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anti-Human ATM Antikörper:
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Human Monoclonal ATM Primary Antibody für ChIP, ELISA - ABIN151775
Naka, Tachibana, Ikeda, Motoyama: Stress-induced premature senescence in hTERT-expressing ataxia telangiectasia fibroblasts. in The Journal of biological chemistry 2004
Show all 114 Pubmed References
Human Polyclonal ATM Primary Antibody für ICC, FACS - ABIN151030
Out, Hoekstra, de Jager, de Vos, van der Westhuyzen, Webb, Van Eck, Biessen, Van Berkel: Adenovirus-mediated hepatic overexpression of scavenger receptor class B type I accelerates chylomicron metabolism in C57BL/6J mice. in Journal of lipid research 2005
Show all 76 Pubmed References
Human Monoclonal ATM Primary Antibody für ICC, IF - ABIN151622
Lai, Chun, Nahas, Mitui, Gamo, Du, Gatti: Correction of ATM gene function by aminoglycoside-induced read-through of premature termination codons. in Proceedings of the National Academy of Sciences of the United States of America 2004
Show all 26 Pubmed References
Human Monoclonal ATM Primary Antibody für ICC, IF - ABIN151772
Yalcin, Zhang, Luciano, Mungamuri, Marinkovic, Vercherat, Sarkar, Grisotto, Taneja, Ghaffari: Foxo3 is essential for the regulation of ataxia telangiectasia mutated and oxidative stress-mediated homeostasis of hematopoietic stem cells. in The Journal of biological chemistry 2008
Show all 19 Pubmed References
Human Polyclonal ATM Primary Antibody für IHC - ABIN362100
Kang, Guo, Tan, Zhao, Tang, Lu: Expression status of ataxia-telangiectasia-mutated gene correlated with prognosis in advanced gastric cancer. in Mutation research 2008
Show all 8 Pubmed References
Human Polyclonal ATM Primary Antibody für IP, PLA - ABIN151739
Kirshner, Jobling, Pajares, Ravani, Glick, Lavin, Koslov, Shiloh, Barcellos-Hoff: Inhibition of transforming growth factor-beta1 signaling attenuates ataxia telangiectasia mutated activity in response to genotoxic stress. in Cancer research 2006
Show all 4 Pubmed References
Human Monoclonal ATM Primary Antibody für ICC, IF - ABIN2668604
Shrivastav, Miller, De Haro, Durant, Chen, Chen, Nickoloff: DNA-PKcs and ATM co-regulate DNA double-strand break repair. in DNA repair 2009
Show all 3 Pubmed References
Human Monoclonal ATM Primary Antibody für ELISA, WB - ABIN965618
ORegan, Kiely, OGara: Expression of the adenyl cyclase-encoding gene (cya) of Rhizobium meliloti F34: existence of two cya genes? in Gene 1990
Show all 4 Pubmed References
Human Monoclonal ATM Primary Antibody für BI, WB - ABIN2688845
Pellegrini, Celeste, Difilippantonio, Guo, Wang, Feigenbaum, Nussenzweig: Autophosphorylation at serine 1987 is dispensable for murine Atm activation in vivo. in Nature 2006
Show all 2 Pubmed References
Human Polyclonal ATM Primary Antibody für IP, WB - ABIN151738
Dirlam, Spike, Macleod: Deregulated E2f-2 underlies cell cycle and maturation defects in retinoblastoma null erythroblasts. in Molecular and cellular biology 2007
Show all 2 Pubmed References
our data indicate that ATR and ATM are both needed for intestinal stem cell maintenance and proliferation; ATR seems to play a bigger role than does ATM.
TCTP (zeige TPT1 Antikörper) has a role in regulating ATM activity to control genome stability and organ development in Drosophila melanogaster
A stringent requirement for the conserved function of Ataxia Telangiectasia Mutated (ATM) in telomere protection during early embryonic development, is identified.
ATM is primarily required for the meiotic DSB repair response, which includes functions in DNA damage repair and negative feedback control over the level of programmed DSBs during meiosis.
Molecular genetic characterization of Drosophila ATM conserved functional domains.
