ArticleDifferentiation; research in biological diversity
A charged multivesicular body protein (CHMP4B) is required for lens growth and differentiation.
Article in Differentiation; research in biological diversity. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 24 citations in OpenAlex.
- ESCRT-III function in membrane fission and repair.Nature reviews. Molecular cell biology · 2026Review
- Candidate Genes for Non-Syndromic Pediatric Cataracts.Clinical ophthalmology (Auckland, N.Z.) · 2026Review
- Transcriptomic Insights into Late-Life Depression and the Role of Environmental Drinking Water Composition: A Study on 18-Month-Old Mice.International journal of molecular sciences · 2025Article
- Exploiting autophagy and related pathways: pioneering new horizons in cataract therapy.Apoptosis : an international journal on programmed cell death · 2025Review
- Extracellular vesicle signatures from eye lavage as novel non-invasive biomarkers for hypoxic ischaemic insult-findings from a neonatal mouse model.Frontiers in medical technology · 2025Article
- Article
- A Cataract-Causing Mutation in the TRPM3 Cation Channel Disrupts Calcium Dynamics in the Lens.Cells · 2024Article
- Application of transgenic mice to the molecular pathogenesis of cataract.International journal of ophthalmology · 2024Review
- HSP90β prevents aging-related cataract formation through regulation of the charged multivesicular body protein (CHMP4B) and p53.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Whole Exome Sequencing of 20 Spanish Families: Candidate Genes for Non-Syndromic Pediatric Cataracts.International journal of molecular sciences · 2023Article
- Charged multivesicular body protein 4b forms complexes with gap junction proteins during lens fiber cell differentiation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Review
- AUTOPHAGY IN THE EYE: FROM PHYSIOLOGY TO PATHOPHYSOLOGY.Autophagy reports · 2023Article
- Lipid Polarization during Cytokinesis.Cells · 2022Review
- Endocytic membrane repair by ESCRT-III controls antigen export to the cytosol during antigen cross-presentation.Cell reports · 2022Article
- Loss of fiber cell communication may contribute to the development of cataracts of many different etiologies.Frontiers in physiology · 2022Review
- PI(3,4)P2-mediated cytokinetic abscission prevents early senescence and cataract formation.Science (New York, N.Y.) · 2021Article
- Article
- Mutation of the TRPM3 cation channel underlies progressive cataract development and lens calcification associated with pro-fibrotic and immune cell responses.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- The regulation of actin dynamics during cell division and malignancy.American journal of cancer research · 2021Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Charged multivesicular body protein 4B (CHMP4B) functions as a core component of the endosome sorting complex required for transport-III (ESCRT-III) machinery that facilitates diverse membrane remodeling and scission processes in eukaryotes. Mutations in the human CHMP4B gene underlie rare, inherited forms of early-onset lens opacities or cataract. Here we have characterized the lens phenotypes of mutant (knock-in) mice harboring a human cataract-associated mutation (p.D129V) in CHMP4B (Chmp4b-mutant) and conditional knockdown mice deficient in lens CHMP4B (Chmp4b-CKD). In situ hybridization localized Chmp4b transcripts to lens epithelial cells and elongating fiber cells at the lens equator. Heterozygous Chmp4b-mutant (D/V) mice were viable and fertile with lenses grossly similar to those of wild-type. However, homozygous Chmp4b-mutant (V/V) mice died by embryonic day 15.5 (E15.5) with grossly abnormal eye and brain histology. Chmp4b-CKD mice displayed variable degrees of lens dysmorphology including lens ablation. Immuno-localization of aquaporin-0 (AQP0) revealed lens fiber cell degeneration in homozygous Chmp4b-mutant (V/V) mouse embryos and in embryonic and postnatal Chmp4b-CKD mice. DNA fragmentation (TUNEL) analysis revealed global cell death in homozygous Chmp4b-mutant (V/V) embryos, whereas, cell death was confined to the lens of Chmp4b-CKD mice. Immuno-localization of the monocyte/macrophage marker macrosialin (CD68) suggested that severe lens degeneration in Chmp4b-CKD mice resulted in an ocular immune cell response. Collectively, these mouse data suggest that (1) heterozygous, germ-line mutations in Chmp4b may not manifest as cataract, (2) homozygous, germ-line mutations in Chmp4b are embryonic lethal, and (3) conditional loss of Chmp4b results in arrest of lens growth and differentiation.
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