ArticleNeuroscience letters2006
Tissue transglutaminase crosslinks ataxin-1: possible role in SCA1 pathogenesis.
Article in Neuroscience letters, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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
10 citing papers in PubMed, 22 citations in OpenAlex.
- Cross-species genetic screens identify transglutaminase 5 as a regulator of polyglutamine-expanded ataxin-1.The Journal of clinical investigation · 2022Article
- Pathogenic mechanisms underlying spinocerebellar ataxia type 1.Cellular and molecular life sciences : CMLS · 2020Review
- Roles of Post-translational Modifications in Spinocerebellar Ataxias.Frontiers in cellular neuroscience · 2018Review
- Transglutaminase 2 has opposing roles in the regulation of cellular functions as well as cell growth and death.Cell death & disease · 2016Review
- Inhibition of transglutaminase exacerbates polyglutamine-induced neurotoxicity by increasing the aggregation of mutant ataxin-3 in an SCA3 Drosophila model.Neurotoxicity research · 2015Article
- Beyond the glutamine expansion: influence of posttranslational modifications of ataxin-1 in the pathogenesis of spinocerebellar ataxia type 1.Molecular neurobiology · 2014Review
- Tissue transglutaminase inhibits the TRPV5-dependent calcium transport in an N-glycosylation-dependent manner.Cellular and molecular life sciences : CMLS · 2012Article
- Cellular functions of tissue transglutaminase.International review of cell and molecular biology · 2012Review
- Transglutaminase induces protofibril-like amyloid beta-protein assemblies that are protease-resistant and inhibit long-term potentiation.The Journal of biological chemistry · 2008Article
- Role of tissue transglutaminase type 2 in calbindin-D28k interaction with ataxin-1.Neuroscience letters · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Transglutaminase type 2 (TG2) has recently been implicated in crosslinking of mutant huntingtin protein into aggregates. Here we show that TG2 also crosslinks spinocerebellar ataxia-1 (SCA1) gene product ataxin-1. HeLa cell lysates expressing GFP tagged ataxin-1 with 2, 30 or 82 glutamines showed covalent crosslinking of ataxin-1 when incubated with exogenously added TG2. This crosslinking was inhibited by TG2 inhibitor cystamine. SCA1 transgenic mice which overexpress the mutant ataxin-1 in cerebellar Purkinje cells showed elevated nuclear TG2 in the absence of ataxin-1 nuclear aggregates. The addition of purified TG2 to the nuclear extracts or addition of SCA1 nuclear TG2 to GFP-Q82 HeLa cell lysates resulted in the formation of insoluble aggregates. These data indicate that ataxin-1 is a substrate of TG2. Further, in SCA1 TG2 may translocate to the nucleus in response to nuclear accumulation of mutant ataxin-1 at early stages of the disease.
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.