ArticleCellular microbiology2008
Invasion of Cryptococcus neoformans into human brain microvascular endothelial cells requires protein kinase C-alpha activation.
Article in Cellular microbiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 62 citations in OpenAlex.
- Trial
- Role of Microbial Toxins in Neurodegenerative Diseases: Insights and Future Perspectives.Biomolecules · 2026Review
- The Pain Is in the Brain With the Sugar-Coated Killer.The Journal of infectious diseases · 2025Review
- Macropinocytosis mediates neurotropism ofResearch square · 2025Article
- Immunometabolic reprogramming in macrophages infected with active and dormantInfection and immunity · 2025Article
- Mechanisms and Virulence Factors ofJournal of fungi (Basel, Switzerland) · 2024Review
- The pathways and the mechanisms by whichMycology · 2024Review
- Macropinocytosis as a potential mechanism driving neurotropism ofFrontiers in cellular and infection microbiology · 2023Review
- Review
- Host immune responses in the central nervous system during fungal infections.Immunological reviews · 2022Review
- Dual-targeted magnetic mesoporous silica nanoparticles reduce brain amyloid-β burden via depolymerization and intestinal metabolism.Theranostics · 2022Article
- Neuroinflammation in neurodegenerationFrontiers in immunology · 2022Review
- Quantitative analysis reveals internalisation of Cryptococcus neoformans by brain endothelial cells in vivo.Cellular microbiology · 2021Article
- Mechanisms of fungal dissemination.Cellular and molecular life sciences : CMLS · 2021Review
- Nutritional Conditions ModulateMicroorganisms · 2020Article
- Cryptococcal Meningitis and Anti-virulence Therapeutic Strategies.Frontiers in microbiology · 2019Review
- Neuroinfections caused by fungi.Infection · 2018Review
- The blood-brain barrier internalises Cryptococcus neoformans via the EphA2-tyrosine kinase receptor.Cellular microbiology · 2018Article
- Innate immune evasion strategies against Cryptococcal meningitis caused byExperimental and therapeutic medicine · 2017Article
- Unraveling the role of membrane microdomains during microbial infections.Cell biology and toxicology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Pathogenic fungus Cryptococcus neoformans has a predilection for the central nervous system causing devastating meningoencephalitis. Traversal of C. neoformans across the blood-brain barrier (BBB) is a crucial step in the pathogenesis of C. neoformans. Our previous studies have shown that the CPS1 gene is required for C. neoformans adherence to the surface protein CD44 of human brain microvascular endothelial cells (HBMEC), which constitute the BBB. In this report, we demonstrated that C. neoformans invasion of HBMEC was blocked in the presence of G109203X, a protein kinase C (PKC) inhibitor, and by overexpression of a dominant-negative form of PKCalpha in HBMEC. During C. neoformans infection, phosphorylation of PKCalpha was induced and the PKC enzymatic activity was detected in the HBMEC membrane fraction. Our results suggested that the PKCalpha isoform might play a crucial role during C. neoformans invasion. Immunofluorescence microscopic images showed that induced phospho-PKCalpha colocalized with beta-actin on the membrane of HBMEC. In addition, cytochalasin D (an F-filament-disrupting agent) inhibited fungus invasion into HBMEC in a dose-dependent manner. Furthermore, blockage of PKCalpha function attenuated actin filament activity during C. neoformans invasion. These results suggest a significant role of PKCalpha and downstream actin filament activity during the fungal invasion into HBMEC.
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.