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| Untersuchte Arbeit: Seite: 38, Zeilen: 1-10 |
Quelle: Martin und Kosik 2002 Seite(n): 815-816, Zeilen: 815:re.Sp. 55-60 - 816:li.Sp. 1-5.54-59 |
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| Another potential candidate for a synaptic tag that has recently received significant attention is the actin microfilament network at the synapse. The actin network in neurons is extremely dynamic, and these dynamics have been shown to change with activity. Studies have shown that ubiquitin-mediated proteolysis of the regulatory subunit of PKA results in a persistently active kinase, and that this degradation involves the transcriptional induction of an ubiquitin carboxy-terminal. Together, these findings raise the possibility that local activation of PKA and local regulation of the ubiquitin-proteasome pathway can serve as synaptic tags that combine with transcriptional events (for example, the induction of the ubiquitin carboxy-terminal hydrolase) to produce persistent increase in synaptic strength due to local protein synthesis (Hegde, 2004).
69. Hegde AN (2004) Ubiquitin-proteasome-mediated local protein degradation and synaptic plasticity. Prog Neurobiol 73: 311-357. |
[Seite 815]
Previous studies have shown that UBIQUITIN-mediated proteolysis of the regulatory subunit of PKA results in a persistently active kinase13, and that this degradation involves the transcriptional induction of a ubiquitin carboxy-terminal hydrolase14,15. Together [Seite 816] PKA and local regulation of the ubiquitin–PROTEASOME pathway can serve as synaptic tags that combine with transcriptional events (for example, the induction of the ubiquitin carboxy-terminal hydrolase) to produce persistent and local synaptic strengthening. [...] Another potential candidate for a synaptic tag that has recently received significant attention is the actin microfilament network at the synapse. The actin network in neurons is extremely dynamic, and these dynamics have been shown to change with activity27,28. 14. Hegde, A. N. et al. Ubiquitin C-terminal hydrolase is an immediate–early gene essential for long-term facilitation in Aplysia. Cell 89, 115–126 (1997). 15. Chain, D. G. et al. Mechanisms for generating the autonomous cAMP-dependent protein kinase required for long-term facilitation in Aplysia. Neuron 22, 147–156 (1999). 27. Fischer, M., Kaech, S., Wagner, U., Brinkhaus, H. & Matus, A. Glutamate receptors regulate actin-based plasticity in dendritic spines. Nature Neurosci. 3, 887–894 (2000). 28. Star, E. N., Kwiatkowski, D. J. & Murthy, V. N. Rapid turnover of actin in dendritic spines and its regulation by activity. Nature Neurosci. 5, 239–246 (2002). |
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