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Details on Person Based on mouse model studies, the JUN transcription factor u...

Class:IdSummation:8868667
_displayNameBased on mouse model studies, the JUN transcription factor u...
_timestamp2016-04-22 18:44:08
created[InstanceEdit:8868665] Orlic-Milacic, Marija, 2016-04-22
literatureReference[LiteratureReference:8868671] Direct and indirect roles of cyclin-dependent kinase 5 as an upstream regulator in the c-Jun NH2-terminal kinase cascade: relevance to neurotoxic insults in Alzheimer's disease
[LiteratureReference:8868669] Cdk5 is a major regulator of p38 cascade: relevance to neurotoxicity in Alzheimer's disease
modified[InstanceEdit:8868672] Orlic-Milacic, Marija, 2016-04-22
[InstanceEdit:8868681] Orlic-Milacic, Marija, 2016-04-22
textBased on mouse model studies, the JUN transcription factor undergoes biphasic activation in Alzheimer's disease. JUN is phosphorylated directly by p25-bound CDK5 at serine residues S63 and S73. CDK5:p25-mediated increase in the level of reactive oxygen species (ROS) triggers activation of JNK kinases (MAPK8, MAPK9, MAPK10), which phosphorylate JUN at S63 and S73 at a later time point (Sun et al. 2009).

Aberrant activation of CDK5 by p25 binding also triggers activation of MKK6 (MAP2K6), a p38 MAP kinase. Levels of phosphorylated MAP2K6 are increased in Alzheimer's disease. Activation of p38 MAP kinase(s) results in increased JUN expression (Chang et al. 2010).

(summation)[Reaction:8868666] CDK5:p25 phosphorylates JUN [Homo sapiens]
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