货号：07-1286

品牌：Merck Millipore

规格：200UL

目录价：￥5053.00

市场价格：￥4295.05

会员价格：￥4042.40

金山科研平台，产品价格货期咨询微信：jinshanbio Description: Anti-ATM Antibody | 07-1286 View All» Promotional Text: Special Shipping Offer on Antibodies100% Performance Guaranteed View All» Trade Name: Upstate (Millipore) View All» Specificity: Detects ATM. View All» Molecular Weight: 350 kDa View All» Epitope: Central View All» Immunogen: KLH-conjugated synthetic peptide containing amino acids of internal human ATM in the Abl interacting domain. View All» Isotype: IgG View All» Background Information: ATM (Ataxia Telangiectasia Mutated kinase) and ATR (Ataxia Telangiectasia and Rad3-related kinase) are related kinases that regulate cell cycle checkpoints and DNA repair. ATM is activated in response to DNA damage and serves to arrest further cell division before the damage can be repaired. Mutation in the ATM gene results in the autosomal recessive disease ataxia telangiectasia (AT). The identified substrates for ATM include p53, p95/NBS1, MDM2, Chk2, BRCA1, CtIP, 4E-BP1 and Chk1. ATM activates p53, increasing p21/Cip1/Waf1 levels, thus blocking activation of Cdk2. That results in Rb hypophosphorylation and blockage of the G1/S transition. Separately, ATM also phosphorylates and activates Chk1, which phosphorylates Cdc25C. This inactivates Cdc25C and prevents it from dephosphorylating the inhibitory phosphotyrosine residue on cdc2/Cdk1, thus preventing the G2/M transition. The complex phenotype of cells derived from patients with AT suggests that ATM has additional cellular substrates. In unirradiated cells, ATM is present as an inactive homodimer or multimer. Double-stranded breaks in DNA caused by ionizing radiation cause rapid ATM kinase activation through dissociation of this complex and ATM autophosphorylation at Ser1981. View All» Species Reactivity:

• Human

• Mouse

• Rat

• Horse

• Bovine
  View All» Species Reactivity Note: Human, Mouse, and Rat. Expected to react with horse and bovine based on 100% sequence homology. View All» Application Notes: Immunofluorescence Confocal Microscopy Analysis:HeLa cells (A & B) and NIH/3T3 cells (C & D) were fixed, permeabilized, and stained using Anti-ATM (Cy3, Red). Cells were co-stained for actin (Phalloidin, AlexaFluor® 488 conjugate, Green) and for panels B & D, staining includes nuclear staining with DAPI (Blue). View All» Control: HeLa nuclear extract View All» Quality Assurance: Routinely evaluated by western blot.Western Blot Analysis: This lot detected ATM at 1:500 dilution in HeLa nuclear extract lysates via SDS-PAGE and transferred to PVDF (Immobilon-P). View All» Purification Method: Antigen affinity purified View All» Presentation: Antigen Affinity purified rabbit serum in 0.1M Tris-Glycine (pH7.4) 15mM NaCl, and 0.05% NaN3. View All» Storage Conditions: Stable for 1 year at 2-8°C from date of receipt.Handling Recommendations: Upon receipt, and prior to removing the cap, centrifuge the vial and gently mix the solution. View All» UniProt Number: Q13315 View All» Entrez Gene Number: NP_000042. View All» Gene Symbol:
  • AT1

  • ATA

  • ATC

  • ATD

  • ATDC

  • ATE

  • DKFZp781A0353 2

  • EC 2.7.11.1 3

  • MGC74674

  • TEL1

  • TELO1
    View All» Alternate Names:
    • ataxia telangiectasia mutated

    • A-T, mutated

    • AT mutated

    • TEL1, telomere maintenance 1, homolog

    • ataxia telangiectasia mutated (includes complementation groups A, C and D)

    • ataxia telangiectasia mutated protein

    • human phosphatidylinositol 3-kinase homolog

    • serine-protein kinase ATM
      View All» Usage Statement: 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. View All» Key Applications:
      • Western Blotting

