AgingResearch.NewsJoin free

ACSS2

Gene

4 papers6 findings

HGNC 15814NCBI Gene 55902Taxon 9606

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.

  • 2 independent labs in 1 country
  • Funders: National Natural Science Foundation of China and 2 more
  • Animals3

Effects

6

DNA repair

downin mouse cells1

1 study

  1. ACSS2 inhibits DNA repair in mouse cells.

    “reduces dNTP pools for DNA repair, exacerbating cytoplasmic chromatin fragment accumulation and SASP”

    Cellsvia limiting purine metabolism and reducing dNTP pools

    ACSS2 drives senescence-associated secretory phenotype by limiting purine biosynthesis through PAICS acetylation

    Nature communications28 Feb 2025

More on DNA repair

Purine metabolism

downin mouse cells1

1 study

  1. ACSS2 inhibits purine metabolism in mouse cells.

    “The acetylation of PAICS promotes autophagy-mediated degradation of PAICS to limit purine metabolism”

    Cellsvia autophagy-mediated degradation of PAICS

    ACSS2 drives senescence-associated secretory phenotype by limiting purine biosynthesis through PAICS acetylation

    Nature communications28 Feb 2025

More on Purine metabolism

Senescence-associated secretory phenotype (SASP)

upin mice1

1 study

  1. ACSS2 increases senescence-associated secretory phenotype (SASP) in mice.

    “pharmacological inhibition and deletion of Acss2 in mice blunts SASP”

    Animalsin senescent cells

    ACSS2 drives senescence-associated secretory phenotype by limiting purine biosynthesis through PAICS acetylation

    Nature communications28 Feb 2025

More on Senescence-associated secretory phenotype (SASP)

IL-1β expression

upin cells1

1 study

  1. ACSS2 increases IL-1β expression in cells.

    “genetic and pharmacologic inhibition of ACSS2 both suppress H3K9cr-mediated IL-1β expression”

    Cellsshown by genetic and pharmacologic inhibition of ACSS2

    Inhibition of ACSS2-mediated histone crotonylation alleviates kidney fibrosis via IL-1β-dependent macrophage activation and tubular cell senescence

    Nature communications13 Apr 2024

More on IL-1β expression

H3K9ac

no changein cells1

1 study

  1. ACSS2 has no effect on H3K9ac in cells.

    “without influencing H3K9ac in kidneys and tubular epithelial cells.”

    Cellstubular epithelial cell

    Inhibition of ACSS2-mediated histone crotonylation alleviates kidney fibrosis via IL-1β-dependent macrophage activation and tubular cell senescence

    Nature communications13 Apr 2024

More on H3K9ac

H3K9cr

upin cells1

1 study

  1. ACSS2 increases H3K9cr in cells.

    “is found to remarkably increase histone 3 lysine 9 crotonylation (H3K9cr) level without influencing H3K9ac in kidneys and tubular epithelial cells.”

    Cellstubular epithelial cell

    Inhibition of ACSS2-mediated histone crotonylation alleviates kidney fibrosis via IL-1β-dependent macrophage activation and tubular cell senescence

    Nature communications13 Apr 2024

More on H3K9cr

Latest

Related