Pathway link TBK1-FNIP1
TBK1 FLCN / FNIP1/2
TBK1 inhibits FLCN / FNIP1/2.
TBK1 tags FNIP1, which turns FLCN off and lets TFEB escape mTORC1's grip.
The conditions it holds under
Human cell lines and ATP6V1B2-mutant follicular lymphoma samples (ESP2026); a nutrient-independent lysosomal-stress route. Single study, not yet replicated.
A parallel input to TFEB, not a refutation of canonical TFEB control by mTORC1 (MTORC1-TFEB): it acts by removing FLCN, which mTORC1 needs in order to reach TFEB.
- Time it takes
- minutes
- Step
- direct (one molecule acts on the other)
- Measured in
- human cells
- Where in the cell
- lysosome
- Reaches people?
- plausible in people, not shown directly
- How settled
- emerging, few independent studies
Studies behind it
| Year | Evidence | Study |
|---|---|---|
| 2026 | M | A TBK1/ULK1 signalling axis couples lysosomal stress to TFEB activation.ESP2026 Identifies a nutrient-independent lysosomal pathway in which v-ATPase recruits TBK1/ULK1 to phosphorylate FNIP1, inhibiting the FLCN:FNIP complex and releasing TFEB for nuclear translocation; recurrent ATP6V1B2 mutations found in follicular lymphoma patients constitutively hyperactivate this axis, driving TFEB-dependent tumor proliferation. |
Points the other way
No study in the Atlas contradicts this link. That means none in this curated set, not none in the literature.
Who has checked this
- Checked by
- No researcher outside the project has checked this link yet.
- Curator sign-off
- Not signed off yet. This link was drafted with AI help and has not been reviewed link by link; treat it as a proposal until it is.
- Curated by
- Oliver Barton, with AI help for drafting; see how links are checked.
← The whole pathway · This link as JSON
Thank you. Your answer was counted anonymously.
Thank you. That helps us know which pages have been read by someone who knows the work.
Thank you. We will check it and correct the page.