RGD Reference Report - Reciprocal actions of NCAM and tPA via a Ras-dependent MAPK activation in rat hippocampal neurons. - Rat Genome Database

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Reciprocal actions of NCAM and tPA via a Ras-dependent MAPK activation in rat hippocampal neurons.

Authors: Son, H  Seuk Kim, J  Mogg Kim, J  Lee, SH  Lee, YS 
Citation: Son H, etal., Biochem Biophys Res Commun 2002 Oct 25;298(2):262-8.
RGD ID: 729413
Pubmed: PMID:12387826   (View Abstract at PubMed)

In an attempt to identify the functions of neural cell adhesion molecule (NCAM) and tissue plasminogen activator (tPA) in hippocampal synaptic plasticity, we investigated the relationship between the two molecules by focusing on mitogen-activated protein kinase (MAPK), an essential enzyme in this process. NCAM clustering in cultured hippocampal neurons transiently induced MAPK within 10min. Moreover, soluble NCAM also induced a Ras-dependent MAPK activation. Conversely, MAPK activation led to an increase in the expressions of all three isoforms of NCAM. Treatment of neurons with tPA and plasminogen induced a Ras-dependent MAPK activation and tPA-plasmin degradation of NCAM was mediated in a MAPK-dependent manner. Soluble NCAM transiently inhibited tPA mRNA expression levels in a MAPK-dependent manner, while stimulation of MAPK alone induced tPA reduction in cells. These results collectively indicate that NCAM and tPA reciprocally act as important regulators in the modulation of synaptic plasticity via a Ras-MAPK-involved signaling pathway. In turn, MAPK activation may cause tPA degradation or a decrease in expression to promote synaptic plasticity.

Objects referenced in this article
Gene Ncam1 neural cell adhesion molecule 1 Rattus norvegicus
Gene Plat plasminogen activator, tissue type Rattus norvegicus

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