Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Tyrosine phosphorylation is a powerful mechanism of modulation for proliferation, differentiation, and functioning of neurons. The protein products of the neuronal mouse gene PTPRR are physiological regulators of mitogen-activated protein kinase (MAPK) activities. PTPRR(-/-) mice display deficits of motor coordination and balance skills. PTPRR gene orthologues are found in many vertebrates. Recent observations suggest that the human episodic ataxia 2 (EA2) and spinocerebellar ataxia types 6 (SCA6), 12 (SCA12), and 14 (SCA14) might be associated with impaired phosphorylation levels of cerebellum calcium channels and receptors. The concept that MAPK signaling is a key process in tuning synaptic plasticity in cerebellar circuits is now emerging, with numerous implications for understanding cerebellar functions and cerebellar disorders.

Original publication

DOI

10.1007/s12311-009-0118-4

Type

Journal article

Journal

Cerebellum

Publication Date

06/2009

Volume

8

Pages

71 - 73

Keywords

Animals, Calcium Signaling, Cerebellar Ataxia, Cerebellar Diseases, Cerebellum, Humans, MAP Kinase Signaling System, Mice, Mice, Knockout, Neuronal Plasticity, Phosphorylation, Receptor-Like Protein Tyrosine Phosphatases, Class 7