ATM checkpoint kinase (zeige ATR Antikörper) plays a role in telomere maintenance that is independent of telomerase regulation.
Drosophila ATM and Mre11 (zeige MRE11A Antikörper) are essential for the G2/M checkpoint induced by low-dose irradiation.
Results suggest that ATM and ATR protect telomere integrity by safeguarding chromatin architecture that favors the loading of telomere-elongating, capping, and silencing proteins.
Dna2 (zeige DNA2 Antikörper) co-localizes in foci with RPA (zeige RPA1 Antikörper) and is found in a complex with replication fork components And-1 and Mcm10 (zeige MCM10 Antikörper). Dna2 (zeige DNA2 Antikörper) interacts with the DSB repair and checkpoint proteins Nbs1 (zeige NLRP2 Antikörper) and ATM.
ATM and ATR (zeige ATR Antikörper) prevent accumulation of chromosomal abnormalities by promoting Mre11 (zeige MRE11A Antikörper)/Rad50 (zeige RAD50 Antikörper)/Nbs1 (zeige NLRP2 Antikörper) dependent recovery of collapsed replication forks.
ATM and ATR (zeige ATR Antikörper) phosphorylate the functionally critical replication protein Mcm2 (zeige MCM2 Antikörper) during both DNA damage and replication checkpoint responses in Xenopus egg extracts
PP2A counteracts ATM and ATR in a DNA damage checkpoint in Xenopus egg extracts
Data show that ATM (ataxia-telangiectasia mutated) regulates Xenopus TopBP1 (zeige TOPBP1 Antikörper) by phosphorylating serine 1131 and thereby strongly enhancing association of TopBP1 (zeige TOPBP1 Antikörper) with ATR (zeige ATR Antikörper)(ATM and Rad3-related).
ATM and ATR (zeige ATR Antikörper) control mitotic events in vertebrate cells by targeting CEP63 (zeige CEP63 Antikörper) and centrosome dependent spindle assembly.
These findings suggest that the MRN complex is a crucial mediator in the process whereby ATM promotes the TopBP1 (zeige TOPBP1 Antikörper)-dependent activation of ATR (zeige ATR Antikörper)-ATRIP (zeige ATRIP Antikörper) in response to double-stranded DNA breaks.
The Fanconi anemia protein (zeige FANCF Antikörper) FANCM (zeige FANCM Antikörper) is controlled by FANCD2 (zeige FANCD2 Antikörper) and the ATR (zeige ATR Antikörper)/ATM pathways.
molecular cloning of the coding sequence of the catalytic domain of the zebrafish homologue of ATM
Characterization of ataxia telangiectasia protein.
NOTCH1 (zeige NOTCH1 Antikörper) inhibits activation of ATM by impairing the formation of an ATM-FOXO3a (zeige FOXO3 Antikörper)-KAT5 (zeige KAT5 Antikörper) complex.
No strong correlation was observed between ATM mutation and function. Therefore, mutation status may not be taken as an indicator of ATM function. Rather, a direct assay of the kinase activity should be used in the development of therapies.
Results show that ATM protein expression is lost in 31% of patients with breast cancer. ATM loss is frequently observed in a distinct group with more advanced-stage disease.
ATM mutation impacts on the age-related telomere length shortening and is not related to cancer risk.
although recruitment of the MRE11 (zeige MRE11A Antikörper)-RAD50 (zeige RAD50 Antikörper)-NBS1 (zeige NBN Antikörper) (MRN) DSB-sensing complex to viral genomes and activation of the ATM kinase can promote KSHV replication, proteins involved in nonhomologous end joining (NHEJ) repair restrict amplification of viral DNA.
A high frequency of chromothriptic events occurred in cases of acute lymphoblastic anemia arising in patients with ataxia telangectasia, specifically on acrocentric chromosomes, as compared with tumors from individuals with other types of DNA repair syndromes, due to the short telomeres and poor DNA repair caused by their two ATM mutations. ATM loss in other tumors also increases chromothripsis.
