Caspase-6 does not contribute to the proteolysis of mutant huntingtin in the HdhQ150 knock-in mouse model of Huntington's disease.

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

8 citing papers in PubMed, 22 citations in OpenAlex.

1. Truncation of mutant huntingtin in knock-in mice demonstrates exon1 huntingtin is a key pathogenic form.Nature communications · 2020
   Article
2. A patient-derived cellular model for Huntington's disease reveals phenotypes at clinically relevant CAG lengths.Molecular biology of the cell · 2018
   Article
3. Differential susceptibility of striatal, hippocampal and cortical neurons to Caspase-6.Cell death and differentiation · 2018
   Article
4. A Huntingtin-based peptide inhibitor of caspase-6 provides protection from mutant Huntingtin-induced motor and behavioral deficits.Human molecular genetics · 2015
   Article
5. Comparative study of naturally occurring huntingtin fragments in Drosophila points to exon 1 as the most pathogenic species in Huntington's disease.Human molecular genetics · 2015
   Article
6. Identification of a post-translationally myristoylated autophagy-inducing domain released by caspase cleavage of huntingtin.Human molecular genetics · 2014
   Article
7. From pathways to targets: understanding the mechanisms behind polyglutamine disease.BioMed research international · 2014
   Review
8. Genetic manipulations of mutant huntingtin in mice: new insights into Huntington's disease pathogenesis.The FEBS journal · 2013
   Review

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

Authors and funding

5 authors at 3 institutions in 3 countries.

Funding

No grant is acknowledged in the PubMed record.

Abstract

PubMed holds no abstract for this paper.