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Human Monoclonal ATM Primary Antibody for 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 117 Pubmed References
Human Polyclonal ATM Primary Antibody for 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 84 Pubmed References
Human Monoclonal ATM Primary Antibody for 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 27 Pubmed References
Human Monoclonal ATM Primary Antibody for 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 22 Pubmed References
Polyclonal ATM Primary Antibody for IF, WB - ABIN540777
Hovest, Brüggenolte, Hosseini, Krieg, Herrmann: Senescence of human fibroblasts after psoralen photoactivation is mediated by ATR kinase and persistent DNA damage foci at telomeres. in Molecular biology of the cell 2006
Show all 5 Pubmed References
Human Polyclonal ATM Primary Antibody for 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
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Human Polyclonal ATM Primary Antibody for 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
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Human Monoclonal ATM Primary Antibody for IP, ELISA - ABIN532709
Hurley, Bunz: ATM and ATR: components of an integrated circuit. in Cell cycle (Georgetown, Tex.) 2007
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Human Monoclonal ATM Primary Antibody for 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
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Monoclonal ATM Primary Antibody for IF, WB - ABIN534124
Ye, Franco, Santos, Nelson, Kaufman, Adams: Defective S phase chromatin assembly causes DNA damage, activation of the S phase checkpoint, and S phase arrest. in Molecular cell 2003
Show all 3 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 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 plays a role in telomere maintenance that is independent of telomerase regulation.
Drosophila ATM and Mre11 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 co-localizes in foci with RPA and is found in a complex with replication fork components And-1 and Mcm10. Dna2 interacts with the DSB repair and checkpoint proteins Nbs1 and ATM.
ATM and ATR prevent accumulation of chromosomal abnormalities by promoting Mre11/Rad50/Nbs1 dependent recovery of collapsed replication forks.
ATM and ATR phosphorylate the functionally critical replication protein Mcm2 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 by phosphorylating serine 1131 and thereby strongly enhancing association of TopBP1 with ATR(ATM and Rad3-related).
ATM and ATR control mitotic events in vertebrate cells by targeting CEP63 and centrosome dependent spindle assembly.
These findings suggest that the MRN complex is a crucial mediator in the process whereby ATM promotes the TopBP1-dependent activation of ATR-ATRIP in response to double-stranded DNA breaks.
The Fanconi anemia protein FANCM is controlled by FANCD2 and the ATR/ATM pathways.
molecular cloning of the coding sequence of the catalytic domain of the zebrafish homologue of ATM
Characterization of ataxia telangiectasia protein.
ATDC is required for TP63-induced bladder tumor invasion and metastasis.
a case of a 4-month-old infant homozygous for the 2 ATM mutations, who developed malignant peritoneal mesothelioma and died by the age of 2 years.
the mitochondrial functional recovery by ATM inhibition might represent a promising strategy to ameliorate the accelerated aging phenotypes and to treat age-related disease.
The regulation of ATM in autophagy is including mitophagy, pexophagy, and lipophagy, which would enhance our understanding of its role in cell dynamics and homeostasis.
Here, the authors show that ARP8, a subunit of the INO80 chromatin remodeling complex, is phosphorylated after etoposide treatment. The etoposide-induced phosphorylation of ARP8 is regulated by ATM and ATR, and attenuates its interaction with INO80.
SIM2s interacts with ATM and is stabilized through ATM-dependent phosphorylation in response to IR.
In each of these domains, key molecules and pathways have now been identified, including the glycolytic enzymes PFKFB3 and G6PD; the DNA repair molecules ATM, DNA-PKcs and MRE11A; and the podosome marker protein TKS5. Some of these molecules may help in defining targetable pathways to slow the T cell aging process. [review]
Rare germline variants in ATM are associated with chronic lymphocytic leukemia.
Which was induced by phosphorylation and ATM gene expression.
Study findings reveal that ufmylation of histone H4 by UFL1 is an important step for amplification of ATM activation and maintenance of genomic integrity.
associations between CD40L/IL-4 response and baseline ATM levels, induction of ATM, and phosphorylation of the ATM targets, p53 and H2AX. X-irradiation was used to demonstrate that CD40L/IL-4 stimulation tended to improve DNA damage repair.
This non-canonical activation of STING is mediated by the DNA binding protein IFI16, together with the DNA damage response factors ATM and PARP-1.
ATM activation at mammalian telomeres with reduced TRF2 or at human telomeres during mitotic arrest occurs specifically with a structural change from telomere loops (t-loops) to linearized telomeres.
Although ATM is involved in the DNA damage response, ATM-associated tumours are distinct from BRCA1-associated tumours in terms of morphological characteristics and genomic alterations, and they are also distinguishable from sporadic breast tumours, thus opening up the possibility to identify ATM variant carriers outside the ataxia-telangiectasia disorder and direct them towards effective cancer risk management and therap
Invasive breast carcinomas with variants of uncertain significance in the ATM gene showed similar histopathologic features.
