ArticlePloS one2011
The proteolipid protein promoter drives expression outside of the oligodendrocyte lineage during embryonic and early postnatal development.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 48 citations in OpenAlex.
- Analysis of Oligodendrocyte Lineage Cell Progression with Cre-Mediated RiboTag Reporter Lines.ASN neuro · 2025Article
- Myelin Repair as a Novel Mechanism for Ketamine's Sustained Antidepressant Effects.Current neuropharmacology · 2025Review
- Genetically Labeled Premyelinating Oligodendrocytes: Bridging Oligodendrogenesis and Neuronal Activity.bioRxiv : the preprint server for biology · 2024Article
- The roles of neural stem cells in myelin regeneration and repair therapy after spinal cord injury.Stem cell research & therapy · 2024Review
- Features, Fates, and Functions of Oligodendrocyte Precursor Cells.Cold Spring Harbor perspectives in biology · 2024Review
- Gender-Specific Fine Motor Skill Learning Is Impaired by Myelin-Targeted Neurofibromatosis Type 1 Gene Mutation.Cancers · 2024Article
- Deletion of the Sodium-Dependent Glutamate Transporter GLT-1 in Maturing Oligodendrocytes Attenuates Myelination of Callosal Axons During a Postnatal Phase of Central Nervous System Development.Frontiers in cellular neuroscience · 2022Article
- Ion Channels as New Attractive Targets to Improve Re-Myelination Processes in the Brain.International journal of molecular sciences · 2021Review
- Review
- Aquaporin-4-antibody-positive Neuromyelitis Optica Spectrum Disorder in a Patient with Charcot-Marie-Tooth Disease Type 1A.Internal medicine (Tokyo, Japan) · 2021Article
- Age-dependent decline in remyelination capacity is mediated by apelin-APJ signaling.Nature aging · 2021Article
- N-acetylglucosamine drives myelination by triggering oligodendrocyte precursor cell differentiation.The Journal of biological chemistry · 2020Article
- Review
- Anti-Myelin Proteolipid Protein Peptide Monoclonal Antibodies Recognize Cell Surface Proteins on Developing Neurons and Inhibit Their Differentiation.Journal of neuropathology and experimental neurology · 2019Article
- Severe Convulsions and Dysmyelination in Both Jimpy and Cx32/47Neurochemical research · 2017Review
- VCAM1 acts in parallel with CD69 and is required for the initiation of oligodendrocyte myelination.Nature communications · 2016Article
- Oligodendroglial membrane dynamics in relation to myelin biogenesis.Cellular and molecular life sciences : CMLS · 2016Review
- Oligodendroglial defects during quakingviable cerebellar development.Developmental neurobiology · 2016Article
- Regulation of DM-20 mRNA expression and intracellular translocation of glutathione-S-transferase pi isoform during oligodendrocyte differentiation in the adult rat spinal cord.Histochemistry and cell biology · 2016Article
- The expression of PLP/DM-20 mRNA is restricted to the oligodendrocyte-lineage cells in the adult rat spinal cord.Histochemistry and cell biology · 2016Article
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
No grant is acknowledged in the PubMed record.
Abstract
The proteolipid protein (Plp) gene promoter is responsible for driving expression of one of the major components of myelin--PLP and its splice variant DM-20. Both products are classically thought to express predominantly in oligodendrocytes. However, accumulating evidence suggests Plp expression is more widespread than previously thought. In an attempt to create a mouse model for inducing oligodendrocyte-specific gene deletions, we have generated transgenic mice expressing a Cre recombinase cDNA under control of the mouse Plp promoter. We demonstrate Plp promoter driven Cre expression is restricted predominantly to mature oligodendrocytes of the central nervous system (CNS) at postnatal day 28. However, crosses into the Rosa26(LacZ) and mT/mG reporter mouse lines reveal robust and widespread Cre activity in neuronal tissues at E15.5 and E10.5 that is not strictly oligodendrocyte lineage specific. By P28, all CNS tissues examined displayed high levels of reporter gene expression well outside of defined white matter zones. Importantly, our study reinforces the emerging idea that Plp promoter activity is not restricted to the myelinating cell lineage, but rather, has widespread activity both during embryonic and early postnatal development in the CNS. Specificity of the promoter to the oligodendrocyte cell lineage, as shown through the use of a tamoxifen inducible Plp-CreER(t) line, occurs only at later postnatal stages. Understanding the temporal shift in Plp driven expression is of consequence when designing experimental models to study oligodendrocyte biology.
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.