ArticleHuman molecular genetics2009
Interactions between the juvenile Batten disease gene, CLN3, and the Notch and JNK signalling pathways.
Article in Human molecular genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 50 citations in OpenAlex.
- The calcium channel blocker diltiazem ameliorates parthanatos in juvenile neuronal ceroid lipofuscinosis.Journal of molecular medicine (Berlin, Germany) · 2026Article
- CLN3, at the crossroads of endocytic trafficking.Neuroscience letters · 2021Article
- Exploiting the Potential ofBiomedicines · 2021Review
- Loss of CLN3, the gene mutated in juvenile neuronal ceroid lipofuscinosis, leads to metabolic impairment and autophagy induction in retinal pigment epithelium.Biochimica et biophysica acta. Molecular basis of disease · 2020Article
- Cellular models of Batten disease.Biochimica et biophysica acta. Molecular basis of disease · 2020Review
- Lysosomal proteome analysis reveals that CLN3-defective cells have multiple enzyme deficiencies associated with changes in intracellular trafficking.The Journal of biological chemistry · 2019Article
- Article
- Proteomic mapping of differentially vulnerable pre-synaptic populations identifies regulators of neuronal stability in vivo.Scientific reports · 2017Article
- in vivo localization of the neuronal ceroid lipofuscinosis proteins, CLN3 and CLN7, at endogenous expression levels.Neurobiology of disease · 2017Article
- A saposin deficiency model in Drosophila: Lysosomal storage, progressive neurodegeneration and sensory physiological decline.Neurobiology of disease · 2017Article
- Royal Decree: Gene Expression in Trans-Generationally Immune Primed Bumblebee Workers Mimics a Primary Immune Response.PloS one · 2016Article
- A central role for TOR signalling in a yeast model for juvenile CLN3 disease.Microbial cell (Graz, Austria) · 2015Article
- Diminished MTORC1-Dependent JNK Activation Underlies the Neurodevelopmental Defects Associated with Lysosomal Dysfunction.Cell reports · 2015Article
- Wnt/β-catenin signaling integrates patterning and metabolism of the insect growth zone.Development (Cambridge, England) · 2014Article
- Genetic studies in Drosophila and humans support a model for the concerted function of CISD2, PPT1 and CLN3 in disease.Biology open · 2014Article
- The FTLD risk factor TMEM106B and MAP6 control dendritic trafficking of lysosomes.The EMBO journal · 2014Article
- Modification of the Drosophila model of in vivo Tau toxicity reveals protective phosphorylation by GSK3β.Biology open · 2014Article
- Odd-skipped labels a group of distinct neurons associated with the mushroom body and optic lobe in the adult Drosophila brain.The Journal of comparative neurology · 2013Article
- Neuronal ceroid lipofuscinosis protein CLN3 interacts with motor proteins and modifies location of late endosomal compartments.Cellular and molecular life sciences : CMLS · 2012Article
- Invertebrate models of lysosomal storage disease: what have we learned so far?Invertebrate neuroscience : IN · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in the gene CLN3 are responsible for the neurodegenerative disorder juvenile neuronal ceroid lipofuscinosis or Batten disease. CLN3 encodes a multi-spanning and hydrophobic transmembrane protein whose function is unclear. As a consequence, the cell biology that underlies the pathology of the disease is not well understood. We have developed a genetic gain-of-function system in Drosophila to identify functional pathways and interactions for CLN3. We have identified previously unknown interactions between CLN3 and the Notch and Jun N-terminal kinase signalling pathways and have uncovered a potential role for the RNA splicing and localization machinery in regulating CLN3 function.
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.