ReviewJournal of neurochemistry2009
Transglutaminases and neurodegeneration.
Review in Journal of neurochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 86 citations in OpenAlex.
- Development of peptide-based biosensors for detecting cross-linking and deamidation activities of transglutaminases.Amino acids · 2023Article
- Review
- Transglutaminase 6 Is Colocalized and Interacts with Mutant Huntingtin in Huntington Disease Rodent Animal Models.International journal of molecular sciences · 2021Article
- Probing tissue transglutaminase mediated vascular smooth muscle cell aging using a novel transamidation-deficient Tgm2-C277S mouse model.Cell death discovery · 2021Article
- Review
- Neither a Novel Tau Proteinopathy nor an Expansion of a Phenotype: Reappraising Clinicopathology-Based Nosology.International journal of molecular sciences · 2021Article
- Zinc as a modulator of transglutaminase activity - Laboratory and pathophysiological aspects.Journal of translational autoimmunity · 2021Review
- The Rate of Decrease in Brain Perfusion in Progressive Supranuclear Palsy and Corticobasal Syndrome May Be Impacted by Glycemic Variability-A Pilot Study.Frontiers in neurology · 2021Article
- Ablation of polyamine catabolic enzymes provokes Purkinje cell damage, neuroinflammation, and severe ataxia.Journal of neuroinflammation · 2020Article
- The Tubulin Code in Microtubule Dynamics and Information Encoding.Developmental cell · 2020Review
- New directions in therapeutics for Huntington disease.Future neurology · 2018Review
- Calcium-dependent activation of transglutaminase 2 by nanosecond pulsed electric fields.FEBS open bio · 2017Article
- Amphotericin B Increases Transglutaminase 2 Expression Associated with Upregulation of Endocytotic Activity in Mouse Microglial Cell Line BV-2.Neurochemical research · 2017Article
- 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
- Transglutaminase 2 exacerbates α-synuclein toxicity in mice and yeast.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- Aberrant calcium signaling by transglutaminase-mediated posttranslational modification of inositol 1,4,5-trisphosphate receptors.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Transglutaminase and polyamination of tubulin: posttranslational modification for stabilizing axonal microtubules.Neuron · 2013Article
- Overlapped metabolic and therapeutic links between Alzheimer and diabetes.Molecular neurobiology · 2013Review
- γ-Glutamylamines and neurodegenerative diseases.Amino acids · 2013Review
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 2 institutions in 1 country.
Funding
Abstract
Transglutaminases (TGs) are Ca2+-dependent enzymes that catalyze a variety of modifications of glutaminyl (Q) residues. In the brain, these modifications include the covalent attachment of a number of amine-bearing compounds, including lysyl (K) residues and polyamines, which serve to either regulate enzyme activity or attach the TG substrates to biological matrices. Aberrant TG activity is thought to contribute to Alzheimer disease, Parkinson disease, Huntington disease, and supranuclear palsy. Strategies designed to interfere with TG activity have some benefit in animal models of Huntington and Parkinson diseases. The following review summarizes the involvement of TGs in neurodegenerative diseases and discusses the possible use of selective inhibitors as therapeutic agents in these diseases.
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.