Tankyrase-2 regulates adipocyte differentiation through AMPK/mTOR signaling.
What this study shows
Deleting TNKS1 or TNKS2 slows adipocyte differentiation, with inhibited autophagy, AMPK activation and suppressed mTORC1; the TNKS2-knockout defect is rescued by NV-5138 or by LKB1 inhibition, and TNKS2 ADP-ribosylates LKB1 (cell line).
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Cell line (adipocytes)) 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 | Cell line (adipocytes) |
| Journal | The FEBS journal |
| Year | 2026 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1111/febs.70676 · PMID 42563506 |
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 | TNKS2 knockout / NV-5138 (autophagy activator) |
| Target | AMPK/mTORC1 |
| Model | Cell line |
| Effect | Reduces adipocyte differentiation rate; AMPK activation suppresses mTORC1 |
In the Atlas
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