ATM Antibody (N-term) Blocking Peptide
€363.00
In stock
SKU
AC-BP8046a
Background:
ATM is involved in signal transduction, cell cycle control and DNA repair, and may function as a tumor suppressor. It is necessary for activation of ABL1 and SAPK, and phosphorylates p53, NFKBIA, BRCA1, CTIP, NIBRIN (NBS1), TERF1, and RAD9. This protein has potential roles in vesicle and/or protein transport, T-cell development, gonad and neurological function. ATM is also part of the BRCA1-associated genome surveillance complex. ATM is induced by ionizing radiation. Defects in ATM are the cause of ataxia talangiectasia (AT), also known as Louis-Bar syndrome, a rare recessive disorder characterized by progressive cerebellar ataxia, dilation of the blood vessels in the conjunctiva and eyeballs, immunodeficiency, growth retardation and sexual immaturity. About 30% of AT patients develop lymphomas and leukemias. Defects in ATM also contribute to T-cell acute lymphoblastic leukemia (TALL) and T-prolymphocytic leukemia (TPLL). TPLL is characterized by a high white blood cell count, with a predominance of prolymphocytes, marked splenomegaly, lymphadenopathy, skin lesions and serous effusion. Defects in ATM also contribute to B-cell non-Hodgkin's lymphomas, and to B-cell chronic lymphocytic leukemia, a disease characterized by accumulation of mature CD5+ B lymphocytes, lymphadenopathy, immunodeficiency and bone marrow failure.
Other Names:
Serine-protein kinase ATM, Ataxia telangiectasia mutated, A-T mutated, ATM
Target/Specificity:
The synthetic peptide sequence used to generate the antibody AP8046a was selected from the N-term region of human ATM . A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.
Gene Name: ATM
Gene ID: 472
Primary Accession: Q13315
Format: Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed.
ATM is involved in signal transduction, cell cycle control and DNA repair, and may function as a tumor suppressor. It is necessary for activation of ABL1 and SAPK, and phosphorylates p53, NFKBIA, BRCA1, CTIP, NIBRIN (NBS1), TERF1, and RAD9. This protein has potential roles in vesicle and/or protein transport, T-cell development, gonad and neurological function. ATM is also part of the BRCA1-associated genome surveillance complex. ATM is induced by ionizing radiation. Defects in ATM are the cause of ataxia talangiectasia (AT), also known as Louis-Bar syndrome, a rare recessive disorder characterized by progressive cerebellar ataxia, dilation of the blood vessels in the conjunctiva and eyeballs, immunodeficiency, growth retardation and sexual immaturity. About 30% of AT patients develop lymphomas and leukemias. Defects in ATM also contribute to T-cell acute lymphoblastic leukemia (TALL) and T-prolymphocytic leukemia (TPLL). TPLL is characterized by a high white blood cell count, with a predominance of prolymphocytes, marked splenomegaly, lymphadenopathy, skin lesions and serous effusion. Defects in ATM also contribute to B-cell non-Hodgkin's lymphomas, and to B-cell chronic lymphocytic leukemia, a disease characterized by accumulation of mature CD5+ B lymphocytes, lymphadenopathy, immunodeficiency and bone marrow failure.
Other Names:
Serine-protein kinase ATM, Ataxia telangiectasia mutated, A-T mutated, ATM
Target/Specificity:
The synthetic peptide sequence used to generate the antibody AP8046a was selected from the N-term region of human ATM . A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.
Gene Name: ATM
Gene ID: 472
Primary Accession: Q13315
Format: Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed.
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