Study · In vitro (cells) · 2011
9 resultsZajkowicz A, Rusin M
Mechanisms of ageing and development21 Sept 2011Cited by 18 (Europe PMC)
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Text rights: Publisher copyright. Results still quote short attributed sentences.
5 results from studies that gave the peptide. No result from this study comes from people.
In LKB1-deficient cells, AICAR activated the p53 pathway.
In plain wordsIn cells without LKB1, AICAR activated the p53 pathway.
n: not reported in source
LKB1-deficient cellsSource sentences
We showed that AICAR activated the p53 pathway in LKB1-deficient cells.
In cells, AICAR did not induce the DNA damage response reported with resveratrol.
In plain wordsIn cells, AICAR did not induce the DNA damage response seen with resveratrol.
n: not reported in source
Source sentences
Rapamycin did not block p53 activation by resveratrol, which, in contrast to AICAR, induced the DNA damage response, senescence-like growth inhibition, a high level of post-translational modification of p53, and weak upregulation of MDM2 (the negative regulator of p53).
In cells, AICAR did not induce the senescence-like growth inhibition reported with resveratrol.
In plain wordsIn cells, AICAR did not induce the senescence-like growth inhibition seen with resveratrol.
n: not reported in source
Source sentences
Rapamycin did not block p53 activation by resveratrol, which, in contrast to AICAR, induced the DNA damage response, senescence-like growth inhibition, a high level of post-translational modification of p53, and weak upregulation of MDM2 (the negative regulator of p53).
In cells, AICAR differed from resveratrol, which induced a high level of p53 post-translational modification.
In plain wordsIn cells, AICAR differed from resveratrol, which caused high p53 modification.
n: not reported in source
Source sentences
Rapamycin did not block p53 activation by resveratrol, which, in contrast to AICAR, induced the DNA damage response, senescence-like growth inhibition, a high level of post-translational modification of p53, and weak upregulation of MDM2 (the negative regulator of p53).
In cells, AICAR differed from resveratrol, which induced weak MDM2 upregulation.
In plain wordsIn cells, AICAR differed from resveratrol, which weakly increased MDM2.
n: not reported in source
Source sentences
Rapamycin did not block p53 activation by resveratrol, which, in contrast to AICAR, induced the DNA damage response, senescence-like growth inhibition, a high level of post-translational modification of p53, and weak upregulation of MDM2 (the negative regulator of p53).
In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking AICAR (acadesine).
In cells, caffeine and Ku-55933 strongly attenuated AICAR-induced p53 pathway activation.
In plain wordsIn cells, caffeine and Ku-55933 reduced p53 pathway activation induced by AICAR.
n: not reported in source
LKB1-deficient cellsSource sentences
This activation was strongly attenuated by two inhibitors of the ATM kinase (caffeine and Ku-55933), which is dysfunctional in ataxia-telanagiectasia patients.
We showed that AICAR activated the p53 pathway in LKB1-deficient cells.
In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).
In cells with ATM silenced by shRNA, AICAR-induced p53 phosphorylation at Ser(15) was attenuated.
In plain wordsIn cells, ATM gene silencing reduced p53 phosphorylation at Ser(15) induced by AICAR.
n: not reported in source
Cells expressing ATM-targeting shRNASource sentences
In cells with ATM expression silenced by shRNA, AICAR-induced p53 phosphorylation at Ser(15) and Ser(37) was attenuated.
In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).
In cells with ATM silenced by shRNA, AICAR-induced p53 phosphorylation at Ser(37) was attenuated.
In plain wordsIn cells, ATM gene silencing reduced p53 phosphorylation at Ser(37) induced by AICAR.
n: not reported in source
Cells expressing ATM-targeting shRNASource sentences
In cells with ATM expression silenced by shRNA, AICAR-induced p53 phosphorylation at Ser(15) and Ser(37) was attenuated.
In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).
In cells, rapamycin blocked p53 activation induced by AICAR.
In plain wordsIn cells, rapamycin blocked p53 activation induced by AICAR.
n: not reported in source
LKB1-deficient cellsSource sentences
Furthermore, p53 activation by AICAR was blocked by rapamycin, a specific inhibitor of the mTOR kinase, which is a crucial regulator of cell growth.
In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).
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21 Oct 2026, 12:50 UTC
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