ArticleThe Journal of cell biology1998
Occludin-deficient embryonic stem cells can differentiate into polarized epithelial cells bearing tight junctions.
Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 191 papers.
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Who cites it
191 citing papers in PubMed, 540 citations in OpenAlex.
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- Occludin Is Essential to Maintain Normal Alveolar Barrier Integrity and Its Protective Role During ARDS Progression.International journal of molecular sciences · 2024Article
- Molecular hydrogen supplementation in mice ameliorates lipopolysaccharide-induced loss of interest.PCN reports : psychiatry and clinical neurosciences · 2024Article
- Tight Junction Component Occludin Binds to FIP5 to Regulate Endosome Trafficking and Mitotic Spindle Function.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Ageratina adenophora damages the rumen epithelium via inducing the expression of inflammatory factors in goats.Journal of animal science · 2024Article
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- A20 regulates lymphocyte adhesion in murine neuroinflammation by restricting endothelial ICOSL expression in the CNS.The Journal of clinical investigation · 2023Article
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- The Rare Marine Bioactive Compounds in Neurological Disorders and Diseases: Is the Blood-Brain Barrier an Obstacle or a Target?Marine drugs · 2023Review
- The tight junction protein occludin modulates blood-brain barrier integrity and neurological function after ischemic stroke in mice.Scientific reports · 2023Article
- Phase separation of an actin nucleator by junctional microtubules regulates epithelial function.Science advances · 2023Article
- Article
131 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Occludin is the only known integral membrane protein of tight junctions (TJs), and is now believed to be directly involved in the barrier and fence functions of TJs. Occludin-deficient embryonic stem (ES) cells were generated by targeted disruption of both alleles of the occludin gene. When these cells were subjected to suspension culture, they aggregated to form simple, and then cystic embryoid bodies (EBs) with the same time course as EB formation from wild-type ES cells. Immunofluorescence microscopy and ultrathin section electron microscopy revealed that polarized epithelial (visceral endoderm-like) cells were differentiated to delineate EBs not only from wild-type but also from occludin-deficient ES cells. Freeze fracture analyses indicated no significant differences in number or morphology of TJ strands between wild-type and occludin-deficient epithelial cells. Furthermore, zonula occludens (ZO)-1, a TJ-associated peripheral membrane protein, was still exclusively concentrated at TJ in occludin-deficient epithelial cells. In good agreement with these morphological observations, TJ in occludin-deficient epithelial cells functioned as a primary barrier to the diffusion of a low molecular mass tracer through the paracellular pathway. These findings indicate that there are as yet unidentified TJ integral membrane protein(s) which can form strand structures, recruit ZO-1, and function as a barrier without occludin.
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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.