      • Immunofluorescence
        View All» Entrez Gene Summary: The protein encoded by this gene belongs to the PI3/PI4-kinase family. This protein is an important cell cycle checkpoint kinase that phosphorylates; thus, it functions as a regulator of a wide variety of downstream proteins, including tumor suppressor proteins p53 and BRCA1, checkpoint kinase CHK2, checkpoint proteins RAD17 and RAD9, and DNA repair protein NBS1.This protein and the closely related kinase ATR are thought to be master controllers of cell cycle checkpoint signaling pathways that are required for cell response to DNA damage and for genome stability. Mutations in this gene are associated with ataxia telangiectasia, an autosomal recessive disorder. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq]. View All» UniProt Summary: FUNCTION: Serine/threonine protein kinase which activates checkpoint signaling upon double strand breaks (DSBs), apoptosis and genotoxic stresses such as ionizing ultraviolet A light (UVA), thereby acting as a DNA damage sensor. Recognizes the substrate consensus sequence [ST]-Q. Phosphorylates 'Ser-139' of histone variant H2AX/H2AFX at double strand breaks (DSBs), thereby regulating DNA damage response mechanism. Also involved in signal transduction and cell cycle control. May function as a tumor suppressor. Necessary for activation of ABL1 and SAPK. Phosphorylates p53/TP53, FANCD2, NFKBIA, BRCA1, CTIP, nibrin (NBN), TERF1, RAD9 and DCLRE1C. May play a role in vesicle and/or protein transport. Could play a role in T-cell development, gonad and neurological function. CATALYTIC ACTIVITY: ATP + a protein = ADP + a phosphoprotein. ENZYME REGULATION: Inhibited by wortmannin. SUBUNIT: Exists in monomeric and tetrameric state. Binds DNA ends, p53/TP53, ABL1, BRCA1, NBN/nibrin and TERF1. Part of the BRCA1-associated genome surveillance complex (BASC), which contains BRCA1, MSH2, MSH6, MLH1, ATM, BLM, PMS2 and the RAD50-MRE11-NBN protein complex. This association could be a dynamic process changing throughout the cell cycle and within subnuclear domains. DNA damage promotes association with RAD17. Interacts with EEF1E1. This interaction, which takes place independently of TP53, is induced by DNA damage that may occur during genotoxic stress or cell growth. Interacts with DCLRE1C. Interacts with MYST1. Interacts with HTATIP. Interacts with OBFC2B. SUBCELLULAR LOCATION: Nucleus. Cytoplasmic vesicle. Note=Primarily nuclear. Found also in endocytic vesicles in association with beta-adaptin. TISSUE SPECIFICITY: Found in pancreas, kidney, skeletal muscle, liver, lung, placenta, brain, heart, spleen, thymus, testis, ovary, small intestine, colon and leukocytes. INDUCTION: By ionizing radiation. DOMAIN: The FATC domain is required for interaction with HTATIP. PTM: Phosphorylated by ARK5. Autophosphorylated on Ser-1981 upon DNA damage. PTM: Acetylated by HTATIP upon DNA damage; which is required for autophosphorylation and subsequent activation. DISEASE: Defects in ATM are the cause of ataxia telangiectasia (AT) [MIM:208900]; also known as Louis-Bar syndrome, which includes four complementation groups: A, C, D and E. This rare recessive disorder is characterized by progressive cerebellar ataxia, dilation of the blood vessels in the conjunctiva and eyeballs, immunodeficiency, growth retardation and sexual immaturity. AT patients have a strong predisposition to cancer; about 30% of patients develop tumors, particularly lymphomas and leukemias. Cells from affected individuals are highly sensitive to damage by ionizing radiation and resistant to inhibition of DNA synthesis following irradiation. DISEASE: Defects in ATM 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. The clinical course is highly aggressive, with poor response to chemotherapy and short survival time. TPLL occurs both in adults as a sporadic disease and in younger AT patients. Defects in ATM contribute to DISEASE:B-cell non-Hodgkin lymphomas (BNHL), including mantle cell lymphoma (MCL). DISEASE: Defects in ATM contribute to B-cell chronic lymphocytic leukemia (BCLL). BCLL is the commonest form of leukemia in the elderly. It is characterized by the accumulation of mature CD5+ B lymphocytes, lymphadenopathy, immunodeficiency and bone marrow failure. SIMILARITY: Belongs to the PI3/PI4-kinase family. ATM subfamily. SIMILARITY: Contains 1 FAT domain. SIMILARITY: Contains 1 FATC domain. SIMILARITY: Contains 1 PI3K/PI4K domain. View All» Product Name: Anti-ATM View All» Concentration: 1.0 mg/mL View All» Antibody Type: Polyclonal Antibody View All» Qty/Pk: 200 μL View All» Format: Affinity Purified View All» Host: Rabbit View All»
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