Selective activation of PFKL suppresses the phagocytic oxidative burst is a research paper published in Cell (2021). On theSindex it has a DataRank of 0. It has been cited 160 times.
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Genentech
Grant: 1008579R
National Institutes of Health
Grant: R01GM118396
Indiana Clinical and Translational Sciences Institute
Grant: U54 GM104942
NIH HHS
Grant: S10 OD023476
Fundação para a Ciência e a Tecnologia, I.P.
Grant: PTDC/CCI-INF/6762/2020
MS3: New foundations for micro-services and serverless systems
National Institutes of Health
Grant: 2U54GM104942-02
West Virginia Clinical and Translational Science Institute: Improving Health through Partnerships and Transformative Research
National Institutes of Health
Grant: 1R01GM118396-01
The Structure and Function of Metabolic Filaments
University of Washington
West Virginia University
FWCI
8.21
Citation Percentile
1.0%
Citation Trend
Fields of Study
MeSH Terms
Keywords
Sustainable Development Goals
Additional file 1 of Cyclosporine A alleviates colitis by inhibiting the formation of neutrophil extracellular traps via the regulating pentose phosphate pathway
Additional file 1 of Cyclosporine A alleviates colitis by inhibiting the formation of neutrophil extracellular traps via the regulating pentose phosphate pathway
Additional file 1 of G6PD maintains the VSMC synthetic phenotype and accelerates vascular neointimal hyperplasia by inhibiting the VDAC1–Bax-mediated mitochondrial apoptosis pathway
Additional file 1 of G6PD maintains the VSMC synthetic phenotype and accelerates vascular neointimal hyperplasia by inhibiting the VDAC1–Bax-mediated mitochondrial apoptosis pathway
Additional file 2 of G6PD maintains the VSMC synthetic phenotype and accelerates vascular neointimal hyperplasia by inhibiting the VDAC1–Bax-mediated mitochondrial apoptosis pathway
Additional file 2 of G6PD maintains the VSMC synthetic phenotype and accelerates vascular neointimal hyperplasia by inhibiting the VDAC1–Bax-mediated mitochondrial apoptosis pathway
Additional file 3 of Cyclosporine A alleviates colitis by inhibiting the formation of neutrophil extracellular traps via the regulating pentose phosphate pathway
Additional file 3 of Cyclosporine A alleviates colitis by inhibiting the formation of neutrophil extracellular traps via the regulating pentose phosphate pathway
Additional file 3 of G6PD maintains the VSMC synthetic phenotype and accelerates vascular neointimal hyperplasia by inhibiting the VDAC1–Bax-mediated mitochondrial apoptosis pathway
Additional file 3 of G6PD maintains the VSMC synthetic phenotype and accelerates vascular neointimal hyperplasia by inhibiting the VDAC1–Bax-mediated mitochondrial apoptosis pathway
Additional file 1 of Reversing the directionality of reactions between non-oxidative pentose phosphate pathway and glycolytic pathway boosts mycosporine-like amino acid production in Saccharomyces cerevisiae
Additional file 1 of Reversing the directionality of reactions between non-oxidative pentose phosphate pathway and glycolytic pathway boosts mycosporine-like amino acid production in Saccharomyces cerevisiae
Additional file 2 of Reversing the directionality of reactions between non-oxidative pentose phosphate pathway and glycolytic pathway boosts mycosporine-like amino acid production in Saccharomyces cerevisiae
Additional file 2 of Reversing the directionality of reactions between non-oxidative pentose phosphate pathway and glycolytic pathway boosts mycosporine-like amino acid production in Saccharomyces cerevisiae
Additional file 2 of Cyclosporine A alleviates colitis by inhibiting the formation of neutrophil extracellular traps via the regulating pentose phosphate pathway
Additional file 2 of Cyclosporine A alleviates colitis by inhibiting the formation of neutrophil extracellular traps via the regulating pentose phosphate pathway