly activates other kinases that phosphorylate the same molecule on additional sites. Furthermore, human homolog of double minute 2 (Hdm2) is phosphorylated by ATM on Ser395 and this phosphorylation inhibits Hdm2-mediated degradation of p53.
Monoclonal Anti-ATM antibody reacts specifically with mouse and human ATM.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
General description
Monoclonal Anti-ATM (mouse IgG1 isotype) is derived from the hybridoma MAT3-4G10/8 produced by the fusion of mouse myeloma cells (NSO) and splenocytes from BALB/c mice immunized with a peptide.
Immunogen
peptide spanning positions 1967-1988 of mouse ATM containing a cysteine at its NH2 terminus coupled to KLH.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide
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保管分類
10 - Combustible liquids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
ATM-dependent phosphorylation of Mdm2 on serine 395: role in p53 activation by DNA damage
Maya R, et al.
Genes & Development, 15(9), 1067-1067 (2001)
Jasmin Roohi et al.
Journal of human genetics, 62(5), 581-584 (2017-01-27)
Ataxia-telangiectasia (A-T) is an autosomal recessive chromosome breakage disorder caused by mutations in the ATM gene. Typically, it presents in early childhood with progressive cerebellar dysfunction along with immunodeficiency and oculocutaneous telangiectasia. An increased risk of malignancy is also associated
Phosphorylation of Hdmx mediates its Hdm2- and ATM-dependent degradation in response to DNA damage
Pereg Y, et al.
Proceedings of the National Academy of Sciences of the USA, 102(14), 5056-5061 (2005)
Tatiana N Moiseeva et al.
DNA repair, 43, 9-17 (2016-05-29)
We describe a dynamic phosphorylation on serine-1940 of the catalytic subunit of human Pol ε, POLE1, following DNA damage. We also describe novel interactions between POLE1 and the iron-sulfur cluster assembly complex CIA proteins CIAO1 and MMS19. We show that
Domenico Delia et al.
Human molecular genetics, 13(18), 2155-2163 (2004-07-23)
Hypomorphic mutations of the MRE11 gene are the hallmark of the radiosensitive ataxia-telangiectasia-like disorder (ATLD). Here, we describe a new family with two affected siblings, ATLD5 and ATLD6, now aged 37 and 36, respectively. They presented with late onset cerebellar
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