Author: Yen, Wei-Chen; Wu, Yi-Hsuan; Wu, Chih-Ching; Lin, Hsin-Ru; Stern, Arnold; Chen, Shih-Hsiang; Shu, Jwu-Ching; Tsun-Yee Chiu, Daniel
Title: Impaired inflammasome activation and bacterial clearance in G6PD deficiency due to defective NOX/p38 MAPK/AP-1 redox signaling Document date: 2019_11_2
ID: 6fw4thkq_52
Snippet: activation. Such defect in NLRP3 inflammasome activation could be attributed to the inhibition of p38-MAPK and AP-1 signaling upon LPS stimulation. The underlying mechanism is due to decreased superoxide production by NOX, as found in G6PD-kd THP-1 cells. Together, these results indicate that G6PD deficiency impairs the cellular innate immune response by a disturbance in redox homeostasis, which can have clinical implications in G6PD-deficient in.....
Document: activation. Such defect in NLRP3 inflammasome activation could be attributed to the inhibition of p38-MAPK and AP-1 signaling upon LPS stimulation. The underlying mechanism is due to decreased superoxide production by NOX, as found in G6PD-kd THP-1 cells. Together, these results indicate that G6PD deficiency impairs the cellular innate immune response by a disturbance in redox homeostasis, which can have clinical implications in G6PD-deficient individuals with infectious diseases.
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