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Abcam rabbit polyclonal anti p cdc25c
ALKBH5 induces posttranscriptional activation of PER1 to inhibit PC progression in an m6A-YTHDF2-dependent manner. ALKBH5 loss that abrogates mRNA demethylation leads to an upregulation of PER1 m6A levels in PC cells. Then, degradation of PER1 mRNA occurs on the basis of the m6A-YTHDF2 interaction. PER1 downregulation results in the inhibition of ATM phosphorylation and inactivation of the <t>ATM-CHK2-P53/CDC25C</t> pathways. G2/M arrest in PC cells was suppressed as a result. The PER1-related P53 downregulation and P53-dependent transcriptional inactivation of ALKBH5 indicates a feedback loop underlying the progression of PC
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1) Product Images from "RNA demethylase ALKBH5 prevents pancreatic cancer progression by posttranscriptional activation of PER1 in an m6A-YTHDF2-dependent manner"

Article Title: RNA demethylase ALKBH5 prevents pancreatic cancer progression by posttranscriptional activation of PER1 in an m6A-YTHDF2-dependent manner

Journal: Molecular Cancer

doi: 10.1186/s12943-020-01158-w

ALKBH5 induces posttranscriptional activation of PER1 to inhibit PC progression in an m6A-YTHDF2-dependent manner. ALKBH5 loss that abrogates mRNA demethylation leads to an upregulation of PER1 m6A levels in PC cells. Then, degradation of PER1 mRNA occurs on the basis of the m6A-YTHDF2 interaction. PER1 downregulation results in the inhibition of ATM phosphorylation and inactivation of the ATM-CHK2-P53/CDC25C pathways. G2/M arrest in PC cells was suppressed as a result. The PER1-related P53 downregulation and P53-dependent transcriptional inactivation of ALKBH5 indicates a feedback loop underlying the progression of PC
Figure Legend Snippet: ALKBH5 induces posttranscriptional activation of PER1 to inhibit PC progression in an m6A-YTHDF2-dependent manner. ALKBH5 loss that abrogates mRNA demethylation leads to an upregulation of PER1 m6A levels in PC cells. Then, degradation of PER1 mRNA occurs on the basis of the m6A-YTHDF2 interaction. PER1 downregulation results in the inhibition of ATM phosphorylation and inactivation of the ATM-CHK2-P53/CDC25C pathways. G2/M arrest in PC cells was suppressed as a result. The PER1-related P53 downregulation and P53-dependent transcriptional inactivation of ALKBH5 indicates a feedback loop underlying the progression of PC

Techniques Used: Activation Assay, Inhibition



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ALKBH5 induces posttranscriptional activation of PER1 to inhibit PC progression in an m6A-YTHDF2-dependent manner. ALKBH5 loss that abrogates mRNA demethylation leads to an upregulation of PER1 m6A levels in PC cells. Then, degradation of PER1 mRNA occurs on the basis of the m6A-YTHDF2 interaction. PER1 downregulation results in the inhibition of ATM phosphorylation and inactivation of the <t>ATM-CHK2-P53/CDC25C</t> pathways. G2/M arrest in PC cells was suppressed as a result. The PER1-related P53 downregulation and P53-dependent transcriptional inactivation of ALKBH5 indicates a feedback loop underlying the progression of PC
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ALKBH5 induces posttranscriptional activation of PER1 to inhibit PC progression in an m6A-YTHDF2-dependent manner. ALKBH5 loss that abrogates mRNA demethylation leads to an upregulation of PER1 m6A levels in PC cells. Then, degradation of PER1 mRNA occurs on the basis of the m6A-YTHDF2 interaction. PER1 downregulation results in the inhibition of ATM phosphorylation and inactivation of the <t>ATM-CHK2-P53/CDC25C</t> pathways. G2/M arrest in PC cells was suppressed as a result. The PER1-related P53 downregulation and P53-dependent transcriptional inactivation of ALKBH5 indicates a feedback loop underlying the progression of PC
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ALKBH5 induces posttranscriptional activation of PER1 to inhibit PC progression in an m6A-YTHDF2-dependent manner. ALKBH5 loss that abrogates mRNA demethylation leads to an upregulation of PER1 m6A levels in PC cells. Then, degradation of PER1 mRNA occurs on the basis of the m6A-YTHDF2 interaction. PER1 downregulation results in the inhibition of ATM phosphorylation and inactivation of the <t>ATM-CHK2-P53/CDC25C</t> pathways. G2/M arrest in PC cells was suppressed as a result. The PER1-related P53 downregulation and P53-dependent transcriptional inactivation of ALKBH5 indicates a feedback loop underlying the progression of PC
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ALKBH5 induces posttranscriptional activation of PER1 to inhibit PC progression in an m6A-YTHDF2-dependent manner. ALKBH5 loss that abrogates mRNA demethylation leads to an upregulation of PER1 m6A levels in PC cells. Then, degradation of PER1 mRNA occurs on the basis of the m6A-YTHDF2 interaction. PER1 downregulation results in the inhibition of ATM phosphorylation and inactivation of the ATM-CHK2-P53/CDC25C pathways. G2/M arrest in PC cells was suppressed as a result. The PER1-related P53 downregulation and P53-dependent transcriptional inactivation of ALKBH5 indicates a feedback loop underlying the progression of PC

Journal: Molecular Cancer

Article Title: RNA demethylase ALKBH5 prevents pancreatic cancer progression by posttranscriptional activation of PER1 in an m6A-YTHDF2-dependent manner

doi: 10.1186/s12943-020-01158-w

Figure Lengend Snippet: ALKBH5 induces posttranscriptional activation of PER1 to inhibit PC progression in an m6A-YTHDF2-dependent manner. ALKBH5 loss that abrogates mRNA demethylation leads to an upregulation of PER1 m6A levels in PC cells. Then, degradation of PER1 mRNA occurs on the basis of the m6A-YTHDF2 interaction. PER1 downregulation results in the inhibition of ATM phosphorylation and inactivation of the ATM-CHK2-P53/CDC25C pathways. G2/M arrest in PC cells was suppressed as a result. The PER1-related P53 downregulation and P53-dependent transcriptional inactivation of ALKBH5 indicates a feedback loop underlying the progression of PC

Article Snippet: The primary antibodies were rabbit monoclonal anti-ALKBH5 (ab195377, Abcam), mouse monoclonal anti-PER1 (sc-398,890, Santa Cruz), mouse monoclonal anti-p-ATM (Ser-1981; sc-47,739, Santa Cruz), rabbit monoclonal anti-p-CHK2 (Thr-68; ab32148, Abcam), rabbit polyclonal anti-p-CDC25C (Ser216; ab47322, Abcam), rabbit monoclonal anti-p-P53 (Ser-15; ab1431, Abcam), mouse monoclonal anti-P21 (sc-71,811, Santa Cruz), mouse monoclonal anti-CYCLIN B1 (ab72, Abcam), rabbit polyclonal anti-p-CDK1 (Tyr15; ab47594), mouse monoclonal anti-CDK1 (A17, Abcam) and rabbit polyclonal anti-β-ACTIN (ab8227, Abcam).

Techniques: Activation Assay, Inhibition