Author

D. Foguel

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Biochemistry· 1 Microbiology· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Organism:human· 3 Research Focus:cell signaling & trafficking· 2 Approach:experimental assay· 2 Research Focus:host-pathogen & immune response· 2 Assay:proteomics· 2 Assay:bulk RNA-seq· 1 Research Focus:development & morphogenesis· 1 Organism:mouse· 1

Frequent Co-Authors

L. Oliveira· 2 shared A. C. C. de Carvalho· 1 shared A. J. Guimaraes· 1 shared D. De Oliveira· 1 shared D. F. Oliveira· 1 shared F. Mesquita· 1 shared F. Palhano· 1 shared G. H. P. Nunes· 1 shared

Activity by Year

2019-2021 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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Curved chords = mutual co-authorship

2 shared papersMicrobiology

L. Oliveira

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Paving the way towards understanding the inflammatory pathways triggered by giant viruses in mammalian cells: effect of mimivirus-cell interactions on IκBα degradation

J. d. S. Oliveira, D. F. Oliveira, V. A. Essus, G. H. P. Nunes, L. Honorato, L. Oliveira, L. Nimrichter, J. M. Peralta, A. J. Guimaraes, D. Foguel, J. R. Cortines

This study investigates how APMV and Tupanvirus interact with mammalian cells, activating TLR4 and triggering inflammatory responses, including IκBα degradation.

bioRxiv · Sep 16, 2021 · PreprintMicrobiology

Peptides derived from gp43, the most antigenic protein from Paracoccidioides brasiliensis, form amyloid fibrils in vitro: implications for vaccine development

T. R. Cardim-Pires, S. Ricardo, D. Foguel

This study shows that a peptide from gp43, a key antigen in Paracoccidioides brasiliensis, forms amyloid fibrils in vitro, which may hinder vaccine development, and proposes a redesigned sequence to reduce aggregation.

bioRxiv · Jul 8, 2021Biochemistry

Cerebral dopamine neurotrophic factor (CDNF) reduces myocardial ischemia/reperfusion injuries by the activation of PI3K-AKT via KDEL-receptor binding

L. Maciel, D. De Oliveira, F. Mesquita, H. A. d. S. Souza, L. Oliveira, F. Palhano, A. C. C. de Carvalho, J. Nascimento, D. Foguel

This study shows CDNF reduces myocardial ischemia/reperfusion injuries by activating PI3K-AKT through KDEL-receptor binding in cardiomyocytes.

bioRxiv · Jun 27, 2019Physiology