The checkpoint kinase ATM (ataxia telangiectasia mutated) transduces genomic stress signals to halt cell cycle progression and promote DNA repair in response to DNA damage.
| Institute |
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| Cancer Research UK, London Research Institute: Lincoln's Inn Fields |
| Cat. #: | 151460 |
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| Tool sub type: | Primary antibody |
| Unit size: | 100 ug |
| Research Fields: | Genetics |
| Application: | IF ; IP ; WB |
| Target: | Ataxia Telangiectasia Mutated Interacting protein (ATMIN, ASCIZ) |
| Reactivity: | Human |
| Clone: | ATMIN 11F4 |
| Host: | Mouse |
| Class: | Monoclonal |
| Product description: | The checkpoint kinase ATM (ataxia telangiectasia mutated) transduces genomic stress signals to halt cell cycle progression and promote DNA repair in response to DNA damage. ATMIN (ATM INteracting protein) is an essential cofactor for ATM. ATMIN interacts with ATM through a C-terminal motif, which is also present in Nijmegen breakage syndrome (NBS) 1. |
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| Conjugation: | Unconjugated |
| Isotype: | IgG2a |
| Immunogen: | Synthetic peptide |
| Myeloma used: | Sp2/0-Ag14 |
| Target background: | The checkpoint kinase ATM (ataxia telangiectasia mutated) transduces genomic stress signals to halt cell cycle progression and promote DNA repair in response to DNA damage. ATMIN (ATM INteracting protein) is an essential cofactor for ATM. ATMIN interacts with ATM through a C-terminal motif, which is also present in Nijmegen breakage syndrome (NBS) 1. |
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| Format: | Liquid |
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| Storage buffer: | PBS with 0.02% azide |
| Storage conditions: | -80° C |
| Shipping conditions: | Dry ice |
| References: |
Kanu et al. 2007. EMBO J. 26(12):2933-41. PMID: 17525732. ATMIN defines an NBS1-independent pathway of ATM signalling. |
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