Literature summary for 1.6.3.1 extracted from

Fan, J.; Li, Y.; Levy, R.M.; Fan, J.J.; Hackam, D.J.; Vodovotz, Y.; Yang, H.; Tracey, K.J.; Billiar, T.R.; Wilson, M.A.
Hemorrhagic shock induces NAD(P)H oxidase activation in neutrophils: role of HMGB1-TLR4 signaling (2007), J. Immunol., 178, 6573-6580.

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Application

Application	Comment	Organism
medicine	neutropjhil NAD(P)H oxidase activation, induced by hemorrhagic shock/resuscitation and as mediated by high-mobility group box HMGB1/TLR4 signaling, is an important mechanism responsible for hemorrhagic shock/resuscitation-mediated inflammation and organ injury after hemorrhage	Mus musculus

Organism

Organism	UniProt	Comment	Textmining
Mus musculus	-	-	-

Posttranslational Modification

Posttranslational Modification	Comment	Organism
phosphoprotein	hemorrhagic shock/resuscitation activates NAD(P)H oxidase by phosphorylation of subunit p47phox	Mus musculus

Source Tissue

Source Tissue	Comment	Organism	Textmining
neutrophil	hemorrhagic shock/resuscitation activates NAD(P)H oxidase by phosphorylation of subunit p47phox. Activation is significantly diminshed in C3H/HeJ mice, which are not responsive to lipopolysaccharide because of a point mutation of tlr4 affecting the TIR domain. In wild-type, in vitro stimulation of hemorrhagic shock/resuscitation-activated neutrophils with recombinant high-mobility group box HMGB1 causes TLR4-dependent activation of NAD(P)H oxidase as well as increased reactive oxygen species production through both MyD88-IRAK4-p38 MAPK and MyD88-IRAK4-Akt signaling pathways	Mus musculus	-

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Release 2023.1 (January 2023)