Ulk1-mediated phosphorylation of AMPK constitutes a negative regulatory feedback loop
What this study shows
ULK1 phosphorylates and inhibits AMPK in return, showing autophagy signaling is a bidirectional feedback loop, not a one-way switch.
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Human cells; mouse) 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 cells; mouse |
| Journal | Autophagy |
| Year | 2011 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.4161/auto.7.7.15451 · PMID 21460634 |
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 | Biochemical (ULK1–AMPK) |
| Target | ULK1 / AMPK / mTORC1 |
| Model | Human cells; mouse |
| Effect | ULK1 phosphorylates and inhibits AMPK – a negative feedback loop in autophagy signaling |
In the Atlas
Related topics
Links in the pathway map
- Supports ULK1 inhibits AMPK
More studies on this topic
- A systems study reveals concurrent activation of AMPK and mTOR by amino acids (2016)
- 5-Fluorouracil-based chemotherapy disrupts autophagy flux and protein synthesis in cultured myotubes: a role for mTORC1 signaling (2026)
- AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1 (2011)
- Urolithin A activates mitophagy via the AMPK-mTOR axis and modulates the gut-ceramide axis to ameliorate cardiac remodeling in HFpEF (2026)
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