Grb10

Gene/Protein · 2 studies in the Atlas

mTORC1 substrate that, once phosphorylated, damps insulin/IGF-1 receptor signalling - one arm of the negative feedback that makes mTOR inhibitors paradoxically raise upstream Akt activity.

A brake mTORC1 puts on its own upstream signal. A protein that mTORC1 activates as part of a feedback loop - once switched on, it dials down signaling from the insulin/IGF-1 receptor. It's one reason mTOR inhibitors can paradoxically boost upstream Akt activity.

Stabilised by mTORC1 phosphorylation; one of two arms (with S6K1→IRS-1) of negative feedback onto PI3K, and an imprinted gene with growth phenotypes.

TL;DR. Grb10 appears in 2 curated studies in Oliver's mTOR Atlas: 2 at the molecular level (cells, biochemistry, structure). No study in people is recorded for it in the Atlas yet. It has 2 interactions in the curated pathway model.

In the pathway model

2 interactions in the curated mTOR pathway model (1 acting from Grb10, 1 acting on it). Each row is a claim with the evidence behind it; the evidence code is the kind of study, not its quality.

Interaction	Mechanism	Evidence	Studies
Grb10 inhibits Growth hormone / IGF-1 axis mechanism: signal-relay · this link in full · on the map table	Grb10 dampens insulin/IGF-1 signalling – which is why blocking mTOR can paradoxically make Akt more active. Stabilised Grb10 damps insulin/IGF-1 receptor signalling. This is one of two feedback arms behind the paradox that blocking mTORC1 raises Akt activity; the other is the S6K1-IRS-1 loop. Stabilised Grb10 damps insulin/IGF-1 receptor signalling. This is one of two feedback arms behind the paradox that blocking mTORC1 raises Akt activity; the other is the S6K1-IRS-1 loop. Holds under: Two mammalian cell studies (HSU2011, YUX2011). The feedback is shown in cultured cells. Its size in living tissue and in people, and how it compares with the S6K1-IRS-1 loop, are not measured. plausible in people, not shown directly · settled in the literature	M	HSU2011, YUX2011
mTORC1 activates Grb10 mechanism: stabilization · this link in full · on the map table	mTORC1 stabilises Grb10, kicking off a feedback loop that talks back to the insulin receptor. mTORC1 phosphorylates and stabilises Grb10 - the start of a feedback loop that talks back to the insulin receptor. mTORC1 phosphorylates and stabilises Grb10 - the start of a feedback loop that talks back to the insulin receptor. Holds under: Two mammalian cell studies (HSU2011, YUX2011). Cell culture only; not tested in whole animals or in people. plausible in people, not shown directly · settled in the literature	M	HSU2011, YUX2011

Evidence at a glance

Evidence	What it means	Studies
M	Molecular — cells, biochemistry, structure	2

No direct human evidence in the Atlas for this entity yet — everything below rests on animal or molecular work.

Studies

Year	Evidence	Study
2011	M	The mTOR-regulated phosphoproteome reveals a mechanism of mTORC1-mediated inhibition of growth factor signaling HSU2011 mTOR-dependent phosphoproteomics reveal Grb10 as a substrate mediating feedback inhibition of PI3K.
2011	M	Phosphoproteomic analysis identifies Grb10 as an mTORC1 substrate that negatively regulates insulin signaling YUX2011 Phosphoproteomics identify Grb10 as an mTORC1 substrate driving negative feedback on insulin/PI3K.

Cite this page

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Barton, O. (2026). Grb10 [Entity page]. In Oliver's mTOR Atlas [Data set]. https://mtor-atlas.org/gene/grb10/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_gene_grb10,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}: Grb10},
  howpublished = {Entity page in a data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/gene/grb10/},
  doi          = {10.5281/zenodo.22059963}
}

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