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Fig. 7: a Ribosome-stalling/collision/ribosome dysfunction and aging. The primary clear...

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Fig. 7: a  Ribosome-stalling/collision/ribosome dysfunction and aging. The primary clear...
a Ribosome-stalling/collision/ribosome dysfunction and aging. The primary clearance pathway for ribosome collisions is the degradation of nascent peptides through ribosomal quality control (RQC). RQC decreases with age, and ribosome-stalling/collision triggers ribosome dysfunction. As a result, ribosome dysfunction leads to increased nascent polypeptides and protein aggregation. b Ribosomes and the signaling pathway of cellular senescence. Cellular DNA damage can be induced by radiation or chemotherapy, which activates p53-dependent stress responses and cause cellular senescence. SIRT1, a member of the longevity protein family, directly affects the activity of key proteins in the senescence pathway through deacetylating transcription factors. Moreover, SIRT1 recruits methylation enzymes to affect ribosome biogenesis by regulating chromatin remodeling, and abnormal ribosome biogenesis can directly affect p53 and telomerase activity to accelerate cellular senescence. Genomic instabili
PubMed: 36617563
Metadata
captiona Ribosome-stalling/collision/ribosome dysfunction and aging. The primary clearance pathway for ribosome collisions is the degradation of nascent peptides through ribosomal quality control (RQC). RQC
image_urlhttps://www.ebi.ac.uk/europepmc/articles/PMC9826790/bin/41392_2022_1285_Fig7_HTML.jpg
pmid36617563
doi
pmcidPMC9826790
figure_number7
figure_labelFig. 7
source_strategypmc_api
image_path
description
entities_mentioned
_origin{'type': 'external', 'url': 'https://www.ebi.ac.uk/europepmc/articles/PMC9826790/bin/41392_2022_1285_Fig7_HTML.jpg', 'tracked_at': '2026-04-11T17:19:31.083331'}
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