ArticleInfection and immunity2001
Association of mitogen-activated protein kinase pathways with gingival epithelial cell responses to Porphyromonas gingivalis infection.
Article in Infection and immunity, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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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.
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Who cites it
37 citing papers in PubMed, 75 citations in OpenAlex.
- Inhibition of CD38 by 78c Enhanced NADInternational journal of molecular sciences · 2026Article
- Illuminating the oral microbiome: cellular microbiology.FEMS microbiology reviews · 2023Article
- A bacterial tyrosine phosphatase modulates cell proliferation through targeting RGCC.PLoS pathogens · 2021Article
- Porphyromonas gingivalis adopts intricate and unique molecular mechanisms to survive and persist within the host: a critical update.Journal of oral microbiology · 2020Review
- Metronidazole-Treated Porphyromonas gingivalis Persisters Invade Human Gingival Epithelial Cells and Perturb Innate Responses.Antimicrobial agents and chemotherapy · 2020Article
- Porphyromonas gingivalis bypasses epithelial barrier and modulates fibroblastic inflammatory response in an in vitro 3D spheroid model.Scientific reports · 2018Article
- Microbial Degradation of Cellular Kinases Impairs Innate Immune Signaling and Paracrine TNFα Responses.Scientific reports · 2016Article
- Porphyromonas gingivalis initiates a mesenchymal-like transition through ZEB1 in gingival epithelial cells.Cellular microbiology · 2016Article
- Porphyromonas gingivalis Gingipain-Dependently Enhances IL-33 Production in Human Gingival Epithelial Cells.PloS one · 2016Article
- FOXO responses to Porphyromonas gingivalis in epithelial cells.Cellular microbiology · 2015Article
- Involvement of protease-activated receptor 4 in over-expression of matrix metalloproteinase 9 induced by Porphyromonas gingivalis.Medical microbiology and immunology · 2015Article
- Distinctive pathways characterize A. actinomycetemcomitans and P. gingivalis.Molecular biology reports · 2015Article
- Effects of Intravenous Injection of Porphyromonas gingivalis on Rabbit Inflammatory Immune Response and Atherosclerosis.Mediators of inflammation · 2015Article
- Cleavage of host cytokeratin-6 by lysine-specific gingipain induces gingival inflammation in periodontitis patients.PloS one · 2015Article
- Porphyromonas gingivalis-induced reactive oxygen species activate JAK2 and regulate production of inflammatory cytokines through c-Jun.Infection and immunity · 2014Article
- TNF-α augmented Porphyromonas gingivalis invasion in human gingival epithelial cells through Rab5 and ICAM-1.BMC microbiology · 2014Article
- Genetic diversity in the oral pathogen Porphyromonas gingivalis: molecular mechanisms and biological consequences.Future microbiology · 2013Review
- Integrin α5β1-fimbriae binding and actin rearrangement are essential for Porphyromonas gingivalis invasion of osteoblasts and subsequent activation of the JNK pathway.BMC microbiology · 2013Article
- Porphyromonas gingivalis induction of microRNA-203 expression controls suppressor of cytokine signaling 3 in gingival epithelial cells.Infection and immunity · 2011Article
- Polymeric immunoglobulin receptor-mediated invasion of Streptococcus pneumoniae into host cells requires a coordinate signaling of SRC family of protein-tyrosine kinases, ERK, and c-Jun N-terminal kinase.The Journal of biological chemistry · 2010Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
Mitogen-activated protein (MAP) kinase pathways are key factors in host signaling events and can also play important roles in the internalization of pathogenic bacteria by host cells. Porphyromonas gingivalis, a periodontal pathogen, can efficiently invade human gingival epithelial cells (GECs). In this study, we examined the activation of MAP kinase pathways in GECs infected with P. gingivalis. c-Jun N-terminal kinase (JNK) was activated after 5 min of infection with P. gingivalis, whereas noninvasive Streptococcus gordonii did not have a significant effect on JNK activation. In contrast, extracellular signal-regulated kinase (ERK) 1/2 was downregulated in a dose-dependent manner by P. gingivalis, but not by S. gordonii, after a 15-min exposure. Nonmetabolically active P. gingivalis cells were unable to modulate MAP kinase activity. U0126, a specific inhibitor of MEK1/2 (ERK1/2 kinase), and toxin B, a specific inhibitor of Rho family GTPases, had no effect on P. gingivalis invasion. Genistein, a tyrosine protein kinase inhibitor, blocked uptake of P. gingivalis. The transcriptional regulator NF-kappaB was not activated by P. gingivalis. These results suggest that P. gingivalis can selectively target components of the MAP kinase pathways. ERK1/2, while not involved in P. gingivalis invasion of GECs, may be downregulated by internalized P. gingivalis. Activation of JNK is associated with the invasive process of P. gingivalis.
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