ArticleNature communications2026
Loss of intestinal Akt elicits rapid mortality via intestinal damage which is rescued by mTORC1 activation.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Combined Akt1 and Akt2 systemic deletion in adult mice elicits rapid mortality, preceded by body weight loss, diarrhea, and inflammation. Here, we show that lethality induced by systemic Akt1/Akt2 deletion is caused by intestinal damage, as intestinal Akt1/Akt2 deletion induces mortality phenocopying systemic deletion. Consistently, Akt ablation impairs intestinal organoid formation in vitro. Both in vivo and in vitro results show that Akt is essential for the survival of Paneth cells and survival and proliferation of Lgr5
Indexed as
Identifiers
42918758What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.