TNF-α increases production of reactive oxygen species through Cdk5 activation in nociceptive neurons
R Sandoval, P Lazcano, F Ferrari… - Frontiers in …, 2018 - frontiersin.org
The participation of reactive oxygen species (ROS) generated by NOX1 and NOX2/NADPH
oxidase has been documented during inflammatory pain. However, the molecular
mechanism involved in their activation is not fully understood. We reported earlier a key role
of Cyclin-dependent kinase 5 (Cdk5) during inflammatory pain. In particular, we
demonstrated that TNF-α increased p35 expression, a Cdk5 activator, causing Cdk5-
mediated TRPV1 phosphorylation followed by an increment in Ca2+ influx in nociceptive …
oxidase has been documented during inflammatory pain. However, the molecular
mechanism involved in their activation is not fully understood. We reported earlier a key role
of Cyclin-dependent kinase 5 (Cdk5) during inflammatory pain. In particular, we
demonstrated that TNF-α increased p35 expression, a Cdk5 activator, causing Cdk5-
mediated TRPV1 phosphorylation followed by an increment in Ca2+ influx in nociceptive …
TNF-α increases production of reactive oxygen species through Cdk5 activation in nociceptive neurons
R Sandoval Guzmán, P Lazcano Sánchez… - 2018 - repositorio.uchile.cl
The participation of reactive oxygen species (ROS) generated by NOX1 and NOX2/NADPH
oxidase has been documented during inflammatory pain. However, the molecular
mechanism involved in their activation is not fully understood. We reported earlier a key role
of Cyclin-dependent kinase 5 (Cdk5) during inflammatory pain. In particular, we
demonstrated that TNF-α increased p35 expression, a Cdk5 activator, causing Cdk5-
mediated TRPV1 phosphorylation followed by an increment in Ca2+ influx in nociceptive …
oxidase has been documented during inflammatory pain. However, the molecular
mechanism involved in their activation is not fully understood. We reported earlier a key role
of Cyclin-dependent kinase 5 (Cdk5) during inflammatory pain. In particular, we
demonstrated that TNF-α increased p35 expression, a Cdk5 activator, causing Cdk5-
mediated TRPV1 phosphorylation followed by an increment in Ca2+ influx in nociceptive …
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