Reactivity | HuSpecies Glossary |
Applications | ICC/IF |
Clone | 664703 |
Clonality | Monoclonal |
Host | Mouse |
Conjugate | Unconjugated |
Concentration | LYOPH |
Immunogen | E. coli-derived recombinant human ATM Arg2138-Arg2400 Accession # Q13315 |
Specificity | Detects human ATM in direct ELISAs. In direct ELISAs, no cross-reactivity with recombinant
human ATR is observed. |
Source | N/A |
Isotype | IgG2b |
Clonality | Monoclonal |
Host | Mouse |
Gene | ATM |
Purity Statement | Protein A or G purified from hybridoma culture supernatant |
Innovator's Reward | Test in a species/application not listed above to receive a full credit towards a future purchase. |
Storage | Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
|
Buffer | Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. *Small pack size (SP) is supplied either lyophilized or as a 0.2 µm filtered solution in PBS. |
Preservative | No Preservative |
Concentration | LYOPH |
Reconstitution Instructions | Sterile PBS to a final concentration of 0.5 mg/mL. |
ATM (Ataxia Telangiectasia Mutated) is a 350-370 kDa member of the ATM subfamily, PI3/PI4-kinase family of enzymes. It is ubiquitously expressed, and serves as a DNA damage sensor. ATM is activated via autophosphorylation at double strand breaks. Following activation, multiple substrates are phosphorylated, including Chk2, and ATR is recruited and activated as part of an integrated repair circuit. Human ATM is 3056 amino acids (aa) in length. It contains one FAT (focal adhesion targeting) domain (aa 1960-2566), a PI‑3/PI‑4 kinase catalytic domain (aa 2712-2962) and a second, C-terminal FAT domain (aa 3024-3056). There are at least six Ser and four Thr utilized phosphorylation sites, and one critical acetylation activation site at Lys3016. There are at least four potential splice variants. One shows a Trp substitution for aa 536-3056, a second contains an eight aa substitution for aa 2506-3056, a third possesses a five aa substitution for aa 1637-3056, while a fourth contains a premature truncation after Lys2756. Over aa 2138-2400, human ATM shares 82% aa identity with mouse ATM.
Secondary Antibodies |
Isotype Controls |
Further unraveling the role of gamma H2AX in DNA damage response Our genome experiences a moderate amount of DNA damage in our cells on a daily basis. This DNA damage can be in response to external environmental factors, or be a result of our internal metabolic processes going awry. While normal rates of DNA ... Read full blog post. |
The recent relationship of BRCA1 and 53BP1 The p53-binding protein 1 (53BP1) is a DNA damage response factor, which is recruited to nuclear structures at the site of DNA damage. DNA double-strand breaks (DSBs) are mutations that are detrimental to cell viability and genome stability, and m... Read full blog post. |
Application Highlight: Recent uses of TERF2 in immunofluorescence (IF) Telomeres are a region of repeat nucleotide sequences located at the end of chromosomes to protect our DNA from becoming damaged via end-to-end fusion. TERF2, or telomeric-repeat binding factor 2, is important for telomere integrity and aids in th... Read full blog post. |
ATM - detecting and responding to DNA damage Ataxia telangiectasia mutated (ATM) is essential for the maintenance of genomic stability. ATM is a 370 kDa serine-threonine kinase that is constitutively expressed in various tissues. Although primarily nuclear, ATM is also found at lower levels ... Read full blog post. |
53BP1 - a marker for DNA Double Strand Break 53BP1 (p53 binding protein 1) was originally thought to be an enhancer for p53 transcriptional, but later studies have demonstrated that it is actually a substrate for ataxia telangiectasia mutated (ATM). 53BP1 is a classic late DNA damage response... Read full blog post. |
53BP1 - DNA damage is no fun The 53BP1 (p53 binding protein 1) was initially believed to be a p53 transcriptional enhancing partner, but it has now been established as an ataxia telangiectasia mutated (ATM) substrate. As a late DNA damage response (DDR) marker, 53BP1 appears duri... Read full blog post. |
ATM and DSB Repair in Cancer Ataxia Telangiectasia Mutated (ATM) is a serine/threonine protein kinase that is the master regulator of the DNA double-strand break (DSB) repair pathway. ATM is a key part of the cell cycle machinery that activates checkpoint signaling in response to... Read full blog post. |
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