ArticleProceedings of the National Academy of Sciences of the United States of America2026
Prevention of ubiquitination at K6 and K9 in mutant huntingtin exacerbates disease pathology in a knock-in mouse model.
Article in Proceedings of the National Academy of Sciences of the United States of America, 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
10 authors.
Funding
Abstract
Huntington disease (HD) is caused by an expansion of the polyglutamine (polyQ) tract in the huntingtin protein (HTT), leading to its misfolding and aggregation. The subcellular localization of mutant HTT (mHTT) aggregates critically influences their neuronal toxicity, with nuclear aggregates contributing more significantly to neurodegeneration than those in the neuropil. Our previous findings demonstrated that site-specific ubiquitination of lysine residues at the positions of K6 and K9 in HTT significantly affect the aggregation properties of mHTT and influence cell viability. However, the in vivo functional relevance of this modification remains elusive. To address this, we generated two HD knock-in (KI) mouse models in which the mouse
Indexed as
Identifiers
What 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.