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CDK5


Millipore offers the most comprehensive research tools for cdk5 signaling, including gene knockdown tools, active kinases and antibodies. Cdk5, a serine/ threonine kinase, plays an important role in brain development and is dependent upon binding to one of its two regulatory activators, p35 and p25, for kinase activation. In addition to its role in neuronal migration, cdk5 is also implicated in neurodegeneration through dysregulation of its kinase activity. Dysregulation of cdk5 is induced by extracellular loading of amyloid, resulting in tau hyperphosphorylation. Tau hyperphosphorylation induces cytoskeleton collapse and apoptosis in neurons. In addition, p25 is elevated in Alzheimer’s diseased brains, suggesting that p25 generation and dysregulation of Cdk5 plays a role in the pathogenesis of Alzheimer’s disease. This triggers a signaling cascade, leading to neuronal degeneration. Cdk5 inhibitors, which exert protection against neuronal death, are being examined as possible courses of action for combating neurodegeneration.

Let Millipore provide the products necessary to further explore this important target.


cdk5 Activity Data

Cdk5/p25 active (Millipore cat. no.14-516) phosphorylated 0.1 mg/mL Histone H1 (Millipore cat. no.14-155). Assay background was subtracted from the actual counts to yield the results shown above.

References

  1. Floyd SR, Porro EB, Slepnev VI, Ochoa GC,Tsai LH, De Camilli P. Amphiphysin 1 binds the cyclin-dependent kinase (cdk) 5 regulatory subunitp35 and is phosphorylated by cdk5 andcdc2. JBC. Mar 2001; 276(11): 8104–10.
  2. Morfini G, Szebenyi G, Brown H, Pant HC, Pigino G, DeBoer S, Beffert U, Brady ST. A novel CDK5-dependent pathway for regulating EMBO J. Jun 2004; 23(11): 2235–45.
  3. Ohshima T, Ogawa M, Veeranna, Hirasawa M, Longenecker G, Ishiguro K, Pant HC, Brady RO, Kulkarni AB, Mikoshiba K. Synergistic contributions of cyclin-dependant kinase 5/p35 and Reelin/Dab1 to the positioning of cortical neurons in the developing mouse brain. PNAS. Feb 2001; 98(5): 2764–9.

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