ASF1a (zeige ASF1A Antikörper) promotes non-homologous end joining repair by facilitating phosphorylation of MDC1 (zeige MDC1 Antikörper) by ATM at double-strand breaks.
ectopic expression of Gene 33 triggers DNA damage response in an ATM serine/threonine kinase (ATM)-dependent fashion and through pathways dependent or not dependent on ABL proto-oncogene 1 non-receptor tyrosine kinase (c-Abl).
We demonstrate that, in breast cancer cells, ATM and ATG4C (zeige ATG4C Antikörper) are essential drivers of mammosphere formation, suggesting that their targeting may improve current approaches to eradicate breast cancer cells with a stem-like phenotype.
ATM-reactive oxygen species-iNOS (zeige NOS2 Antikörper) axis regulates nitric oxide mediated cellular senescence.
Ataxia telangiectasia (AT) is a progressive multisystem disorder caused by mutations in the AT-mutated (ATM) gene. We engineered a novel porcine model of AT
ATM influenced the meiotic and cytoplasmic maturation of porcine oocytes.
ATM plays critical role in arsenite induced G2/M phase arrest in aortic endothelial cells possibly via regulation of checkpoint signaling molecules.
radiation-induced eNOS (zeige NOS3 Antikörper) activation in bovine aortic endothelial cells is regulated by ATM and HSP90 (zeige HSP90 Antikörper)
Data show that Tp53 (zeige TP53 Antikörper)- and Atm-defective Chronic lymphocytic leukemia (CLL) mimicking the high-risk form of human disease and that Atm-deficient CLL is sensitive to PARP1 (zeige PARP1 Antikörper) inhibition.
Depletion of H3K9ac in embryonic stem cells by suppression of monocytic leukemia zinc finger protein (MOZ (zeige MYST3 Antikörper)) acetyltransferase improved ATM activation, DNA repair, diminished irradiation-induced apoptosis, and enhanced clonogenic survival.
The data demonstrate ATM is important for the maintenance of telomere homeostasis and the surveillance of telomere dysfunction during neurogenesis.
DNA damage induces a kinetochore-based ATM/ATR-independent spindle assembly checkpoint arrest.
The SAGA deubiquitinase activity was required for optimal irradiation-induced gammaH2AX (zeige H2AFX Antikörper) formation, and failure to remove H2BK120ub inhibits ATM- and DNAPK (zeige PRKDC Antikörper)-induced gammaH2AX (zeige H2AFX Antikörper) formation.
ATM expression by peritoneal B cells is required to facilitate viral reactivation during long-term infection. Thus, this study defines a proviral role of B cell-specific ATM expression during chronic gammaherpesvirus infection.
work reveals that simulated microgravity promotes the apoptotic response through a combined modulation of the Uev1A/TICAM/TRAF (zeige TRAF1 Antikörper)/NF-kappaB (zeige NFKB1 Antikörper)-regulated apoptosis and the p53 (zeige TP53 Antikörper)/PCNA (zeige PCNA Antikörper)- and ATM/ATR (zeige ATR Antikörper)-Chk1 (zeige CHEK1 Antikörper)/2-controlled DNA-damage response pathways.
this study shows that Atm-/- mice are more susceptible to pulmonary Streptococcus pneumoniae infection in a manner consistent with inflammasome defects
This study show that like ataxia telangiectasia cells, ISG15 (zeige ISG15 Antikörper) is elevated in Atm-deficient mouse cerebellums.
This study identifies attenuation of type I interferon (zeige IFNA Antikörper) responses as the primary mechanism underlying proviral function of ATM during gammaherpesvirus infection.
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.
, ataxia telangiectasia mutated
, ataxia telengiesctasia mutated
, ataxia-telangiectasia mutated
, drosophila ATM
, ataxia telangiectasia mutated (includes complementation groups A, C and D)
, ataxia telangiectasia mutated protein
, serine-protein kinase ATM-like
, ataxia telangiectasia mutated (atm)
, A-T mutated
, AT mutated
, TEL1, telomere maintenance 1, homolog
, serine-protein kinase ATM
, Ataxia telangiectasia gene mutated in human beings
, ataxia telangiectasia mutated homolog
, A-T mutated homolog
, ATM (ataxia telangiectasia mutated)
, ataxia telangiectasia gene mutated in human beings