| Reactivity | Hu, Mu, RtSpecies Glossary |
| Applications | WB, Simple Western |
| Clonality | Polyclonal |
| Host | Rabbit |
| Conjugate | Unconjugated |
| Immunogen | Phosphopeptide containing human ATM S1981 site |
| Modification | p Ser1981 |
| Specificity | Detects human ATM when phosphorylated at S1981. Also detects the comparable phosphorylated sites in mouse ATM (S1987) and rat ATM (S1952). |
| Source | N/A |
| Isotype | IgG |
| Clonality | Polyclonal |
| Host | Rabbit |
| Gene | ATM |
| Purity Statement | Antigen Affinity-purified |
| Innovator's Reward | Test in a species/application not listed above to receive a full credit towards a future purchase. |
| Dilutions |
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| Application Notes | In Simple Western only 10-15 uL of the recommended dilution is used per data point. |
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| Storage | Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
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| 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 |
| Reconstitution Instructions | Reconstitute at 0.2 mg/mL in sterile PBS. |
The Ataxia telangiectasia-mutated (ATM) protein kinase exists as a dimer in the cell nucleus. Changes in DNA structure induced by genotoxic stress lead to activation of ATM and phosphorylation of S1981 in trans. Once S1981 is phosphorylated, the dimer dissociates and active ATM monomers signal to downstream targets.
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| Images | Ratings | Applications | Species | Date | Details | ||||||||
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Enlarge |
reviewed by:
Yongkang Yang |
WB | Human | 10/28/2020 |
Summary
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Secondary Antibodies |
Isotype Controls |
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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. |
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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. |
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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. |
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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. |
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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. |
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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. |
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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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| Gene Symbol | ATM |
![TCL cell lines show intrinsic DNA damage and basal activation of DDR. Healthy T lymphocytes isolated from healthy donors and malignant T cell lines (OCI-Ly12, KARPAS-299, SUP-T1, HH, HD-MAR-2, and JURKAT) were subjected to immunofluorescence for the evaluation of gamma H2AX or 53BP1 foci (A,B). The percentage (%) of cells displaying foci and the number of foci/cell in the subsets of cells with detectable foci are reported in (A,B), respectively. Data are expressed as the mean ± SD of independent experiments. Asterisks indicate statistically significant differences between each cell line and healthy T lymphocytes (* p < 0.05; ** p < 0.01; *** p < 0.001; ns: not significant). Representative immunofluorescence images (C,D) of experiments described in (A,B), original microscope magnification 100×. SUP-T1 cells were exposed to increasing concentrations of CHOEP (IC50, 4× and 8×, as in [5]) or to 20 μM etoposide for 3 h. After harvesting, untreated and treated cell lysates were analyzed by Western blot using the indicated antibodies (E). Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/35409194), licensed under a CC-BY license. Not internally tested by R&D Systems.](http://images.novusbio.com/fullsize/af1655_phospho-atm-s1981-affinity-purified-polyclonal-ab-228202417335.jpg "TCL cell lines show intrinsic DNA damage and basal activation of DDR. Healthy T lymphocytes isolated from healthy donors and malignant T cell lines (OCI-Ly12, KARPAS-299, SUP-T1, HH, HD-MAR-2, and JURKAT) were subjected to immunofluorescence for the evaluation of gamma H2AX or 53BP1 foci (A,B). The percentage (%) of cells displaying foci and the number of foci/cell in the subsets of cells with detectable foci are reported in (A,B), respectively. Data are expressed as the mean ± SD of independent experiments. Asterisks indicate statistically significant differences between each cell line and healthy T lymphocytes (* p < 0.05; ** p < 0.01; *** p < 0.001; ns: not significant). Representative immunofluorescence images (C,D) of experiments described in (A,B), original microscope magnification 100×. SUP-T1 cells were exposed to increasing concentrations of CHOEP (IC50, 4× and 8×, as in [5]) or to 20 μM etoposide for 3 h. After harvesting, untreated and treated cell lysates were analyzed by Western blot using the indicated antibodies (E). Image collected and cropped by CiteAb from the following publication (//pubmed.ncbi.nlm.nih.gov/35409194), licensed under a CC-BY license. Not internally tested by R&D Systems.")
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![Western Blot: Goat anti-Rabbit IgG (H+L) Secondary Antibody [HRP] [NB7160] - Western blot showing vemurafenib treatment in BRAFV600E CRC cells inhibits fission mediator DRP1 with no significant effect on fusion proteins (Mfn1 & 2) using MFN-1 antibody (NBP1-51841) and corresponding secondary antibody, goat anti-rabbit IgG-HRP (NB7160). Image collected and cropped by CiteAb from the following publication (https://pubmed.ncbi.nlm.nih.gov/33738242).](https://images.novusbio.com/images/Goat-anti-Rabbit-IgG-H+L-Secondary-Antibody-HRP-Western-Blot-NB7160-img0001.jpg "Western Blot: Goat anti-Rabbit IgG (H+L) Secondary Antibody [HRP] [NB7160] - Western blot showing vemurafenib treatment in BRAFV600E CRC cells inhibits fission mediator DRP1 with no significant effect on fusion proteins (Mfn1 & 2) using MFN-1 antibody (NBP1-51841) and corresponding secondary antibody, goat anti-rabbit IgG-HRP (NB7160). Image collected and cropped by CiteAb from the following publication (https://pubmed.ncbi.nlm.nih.gov/33738242).")
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