ArticleProceedings of the National Academy of Sciences of the United States of America1996
Peptides containing glutamine repeats as substrates for transglutaminase-catalyzed cross-linking: relevance to diseases of the nervous system.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 199 citations in OpenAlex.
- GWA meta-analysis of personality in Korean cohorts.Journal of human genetics · 2015Pooled it
- Anticancer peptide Q7 suppresses the growth and migration of human endometrial cancer by inhibiting DHCR24 expression and modulating the AKT-mediated pathway.International journal of medical sciences · 2022Article
- Neural and mesenchymal stem cells in animal models of Huntington's disease: past experiences and future challenges.Stem cell research & therapy · 2015Review
- Molecular cloning and characterization of amh and dax1 genes and their expression during sex inversion in rice-field eel Monopterus albus.Scientific reports · 2015Article
- Detection of ubiquitinated huntingtin species in intracellular aggregates.Frontiers in molecular neuroscience · 2015Article
- Beyond the glutamine expansion: influence of posttranslational modifications of ataxin-1 in the pathogenesis of spinocerebellar ataxia type 1.Molecular neurobiology · 2014Review
- Monomeric, oligomeric and polymeric proteins in huntington disease and other diseases of polyglutamine expansion.Brain sciences · 2014Article
- Factors Affecting Aggregate Formation in Cell Models of Huntington's Disease and Amyotrophic Lateral Sclerosis.Acta naturae · 2013Article
- Tissue transglutaminase overexpression does not modify the disease phenotype of the R6/2 mouse model of Huntington's disease.Experimental neurology · 2012Article
- Engineered antibody therapies to counteract mutant huntingtin and related toxic intracellular proteins.Progress in neurobiology · 2012Review
- Beta-actin is a target for transglutaminase activity at synaptic endings in chicken telencephalic cell cultures.Journal of molecular neuroscience : MN · 2012Article
- Deimination of human filaggrin-2 promotes its proteolysis by calpain 1.The Journal of biological chemistry · 2011Article
- Mutant huntingtin causes defective actin remodeling during stress: defining a new role for transglutaminase 2 in neurodegenerative disease.Human molecular genetics · 2011Article
- Déjà vu with a twist: transglutaminases in bioenergetics and transcriptional dysfunction in Huntington's disease.EMBO molecular medicine · 2010Article
- Transglutaminase activation in neurodegenerative diseases.Future neurology · 2009Article
- Transglutaminases and neurodegeneration.Journal of neurochemistry · 2009Review
- Molecular identification and expression analysis of filaggrin-2, a member of the S100 fused-type protein family.PloS one · 2009Article
- Method for screening and MALDI-TOF MS sequencing of encoded combinatorial libraries.Analytical chemistry · 2007Article
- Developmental expression of DAX1 in the European sea bass, Dicentrarchus labrax: lack of evidence for sexual dimorphism during sex differentiation.Reproductive biology and endocrinology : RB&E · 2007Article
- Apoptotic cascades as possible targets for inhibiting cell death in Huntington's disease.Journal of neurology · 2006Review
Corrections and comments
- Commented on by
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many proteins contain reiterated glutamine residues, but polyglutamine of excessive length may result in human disease by conferring new properties on the protein containing it. One established property of a glutamine residue, depending on the nature of the flanking residues, is its ability to act as an amine acceptor in a transglutaminase-catalyzed reaction and to make a glutamyl-lysine cross-link with a neighboring polypeptide. To learn whether glutamine repeats can act as amine acceptors, we have made peptides with variable lengths of polyglutamine flanked by the adjacent amino acid residues in the proteins associated with spinocerebellar ataxia type 1 (SCA1), Machado-Joseph disease (SCA3), or dentato-rubral pallidoluysian atrophy (DRPLA) or those residues adjacent to the preferred cross-linking site of involucrin, or solely by arginine residues. The polyglutamine was found to confer excellent substrate properties on any soluble peptide; under optimal conditions, virtually all the glutamine residues acted as amine acceptors in the reaction with glycine ethyl-ester, and lengthening the sequence of polyglutamine increased the reactivity of each glutamine residue. In the presence of transglutaminase, peptides containing polyglutamine formed insoluble aggregates with the proteins of brain extracts and these aggregates contained glutamyl-lysine cross-links. Repeated glutamine residues exposed on the surface of a neuronal protein should form cross-linked aggregates in the presence of any transglutaminase activated by the presence of Ca2+.
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.