NCBI . NLM . NIH . GOV {
}
We began analyzing https://pmc.ncbi.nlm.nih.gov/articles/PMC7658972/, but it redirected us to https://pmc.ncbi.nlm.nih.gov/articles/PMC7658972/. The analysis below is for the second page.
Title[redir]:
The mechanism of m6A methyltransferase METTL3-mediated autophagy in reversing gefitinib resistance in NSCLC cells by ฮฒ-elemene - PMC
Description:
N6-methyladenosine (m6A) modification can alter gene expression by regulating RNA splicing, stability, translocation, and translation. Emerging evidence shows that m6A modification plays an important role in cancer development and progression, ...
Title[redir]:
The mechanism of m6A methyltransferase METTL3-mediated autophagy in reversing gefitinib resistance in NSCLC cells by ฮฒ-elemene - PMC
Description:
N6-methyladenosine (m6A) modification can alter gene expression by regulating RNA splicing, stability, translocation, and translation. Emerging evidence shows that m6A modification plays an important role in cancer development and progression, ...
Matching Content Categories {๐}
- Science
- Education
- Health & Fitness
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What CMS is ncbi.nlm.nih.gov built with?
Custom-built
No common CMS systems were detected on Ncbi.nlm.nih.gov, and no known web development framework was identified.
Traffic Estimate {๐}
What is the average monthly size of ncbi.nlm.nih.gov audience?
๐ Phenomenal Traffic: 5M - 10M visitors per month
Based on our best estimate, this website will receive around 6,399,052 visitors per month in the current month.
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How Does Ncbi.nlm.nih.gov Make Money? {๐ธ}
We see no obvious way the site makes money.
Not every website is profit-driven; some are created to spread information or serve as an online presence. Websites can be made for many reasons. This could be one of them. Ncbi.nlm.nih.gov could be getting rich in stealth mode, or the way it's monetizing isn't detectable.
Keywords {๐}
cells, ฮฒelemene, gefitinib, autophagy, doi, cell, resistance, nsclc, cancer, expression, pubmed, google, scholar, mettl, treatment, fig, chloroquine, pmc, treated, methylation, atg, article, results, free, lung, gefitinibresistant, apoptosis, drugs, drug, mechanism, role, tumor, significantly, study, reverse, reversing, control, modification, inhibiting, analysis, experiments, performed, flow, flux, sqstm, mrna, pcgr, similar, mice, protein,
Topics {โ๏ธ}
pi3k/akt/mtor/p70s6k1 signaling pathway augmented wnt/pi3k-akt signaling egfr-tyrosine kinase inhibitors annexin v-fitc a-cdcp1 signaling axis lyso-tracker red dye lyso-tracker red probe pmc beta search dual-agent regulating autophagy gefitinib-resistant cell lines hrp-conjugated secondary antibody tandem fluorescent-tagged lc3 s-adenosylmethionine binding domain hypoxia/reoxygenation-treated cardiomyocytes tumoural pd-l1 expression quantitative real-time pcr gfp-rfp-lc3 plasmid autophagy-mediated cell death bio-rad pcr instrument qrt-pcr experiments showed m6a modification-related genes lyso-tracker red serum-free conditions cell counting kit-8 publisher site pdf supplementary materials included license information pmcid chinese traditional medicine inhibiting mettl3-mediated autophagy m6a methyltransferase complex zhejiang provincial preponderant wound healing assay low concentration ฮฒ-elemene fitc-annexin autophagy-related gene atg5 egfr signaling pathway 120โฮผg/ml ฮฒ-elemene supplementary figure legends ฮฒ-elemene significantly inhibited serum-free medium serum-free condition reverses mitochondrial defects nsclc gefitinib-resistant cells beta-elemene reverses autophagy-related protein expression autophagy-related drug treatment inflammasome-mediated neuroinflammation irreversible egfr tkis gefitinib-resistant cells treated obtain objective quantification
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