YIF1A–RNF126–G3BP1/2 axis activates mTORC1 at the Golgi and affects senescence
In this abstract, YIF1A is reported as a Golgi-localized regulator of growth factor-mediated mTORC1 signaling; its depletion impaired mTORC1 activity and conferred resistance to etoposide- and doxorubicin-induced cellular senescence, and worms lacking or overexpressing the ortholog yif-1 showed extended or shortened lifespan. [1]
Automatic summary · not editorially reviewed
The key findings
YIF1A is reported as a novel Golgi-localized regulator of growth factor-mediated mTORC1 signaling that interacts with RNF126 to promote K48-linked polyubiquitination of G3BP1/2. [1]
Depletion of YIF1A or RNF126 stabilized G3BP1/2 and impaired mTORC1 activity, and YIF1A knockdown conferred resistance to etoposide- and doxorubicin-induced cellular senescence. [1]
In Caenorhabditis elegans, lacking or overexpressing yif-1, the invertebrate ortholog of YIF1A, was associated with extended or shortened lifespan. [1]
The source at a glance
- Study type / format
- Laboratory study reported in an abstract
- Population / context
- Cells in laboratory experiments and Caenorhabditis elegans worms; no human participants are described.
- Summary based on
- Study abstract
- Original publication
- June 23, 2026
Golgi-localized mTORC1 regulation by YIF1A
The abstract notes that mTORC1 activation occurs on lysosomal membranes and at the Golgi in response to environmental cues, but the Golgi-associated mechanism was poorly understood. The study identifies YIF1A as a novel Golgi-localized regulator of growth factor-mediated mTORC1 signaling. Mechanistically, YIF1A is reported to interact with the E3 ubiquitin ligase RNF126 to facilitate K48-linked polyubiquitination of G3BP1/2, thereby promoting mTORC1 activation.
Supporting source [1]
Depletion, senescence resistance and worm lifespan
Genetic depletion of either YIF1A or RNF126 stabilized G3BP1/2 proteins and significantly impaired mTORC1 activity. Notably, YIF1A knockdown conferred resistance to etoposide- and doxorubicin-induced cellular senescence. The abstract reports evolutionary conservation of this pathway, shown by extended or shortened lifespan in Caenorhabditis elegans lacking or overexpressing yif-1, the invertebrate ortholog of YIF1A.
Supporting source [1]
Abstract-only scope and proposed therapeutic framing
The authors state that their findings elucidate a previously unrecognized Golgi-specific regulatory axis for mTORC1 activation and suggest YIF1A as a potential therapeutic target for modulating aging-related pathologies. This is a proposal, not a validated treatment. The record is an abstract; the full text was not reviewed, so design details, sample sizes, follow-up and the extent of human relevance are not reported here. The worm lifespan results concern an invertebrate ortholog and do not establish human lifespan effects.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Design, sample sizes, follow-up and human relevance are not reported in the supplied text. The lifespan findings concern the invertebrate ortholog yif-1 in Caenorhabditis elegans and do not establish human lifespan effects. The therapeutic-target statement is a proposal, not a validated treatment.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Zhang X, Liu L, Shang M, Hu B, Zhu S, Wang X, Liu J, Han Y, Wei X, Cao Q, Li F, Gao L, Sun J, Yu J, Tan C, Dong M, Tang TS, Wang JQ. · europepmc.org · June 23, 2026