Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05412 (c-Jun)
 11,453 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The MEF2 (myocyte enhancer factor 2) family of transcription factors is composed of four distinct vertebrate genes. These factors were first identified in muscle but are also present in brain. MEF2 is involved in neuronal survival and is able to regulate the growth and pruning of neurons in response to stimulation. Dendrite remodelling is under the control of genes that MEF2 can turn on or off and some of its target genes have been identified. Among them are immediate-early genes such as C-JUN and NUR77 and neuronal-activity-regulated genes such as ARC, SYNGAP, HOMER1A and BDNF. MEF2 is able to control the synapse number in the hippocampus in which its activation inhibits the growth of dendritic spines, highlighting its important role in memory and learning. In addition, mutations in the MEF2 gene has been found in patients with Rett-like disorder. MEF2 has also been implicated in other pathologies such as Alzheimer's and Parkinson's diseases.
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PMID:The MEF2 family and the brain: from molecules to memory. 2339 26

The development of metabolic alterations like insulin resistance has been associated with dysfunctions in mitochondrial oxidative capacity, induction of neuroinflammatory responses, and the appearance of cognitive impairments in the brain. The c-Jun N-terminal Kinase 1 (JNK1) is a potential key modulator of these mechanisms. The current study identifies a protective effect of whole-body JNK1 knockout in the presence of a high-fat diet (HFD). Specifically, the data suggest that mice missing JNK1 show increased insulin sensitivity and mitochondrial activity, as well as reduced body weight, and astrocyte and microglial reactivity. Finally, these animals are also protected against HFD-induced cognitive impairments as assessed through novel object recognition test, the observation of dendritic spines, and the levels of BDNF or other proteins like spinophilin and ARC. Thus, modulation of JNK1 activity seems like a promising approach for the design of therapies aimed at treating metabolic-induced cognitive impairments. KEY MESSAGES: JNK1 is a link between obesity/type 2 diabetes and cognitive loss Inhibition of JNK1 is neuroprotective JNK1 constitutes a therapeutic strategy for cognitive loss.
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PMID:c-Jun N-terminal Kinase 1 ablation protects against metabolic-induced hippocampal cognitive impairments. 3179 11