FERMT3
1 paper5 findings
- 1 lab in 1 country
- Cells1
Effects
3Cellular senescence
upin human cells1
1 study
Cellular senescence
upin human cells1
FERMT3 induces cellular senescence in human cells.
“These findings identify miP-FERMT3 as a novel regulator of protein catabolism and p53-dependent cell cycle arrest and cellular senescence in endothelial cells.”
CellsmiP-FERMT3 overexpressionendothelial cell
bioRxiv (Cold Spring Harbor Laboratory)3 Dec 2025Preprint
Cell-cycle arrest
upin human cells1
1 study
Cell-cycle arrest
upin human cells1
FERMT3 induces cell-cycle arrest in human cells.
“These findings identify miP-FERMT3 as a novel regulator of protein catabolism and p53-dependent cell cycle arrest and cellular senescence in endothelial cells.”
CellsmiP-FERMT3 overexpressionendothelial cell
bioRxiv (Cold Spring Harbor Laboratory)3 Dec 2025Preprint
Proteasomal activity
upin human cells1
1 study
Proteasomal activity
upin human cells1
FERMT3 increases Proteasomal activity in human cells.
“cells expressing miP-FERMT3 exhibited increased global protein ubiquitination, enhanced centrosomal neddylation and elevated proteasomal activity.”
CellsmiP-FERMT3 overexpressionendothelial cell
bioRxiv (Cold Spring Harbor Laboratory)3 Dec 2025Preprint
Associations
1Age
upin silico1
1 study
Age
upin silico1
FERMT3 is associated with age in silico.
“Analyses of independent murine and human transcriptomic and proteomic aging datasets further revealed that FERMT3 expression and protein abundance increase with age.”
In silicotranscriptomic and proteomic aging datasetsendothelial cell
bioRxiv (Cold Spring Harbor Laboratory)3 Dec 2025Preprint
FERMT3 is associated with age in silico.
“Analyses of independent murine and human transcriptomic and proteomic aging datasets further revealed that FERMT3 expression and protein abundance increase with age.”
In silicotranscriptomic and proteomic aging datasetsendothelial cell
bioRxiv (Cold Spring Harbor Laboratory)3 Dec 2025Preprint