Sandbox 210: Difference between revisions
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Deregulation of CDK5 has been implicated in Alzheimer’s disease, amyotrophic lateral sclerosis, Parkinson’s disease, Huntington’s disease and acute neuronal injury. Regulators of CDK5 activity are considered as potential therapeutic molecules for degenerative diseases. | Deregulation of CDK5 has been implicated in Alzheimer’s disease, amyotrophic lateral sclerosis, Parkinson’s disease, Huntington’s disease and acute neuronal injury. Regulators of CDK5 activity are considered as potential therapeutic molecules for degenerative diseases. | ||
Sometimes, p35, the activator of CDK5, is cleaved in p25 by a protease calcium-dependent, the calpain. This cut form of p35 (p25) is able to activate CDK5 and to trigger a modification of its cellular localization. It can increase its activity too. In Alzheimer’s disease or in the amyotrophic lateral sclerosis, when the ratio of p25 over p35 increases, it creates an hyperactivity of CDK5 which could hyperphosphorylate the protein Tau.<ref name="un" /> | Sometimes, p35, the activator of CDK5, is cleaved in p25 by a protease calcium-dependent, the calpain. This cut form of p35 (p25) is able to activate CDK5 and to trigger a modification of its cellular localization. It can increase its activity too. In Alzheimer’s disease or in the amyotrophic lateral sclerosis, when the ratio of p25 over p35 increases, it creates an hyperactivity of CDK5 which could hyperphosphorylate the protein Tau.<ref name="un" /> | ||
== External Resources == | |||
*[http://www.rcsb.org/pdb/explore.do?structureId=1h4l Protein Data Bank file on 1H4L] | |||
==References== | ==References== | ||
