<?xml version="1.0" encoding="UTF-8" standalone="yes"?> <ProteomeXchangeDataset id="PXD043703" formatVersion="1.4.0" xsi:noNamespaceSchemaLocation="proteomeXchange-1.4.0.xsd" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance"> <CvList> <Cv fullName="PSI-MS" uri="https://raw.githubusercontent.com/HUPO-PSI/psi-ms-CV/master/psi-ms.obo" id="MS"/> <Cv fullName="PSI-MOD" uri="https://raw.githubusercontent.com/MICommunity/psidev/master/psi/mod/data/PSI-MOD.obo" id="MOD"/> <Cv fullName="UNIMOD" uri="http://www.unimod.org/obo/unimod.obo" id="UNIMOD"/> </CvList> <ChangeLog> <ChangeLogEntry date="2024-10-22">Updated project metadata.</ChangeLogEntry> </ChangeLog> <DatasetSummary announceDate="2024-10-22" hostingRepository="PRIDE" title="LC3A and Aggresomes: A trigger for UPR-activation, mitochondrial dysfunction, and cellular senescence"> <Description>The protein quality control (PQC) network is crucial for maintaining cellular proteostasis by monitoring protein production, folding, and degradation. Unfolded protein response (UPR) and autophagy are key components of this network along with the compartmentalization of misfolded proteins into inclusion bodies. Among inclusion bodies, aggresomes, a bimolecular condensate, formed by collapsed vimentin cage surrounding misfolded/aggregated proteins at the microtubule organizing center. LC3A, a member of the LC3 family of autophagy-related proteins, has been implicated in regulating protein homeostasis. In this study, we investigated the role of LC3A in aggresome-positive cells. Expression of LC3A-mediated autophagy was associated with activation of the PERK-eIF2-ATF4 axis of the UPR and alterations in mitochondrial morphology. Prolonged expression of LC3A induced cellular senescence in aggresome-positive cells. These findings provide insights into the specialized role of LC3A in cellular homeostasis. 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Faculty of Pharmacy and Biotechnology, German University in Cairo (GUC), Egypt."/> <cvParam cvRef="MS" accession="MS:1002037" name="dataset submitter"/> </Contact> <Contact id="project_lab_head"> <cvParam cvRef="MS" accession="MS:1002332" name="lab head"/> <cvParam cvRef="MS" accession="MS:1000586" name="contact name" value="Shahenda El-Naggar"/> <cvParam cvRef="MS" accession="MS:1000589" name="contact email" value="shahenda.elnaggar@57357.org"/> <cvParam cvRef="MS" accession="MS:1000590" name="contact affiliation" value="Tumor Biology Research Program, Research department, Children's Cancer Hospital in Egypt 57357"/> </Contact> </ContactList> <PublicationList> <Publication id="PMID38777145"> <cvParam cvRef="MS" accession="MS:1000879" name="PubMed identifier" value="38777145"/> <cvParam cvRef="MS" accession="MS:1002866" name="Reference" value="Amer N, Hesham D, Al-Shehaby N, Elshoky HA, Amer M, Magdeldin S, Mansour M, Abou-Aisha K, El-Naggar S. LC3A-mediated autophagy elicits PERK-eIF2α-ATF4 axis activation and mitochondrial dysfunction: Exposing vulnerability in aggresome-positive cancer cells. 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