ATM SNP rs11212617 significantly affected the effect of metformin and metformin plasma concentration.
The ATR-Chk1 and ATM-Chk2 signalings in male breast cancer (MBC).
Localization of active phosphorylated Ataxia Telangiectasia Mutated Protein (pATM) to adenovirus control protein E4 deletion mutants (E4-) viral replication centers (VRCs) is important for its inhibitory effect in viral DNA replication. ATM is necessary for localization of RNF8 and 53BP1 to E4- VRCs, but recruitment of DDR factors Mre11, Mdc1 and gammaH2AX is ATM-independent, indicating that ATM affect viral chromatin ...
study outlined the immunohistochemical expression of p-ATM/p53 in glioblastomas and provided data on their possible prognostic/predictive of response role. A "non-oncogene addiction" to ATM for NEp53 glioblastoma could be postulated, strengthening the rationale for development of ATM inhibiting drugs.
Deficient activation of ATM by the Mre11-Rad50-Nbs1 complex and DNA double-strand breaks resulted in loss of cell viability, checkpoint activation, and DNA end resection in response to DNA damage.
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.
The extensive alternative splicing of the pATM gene resembles the complex splicing observed in the hATM and could provide insights for differences observed between mice and humans with regards to the onset of A-T
radiation-induced eNOS activation in bovine aortic endothelial cells is regulated by ATM and HSP90
Molecularly, ATM phosphorylates SIRT6 deacetylase and thus prevents MDM2-mediated ubiquitination and proteasomal degradation.
An excess of reactive oxygen species stimulates ATM-dependent phosphorylation of DBN at serine-647, which enhances protein stability and accounts for improved stress resilience in dendritic spines.
Old hematopoietic stem cells have diminished ATM activity in response to acute DNA damage induction. Diminished apoptotic priming provide a selective advantage to old HSCs.
Genome-wide CRISPR-Cas9 loss-of-function genetic screens to identify suppressors of cell killing by the TOP1i topotecan in ATM-proficient and ATM-deficient mouse and human cells show that, in the absence of ATM, non-homologous end-joining-mediated repair of single-ended double-strand breaks induced by TOP1 or PARP1 inhibition results in aberrant chromatid fusions and cell death.
Urinary profiles from heterozygous animals exhibited remarkably similar responses to WT before and after radiation exposure. However, genotypic differences (WT or Atm(-/-) ) were the primary driver to responses to gamma radiation.
SOD2 expression is ATM- and RelA-dependent, ATM knockdown renders cells sensitive to pro-oxidant exposure, and SOD mimetics partially rescue this sensitivity. Mice with germline deletion of Atm fail to develop mature mammary glands, but using a conditional knockout approach, we determined that Atm deletion significantly diminished the expression of Sod2.
These data suggest that ATM and ATR are part of the cellular "infrastructure" that maintains the excitatory/inhibitory balance of the nervous system.
ATM has a role in homology-directed repair (HDR) independent of the BRCA1-53BP1 antagonism; its HDR function can become critical in certain contexts
intestinal tuft cells play an important role in regulating the ATM mediated DNA damage response, for epithelial cell survival/self-renewal via a Dclk1 dependent mechanism
in the Atm(-/-) MEFs, the same Radiofrequency electromagnetic fields exposure for 12 h induced both SSBs and double-strand breaks and activated the two repair processes, which also reduced the DNA damage to less than the control level after prolonged exposure. The observed phenomenon is similar to the hormesis of a toxic substance at a low dose
ATM haplodeficiency decreases fibroblast senescence and vascular endothelial growth factor production and impaired angiogenesis in response to myocardial infarction, leading to accelerated heart failure.
H2AX shows a similar influence as ATM.
The ATM protein is a key mediator of H2O2 preconditioning.
ATM is the primary kinase responsible for phosphorylation of Hsp90alpha after exposure ionizing radiation.
These findings define an antagonistic function of ATM and MAPK7 in the thymocyte response to DNA damage, and suggest that the lack of MAPK7 inhibits thymic lymphoma growth in Atm-/- mice by partially restoring the DNA damage response in thymocytes.
ATM/G6PD-driven redox metabolism promotes FLT3 inhibitor resistance in acute myeloid leukemia that can be successfully reversed.
Baf60b, a member of the SWI/SNF chromatin remodeling complex, links chromatin opening to ATM activation by facilitating ATM recruitment to the open chromatin regions of a panel of hepatic gene loci.
Results demonstrate that alterations in ATM levels are responsible for pronounced and anticipated GABAergic development and function. Since GABA transmission is strongly linked to the correct brain development and plasticity, this study lays basics for both a more clear comprehension of mechanisms associated with brain development.
These data indicate that defective Atm reduces the redox homeostasis of the testis and genetic integrity of sperm by regulating glutathione levels independently from G6PDH activity.
WSB1 is one of the key players of early oncogenic events through ATM degradation and destruction of the tumorigenesis barrier.
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