In human cerebral microvascular endothelial cells, MMP9 was upregulated when recombinant PLAT was added. Mmp9 levels were lower in Plat knockout compared with wildtype mice after focal cerebral ischemia. (2003) demonstrated that PLAT upregulates MMP9 ( 120361) in cell culture and in vivo. The findings suggested that tPA plays an important role in synaptic plasticity and learning, perhaps through extracellular proteolysis and synaptic remodeling. (1999) showed that transgenic mice overexpressing tPA in postnatal neurons had increased and prolonged long-term potentiation in the hippocampus and showed improved performance in spatial orientation learning tasks. These findings established a direct role for PLAT in facilitating neuronal migration, and they raised the possibility that late arriving neurons may have altered synaptic interactions. A real-time analysis of granule cell migration in cerebellar slices of the null mice showed that granule neurons are migrating 51% as fast as granule neurons in slices from wildtype mice. (1999) showed that compared with their normal counterparts, mice lacking the tPA gene, Plat -/-, have greater than 2-fold more migrating granule neurons in the cerebellar molecular layer during the most active phase of granule cell migration. In the nervous system, PALT activity is correlated with neurite outgrowth, neuronal migration, learning, and excitotoxic death. Granule neurons both secrete PLAT, an extracellular serine protease that converts the proenzyme plasminogen into the active protease plasmin, and bind PLAT to their cell surface.
PLASMINOGEN ACTIVATOR ACTIVATOR
In the developing cerebellum, granule neurons turn on the gene for tissue plasminogen activator as they begin their migration into the cerebellar molecular layer. They hypothesized that induction of PLAT may play a role in synaptic plasticity. (1996) demonstrated induction of tPA mRNA protein in cerebellar Purkinje cells of rats being trained for a complex motor task. Tissue plasminogen activator is the primary plasminogen activator in the brain and is present at high levels in regions undergoing extensive cell migration during embryonic and neonatal development. (1987) assigned the mouse Plat gene to chromosome 8. They described a common EcoRI RFLP in the PLAT gene that could be useful for genetic linkage studies.īy Southern blot analysis of DNA from mouse-Chinese hamster and mouse-rat somatic cell hybrids, Rajput et al.
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By in situ hybridization and Southern blot analysis of somatic cell hybrid DNA, Yang-Feng et al. The ideogram showing location of grains appeared to have more in 8q11 than in 8p11.
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(1986) assigned PLAT to the pericentromeric area of chromosome 8 by in situ hybridization.
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(1986) provided the definitive report on the work reported in abstract by Visse et al. (1985) corrected the assignment to chromosome 8 using various DNA probes for somatic cell hybrids analysis. (1978) mapped the PLAT gene to chromosome 6 by studying mouse-human hybrid cells, Benham et al.