TNFRSF17

2 papers3 findings

HGNC 11913 NCBI Gene 608 Taxon 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.

1 lab in 1 country
1 trial

1 of 1 trial sponsored by developers of drugs on it

Animals1

Effects

Cellular senescence

upin human cells1upin mice1

1 study

TNFRSF17 increases cellular senescence in human cells.
“TNFRSF17 knockdown alleviated CS-induced mitochondrial membrane depolarization, calcium overload, reactive oxygen species (ROS) accumulation, ATP depletion, IL-6 and TNF-α secretion, and cellular senescence both in vitro and in vivo.”
Cellsin CSE-treated HBE cells
TNFRSF17 Knockdown Alleviates Mitochondrial Dysfunction and Inflammation in COPD Through Suppression of the JAK2/STAT3 Pathway
Drug development research26 Jan 2026
TNFRSF17 increases cellular senescence in mice.
“TNFRSF17 knockdown alleviated CS-induced mitochondrial membrane depolarization, calcium overload, reactive oxygen species (ROS) accumulation, ATP depletion, IL-6 and TNF-α secretion, and cellular senescence both in vitro and in vivo.”
Animalsin CS-treated models
TNFRSF17 Knockdown Alleviates Mitochondrial Dysfunction and Inflammation in COPD Through Suppression of the JAK2/STAT3 Pathway
Drug development research26 Jan 2026