AgingResearch.NewsJoin free

MED15

Gene

1 paper3 findings

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: Fudan University and 3 more
  • Animals1

Effects

3

Learning and memory

downin mice1

1 study

  1. MED15 impairs learning and memory in mice.

    “aging mice harboring dephosphorylated mutation in this phosphosite exhibit improved learning and memory through the attenuation of the SASP across tissues.”

    AnimalsShown by improved learning and memory in mice harboring a MED15 T603 dephosphorylated mutation

    A phosphorylation switch in the Mediator MED15 controls cellular senescence and cognitive decline

    Cell discovery19 Aug 2025

Cellular senescence

upin mouse cells1

1 study

  1. MED15 increases cellular senescence in mouse cells.

    “The MED15 T603 dephosphorylated mutant (T603A) inhibits the SASP and cell senescence, whereas the T603 phosphorylation-mimicking mutant (T603D) has the opposite effect.”

    CellsComparison of MED15 T603A dephosphorylated and T603D phosphorylation-mimicking mutants

    A phosphorylation switch in the Mediator MED15 controls cellular senescence and cognitive decline

    Cell discovery19 Aug 2025

More on Cellular senescence

Senescence-associated secretory phenotype (SASP)

upin mouse cells1

1 study

  1. MED15 increases senescence-associated secretory phenotype (SASP) in mouse cells.

    “The MED15 T603 dephosphorylated mutant (T603A) inhibits the SASP and cell senescence, whereas the T603 phosphorylation-mimicking mutant (T603D) has the opposite effect.”

    CellsComparison of MED15 T603A dephosphorylated and T603D phosphorylation-mimicking mutants

    A phosphorylation switch in the Mediator MED15 controls cellular senescence and cognitive decline

    Cell discovery19 Aug 2025

More on Senescence-associated secretory phenotype (SASP)

Latest

Related