ArticleThe Journal of cell biology2025
Protein Kinase C promotes peroxisome biogenesis and peroxisome-endoplasmic reticulum interaction.
Article in The Journal of cell biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed.
- Mitochondrial-endoplasmic reticulum interactions in lung diseases.Cell death & disease · 2026Review
- Genome-wide CRISPR screen reveals PEX11B as a host restriction factor against ORFV through membrane fluidity regulation.PLoS pathogens · 2026Article
- Peroxisome Carrier SLC25A17: Potential Biomarker for Peroxisome Dysfunction and Human Disease.International journal of molecular sciences · 2026Review
- A mitochondria-driven quality control mechanism for peroxisomal membrane proteins.Nature communications · 2026Article
- Mitochondrial dysfunction triggers a maladaptive peroxisomal response driving lipid accumulation.Redox biology · 2026Article
- Machine Learning-Assisted Quantification of Organelle Abundance.Bio-protocol · 2026Article
- VAPB is a negative regulator of STING-mediated innate immune signaling.Science advances · 2025Article
- Peroxisome dynamics and inter-organelle interactions in neuronal health and disease.Frontiers in molecular neuroscience · 2025Review
- Restoring metabolic flexibility: targeting organelle interaction networks in the pathogenesis and therapy of MASLD.Frontiers in cell and developmental biology · 2025Review
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.
Funding
Abstract
Peroxisomes carry out a diverse set of metabolic functions, including oxidation of very long-chain fatty acids, degradation of D-amino acids and hydrogen peroxide, and bile acid production. Many of these functions are upregulated on demand; therefore, cells control peroxisome abundance, and by extension peroxisome function, in response to environmental and developmental cues. The mechanisms upregulating peroxisomes in mammalian cells have remained unclear. Here, we identify a signaling regulatory network that coordinates cellular demand for peroxisomes and peroxisome abundance by regulating peroxisome proliferation and interaction with ER. We show that PKC promotes peroxisome PEX11b-dependent formation. PKC activation leads to an increase in peroxisome-ER contact site formation through inactivation of GSK3β. We show that removal of VAPA and VAPB impairs peroxisome biogenesis and PKC regulation. During neuronal differentiation, active PKC leads to a significant increase in peroxisome formation. We propose that peroxisomal regulation by transient PKC activation enables fine-tuned responses to the need for peroxisomal activity.
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.