CBX8

3 papers4 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.

2 independent labs in 2 countries

Funders: Department of Science and Technology for Social Development and 1 more

Animals1
Cells2

Effects

DDIT4 expression

downin cells1

1 study

CBX8 decreases DDIT4 expression in cells.
“CBX8 achieves this by recruiting TRIM28 to bind the promoter region of DDIT4, thereby maintaining the H3K27me3 modification status and repressing expression of DDIT4.”
CellsThrough TRIM28 recruitment and maintenance of H3K27me3colorectal cancer cell
CBX8 suppresses autophagy-dependent senescence in colorectal cancer by modulating the mTOR signaling pathway
International journal of biological sciences26 Feb 2026

Upstream

PRKD1

downin human cells1

1 study

PRKD1 decreases CBX8 in human cells.
“PKD1-mediated CBX8 phosphorylation at Thr234 reduced its expression level by promoting its ubiquitination-mediated degradation”
Cellsby phosphorylation at Thr234
Phosphorylation of CBX8 by PKD1 suppresses PRC1 activity and promotes cell senescence
Oncogene15 Dec 2025