LINP1 suppresses radiation-induced cellular senescence in keratinocytes by modulating the mTOR-p53 axis
What this study shows
LncRNA LINP1 binds the FAT domain of mTOR, reduces mTOR-p53 interaction and p53 Ser15 phosphorylation, thereby suppressing radiation-induced cellular senescence in keratinocytes and human skin.
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Human keratinocytes; ex vivo human skin explants) rather than a whole-organism health-outcome study. That is often exactly where causal biology gets established -- the code says which system the finding was shown in, and nothing about how good the work is. |
| Study type | 5 - Mechanistic / In Vitro |
| Model system | Human keratinocytes; ex vivo human skin explants |
| Journal | Molecular and Cellular Biochemistry |
| Year | 2026 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1007/s11010-026-05682-z · PMID 42593644 |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | LINP1 overexpression/knockdown; ionizing radiation |
| Target | mTOR FAT domain; mTOR-p53 interaction; p53 Ser15 phosphorylation; cellular senescence |
| Model | Human |
| Effect | LINP1 directly binds mTOR FAT domain to reduce mTOR-p53 interaction, decrease p53 activation, and suppress radiation-induced senescence |
In the Atlas
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