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anti-Human ATM Antibodies:
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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 114 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 77 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 26 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 20 Pubmed References
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
Show all 8 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
Show all 4 Pubmed References
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
Show all 4 Pubmed References
Human Monoclonal ATM Primary Antibody for 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
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
Human ATM Primary Antibody for IHC - ABIN965619
Gupta, Sharma, Young, Agarwal, Smith, Paull, Lucchesi, Khanna, Ludwig, Pandita: Involvement of human MOF in ATM function. in Molecular and cellular biology 2005
Show all 4 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 (show TPT1 Antibodies) 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 (show ATR Antibodies) plays a role in telomere maintenance that is independent of telomerase regulation.
Drosophila ATM and Mre11 (show MRE11A Antibodies) 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 (show DNA2 Antibodies) co-localizes in foci with RPA (show RPA1 Antibodies) and is found in a complex with replication fork components And-1 and Mcm10 (show MCM10 Antibodies). Dna2 (show DNA2 Antibodies) interacts with the DSB repair and checkpoint proteins Nbs1 (show NLRP2 Antibodies) and ATM.
ATM and ATR (show ATR Antibodies) prevent accumulation of chromosomal abnormalities by promoting Mre11 (show MRE11A Antibodies)/Rad50 (show RAD50 Antibodies)/Nbs1 (show NLRP2 Antibodies) dependent recovery of collapsed replication forks.
ATM and ATR (show ATR Antibodies) phosphorylate the functionally critical replication protein Mcm2 (show MCM2 Antibodies) 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 (show TOPBP1 Antibodies) by phosphorylating serine 1131 and thereby strongly enhancing association of TopBP1 (show TOPBP1 Antibodies) with ATR (show ATR Antibodies)(ATM and Rad3-related).
ATM and ATR (show ATR Antibodies) control mitotic events in vertebrate cells by targeting CEP63 (show CEP63 Antibodies) and centrosome dependent spindle assembly.
These findings suggest that the MRN complex is a crucial mediator in the process whereby ATM promotes the TopBP1 (show TOPBP1 Antibodies)-dependent activation of ATR (show ATR Antibodies)-ATRIP (show ATRIP Antibodies) in response to double-stranded DNA breaks.
The Fanconi anemia protein (show FANCF Antibodies) FANCM (show FANCM Antibodies) is controlled by FANCD2 (show FANCD2 Antibodies) and the ATR (show ATR Antibodies)/ATM pathways.
molecular cloning of the coding sequence of the catalytic domain of the zebrafish homologue of ATM
Characterization of ataxia telangiectasia protein.
Data suggest that ataxia telangiectasia mutated protein (ATM) mutational status in lung cancer is a mechanistic biomarker for MEK (show MAP2K1 Antibodies) inhibitor response.
Data suggest a close association between the nonfunctionality of ATM/p53 (show TP53 Antibodies) pathway and accumulation of p27Kip1 (show CDKN1B Antibodies) in chronic lymphocytic leukemia (CLL) cells in response to DNA damage.
Letter: BRCA2 (show BRCA2 Antibodies)- and ATM-mutated prostate cancer sensitive to high dose testosterone.
Radiation-activated ataxia-telangiectasia mutated kinase/p38 (show CRK Antibodies) signaling positively contributed to the nucleus to cytosol translocation of HuR (show ELAVL1 Antibodies).
No significant differences were presented in DNA methylation (show HELLS Antibodies) levels of RASSF1A (show RASSF1 Antibodies) and ATM between the sporadic breast cancer cases and the healthy controls.
The ATM rs189037, rs664677 and rs664143 gene polymorphisms are risk factors for lung cancer, while the ATM rs189037 variant was significantly associated with radiation-induced pneumonitis risk. [meta-analysis]
Moreover, under positive p53 expression, low expression of ATM was highly predictive of poor survival in ACC (p=0.017). CONCLUSION: These data indicate that combined assessment of ATM and p53 expression can serve as a useful prognostic marker for assessing survival rate in patients with ACC [Adenoid cystic carcinoma] of the salivary glands.
results reveal how alterations in FBXO31 (show FBXO5 Antibodies) phosphorylation, mediated by AKT (show AKT1 Antibodies) and ATM, underlie physiological regulation of FBXO31 (show FBXO5 Antibodies) levels in unstressed and genotoxically stressed cells
Combination of T-cell lymphoma-1 (show TCL1A Antibodies) protein (TCL1 (show TCL1A Antibodies))-overexpression and damaging ataxia telangiectasia mutated protein (ATM) functionally synergistically contribute to T-cell prolymphocytic leukemia (T-PLL) specific phenotype of impaired DNA damage processing.
These findings suggested that the ATM/p21 (show CDKN1A Antibodies) pathway directly participated in the LDIR-induced cell proliferation inhibition in p53null type prostate tumor cells, whereas this mechanism was absent in normal prostate cells. Thus, p53 (show TP53 Antibodies) may affect cell stability following LDIR, and plays a crucial role in regulating the ATM/p21 (show CDKN1A Antibodies) pathway activated by LDIR.
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 (show NOS3 Antibodies) activation in bovine aortic endothelial cells is regulated by ATM and HSP90 (show HSP90 Antibodies)
SOD2 (show SOD2 Antibodies) expression is ATM- and RelA (show NFkBP65 Antibodies)-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 (show SOD2 Antibodies).
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 (show GATA3 Antibodies)) independent of the BRCA1 (show BRCA1 Antibodies)-53BP1 (show TP53BP1 Antibodies) antagonism; its HDR (show GATA3 Antibodies) 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 (show DCLK1 Antibodies) 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 (show VEGF Antibodies) production and impaired angiogenesis in response to myocardial infarction, leading to accelerated heart failure.
H2AX (show H2AFX Antibodies) 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 (show HSP90AA2 Antibodies) after exposure ionizing radiation.
These findings define an antagonistic function of ATM and MAPK7 (show MAPK7 Antibodies) in the thymocyte response to DNA damage, and suggest that the lack of MAPK7 (show MAPK7 Antibodies) inhibits thymic lymphoma growth in Atm-/- mice by partially restoring the DNA damage response in thymocytes.
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