ArticleCells2018
Neuronal Ceroid Lipofuscinoses: Connecting Calcium Signalling through Calmodulin.
Article in Cells, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 11 citations in OpenAlex.
- Neuronal progenitor cells-based metabolomics study reveals dysregulated lipid metabolism and identifies putative biomarkers for CLN6 disease.Scientific reports · 2023Article
- Loss of the batten disease protein CLN3 leads to mis-trafficking of M6PR and defective autophagic-lysosomal reformation.Nature communications · 2023Article
- Ppt1-deficiency dysregulates lysosomal CaJournal of inherited metabolic disease · 2022Article
- Calmodulin binding proteins and neuroinflammation in multiple neurodegenerative diseases.BMC neuroscience · 2022Review
- Altered protein secretion in Batten disease.Disease models & mechanisms · 2021Review
- A Proteomics Analysis of Calmodulin-Binding Proteins inInternational journal of molecular sciences · 2021Article
- Calmodulin-mediated events during the life cycle of the amoebozoan Dictyostelium discoideum.Biological reviews of the Cambridge Philosophical Society · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Despite the increased focus on the role of calcium in the neuronal ceroid lipofuscinoses (NCLs, also known as Batten disease), links between calcium signalling and the proteins associated with the disease remain to be identified. A central protein in calcium signalling is calmodulin (CaM), which regulates many of the same cellular processes affected in the NCLs. In this study, we show that 11 of the 13 NCL proteins contain putative CaM-binding domains (CaMBDs). Many of the missense mutations documented from NCL patients overlap with the predicted CaMBDs and are often key residues of those domains. The two NCL proteins lacking such domains, CLN7 and CLN11, share a commonality in undergoing proteolytic processing by cathepsin L, which contains a putative CaMBD. Since CaM appears to have both direct and indirect roles in the NCLs, targeting it may be a valid therapeutic approach for treating 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.