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tars-1

Gene

1 paper3 findings

Taxon 6239

C, W, M, H: cells, worms or flies, mice, humans. Dark: independent labs found the same change there. Light: one lab or one study. Outline: nothing yet.

Labs are independent when their papers share no last author and no institution.

Against: findings that point the other way from most findings on the same outcome.

On aging: the drug’s trials ARN judged to be about aging, of every trial that tests it for any use.

No results posted: trials that ended more than a year ago with no results on ClinicalTrials.gov and no paper in ARN’s record.

Company ties: findings with an author at a company, or from a paper whose competing-interests statement declares ties to one.

A gene’s or a process’s line counts the gene with the processes named after it, as NLRP3 with the NLRP3 inflammasome, and the trials of drugs aimed at it.

  • 1 lab in 1 country
  • Funders: Chinese Academy of Sciences and 4 more
  • Model organisms1

Effects

3

Mitochondrial unfolded protein response

upin worms1

1 study

  1. tars-1 activates mitochondrial unfolded protein response in worms.

    “Mitochondrial tars-1 deficiency leads to compromised mitochondrial functions including the decrease in oxygen consumption rate, complex I activity and the activation of the mitochondrial unfolded protein response (UPRmt)”

    Model organismsmitochondrial tars-1 deficiency

    Mitochondrial translational defect extends lifespan in C. elegans by activating UPRmt

    Redox biology7 May 2023

More on Mitochondrial unfolded protein response

Motor ability

downin worms1

1 study

  1. tars-1 impairs motor ability in worms.

    “decreased motor ability”

    Model organismsmitochondrial tars-1 knockdown

    Mitochondrial translational defect extends lifespan in C. elegans by activating UPRmt

    Redox biology7 May 2023

Lifespan

upin worms1

1 study

  1. tars-1 extends lifespan in worms.

    “Mitochondrial tars-1 knockdown decreased mitochondrial tRNAThr charging and translation and caused pleotropic phenotypes of delayed development, decreased motor ability and prolonged lifespan”

    Model organismsmitochondrial tars-1 knockdown

    Mitochondrial translational defect extends lifespan in C. elegans by activating UPRmt

    Redox biology7 May 2023

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