Abstract:
:Trk tyrosine kinases are receptors for members of the neurotrophin family and are crucial for growth and survival of specific populations of neurons. Yet, the functions of neurotrophin-Trk signaling in postnatal development as well as maintenance and plasticity of the adult nervous system are less clear. We report here the generation of mice harboring Trk knockin alleles that allow for pharmacological control of Trk kinase activity. Nanomolar concentrations of either 1NMPP1 or 1NaPP1, derivatives of the general kinase inhibitor PP1, inhibit NGF and BDNF signaling in TrkA(F592A) and TrkB(F616A) neurons, respectively, while no such Trk inhibition is observed in wild-type neurons. Moreover, oral administration of 1NMPP1 leads to specific inhibition of TrkA(F592A), TrkB(F616A), and TrkC(F167A) signaling in vivo. Thus, Trk knockin mice provide valuable tools for selective, rapid, and reversible inhibition of neurotrophin signaling in vitro and in vivo.
journal_name
Neuronjournal_title
Neuronauthors
Chen X,Ye H,Kuruvilla R,Ramanan N,Scangos KW,Zhang C,Johnson NM,England PM,Shokat KM,Ginty DDdoi
10.1016/j.neuron.2005.03.009subject
Has Abstractpub_date
2005-04-07 00:00:00pages
13-21issue
1eissn
0896-6273issn
1097-4199pii
S0896-6273(05)00204-7journal_volume
46pub_type
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