ArticleDisease models & mechanisms2017
Loss of
Article in Disease models & mechanisms, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 17 citations in OpenAlex.
- Translational lipidomics reveals BMP and its precursor LPG as biomarkers for CLN5 Batten disease.bioRxiv : the preprint server for biology · 2026Article
- CLN5 deficiency impairs glucose uptake and uncovers PHGDH as a potential biomarker in Batten disease.Molecular psychiatry · 2025Article
- Cln5 represents a new type of cysteine-basedScience advances · 2022Article
- Altered protein secretion in Batten disease.Disease models & mechanisms · 2021Review
- A lysosomal enigma CLN5 and its significance in understanding neuronal ceroid lipofuscinosis.Cellular and molecular life sciences : CMLS · 2021Review
- Article
- Aberrant Autophagy Impacts Growth and Multicellular Development in aFrontiers in cell and developmental biology · 2021Article
- SMC5/6 is required for replication fork stability and faithful chromosome segregation during neurogenesis.eLife · 2020Article
- Novel likely disease-causing CLN5 variants identified in Pakistani patients with neuronal ceroid lipofuscinosis.Journal of the neurological sciences · 2020Article
- Proteomic and functional analyses in disease models reveal CLN5 protein involvement in mitochondrial dysfunction.Cell death discovery · 2020Article
- Functional Analysis of a Novel CLN5 Mutation Identified in a Patient With Neuronal Ceroid Lipofuscinosis.Frontiers in genetics · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neural stem/progenitor cells (NPCs) generate new neurons in the brain throughout an individual's lifetime in an intricate process called neurogenesis. Neurogenic alterations are a common feature of several adult-onset neurodegenerative diseases. The neuronal ceroid lipofuscinoses (NCLs) are the most common group of inherited neurodegenerative diseases that mainly affect children. Pathological features of the NCLs include accumulation of lysosomal storage material, neuroinflammation and neuronal degeneration, yet the exact cause of this group of diseases remains poorly understood. The function of the CLN5 protein, causative of the CLN5 disease form of NCL, is unknown. In the present study, we sought to examine neurogenesis in the neurodegenerative disorder caused by loss of
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.