<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>12(11)</volume><submitter>Zhang Y</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Amyotrophic lateral sclerosis (ALS) can result in the dysfunction of upper and lower motor neurons. A previous study has indicated that TBK1 mutation (hTBK1-c.978T>A) is involved in progression of ALS. However, the mechanism by which TBK1 mutation mediates the progression of ALS remains unclear.&lt;h4>Methods&lt;/h4>NSC-34 cells with hTBK1-c.978T>A mutation (TBK1 mutation status) was used to mimic ALS &lt;i>in vitro&lt;/i>. In addition, cell proliferation was detected by Ki67 staining. Gene and protein expressions in NSC-34 cells were detected by RT-qPCR and western blot, respectively. ROS and PGSK levels in NSC-34 cells were detected by flow cytometry.&lt;h4>Results&lt;/h4>hTBK1-c.978T>A mutation significantly inhibited the proliferation of NSC-34 cells via inducing cell ferroptosis, whi</pubmed_abstract><journal>American journal of translational research</journal><pagination>7386-7394</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7724361</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>hTBK1-c.978T>A mutation promotes the ferroptosis in NSC-34 cells via mediation of KEAP1/NRF2/p62 signaling.</pubmed_title><pmcid>PMC7724361</pmcid><pubmed_authors>Liu X</pubmed_authors><pubmed_authors>Tang L</pubmed_authors><pubmed_authors>He J</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Zhang N</pubmed_authors><pubmed_authors>Fan D</pubmed_authors></additional><is_claimable>false</is_claimable><name>hTBK1-c.978T>A mutation promotes the ferroptosis in NSC-34 cells via mediation of KEAP1/NRF2/p62 signaling.</name><description>&lt;h4>Background&lt;/h4>Amyotrophic lateral sclerosis (ALS) can result in the dysfunction of upper and lower motor neurons. A previous study has indicated that TBK1 mutation (hTBK1-c.978T>A) is involved in progression of ALS. However, the mechanism by which TBK1 mutation mediates the progression of ALS remains unclear.&lt;h4>Methods&lt;/h4>NSC-34 cells with hTBK1-c.978T>A mutation (TBK1 mutation status) was used to mimic ALS &lt;i>in vitro&lt;/i>. In addition, cell proliferation was detected by Ki67 staining. Gene and protein expressions in NSC-34 cells were detected by RT-qPCR and western blot, respectively. ROS and PGSK levels in NSC-34 cells were detected by flow cytometry.&lt;h4>Results&lt;/h4>hTBK1-c.978T>A mutation significantly inhibited the proliferation of NSC-34 cells via inducing cell ferroptosis, whi</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020</publication><modification>2025-04-18T21:00:26.235Z</modification><creation>2025-04-07T08:59:18.391Z</creation></dates><accession>S-EPMC7724361</accession><cross_references><pubmed>33312375</pubmed></cross_references></HashMap>