Seismological investigations in the Gioia Tauro Basin (southern Calabria, Italy)

This study provides new seismological information to characterize the seismically active area of the Gioia Tauro basin (southern Calabria, Italy). Seismic activity recorded by a temporary network from 1985 to 1994 was analyzed for focal mechanisms, stress tensor inversion, P-wave seismic attenuation and earthquake source parameters estimation. Fault plane solutions of selected events showed a variety of different mechanisms, even if a prevalence of normal dip-slip solutions with prevalent rupture orientations occurring along ca. NE-SW directions was observed. Stress tensor inversion analysis disclosed a region governed mainly by a NW-SE extensional stress regime with a nearly vertical σ1. These results are consistent with the structure movements affecting the studied area and with geodetic data. Furthermore, evaluation of P-waves seismic attenuation and earthquake source parameters of a subset of events highlighted a strong heterogeneity of the crust and the presence of fault segments and/or weakened zones where great stress accumulation or long-rupture propagation are hindered

Seismological investigations in the Gioia Tauro Basin (southern Calabria, Italy)

This study provides new seismological information to characterize the seismically active area of the Gioia
 Tauro basin (southern Calabria, Italy). Seismic activity recorded by a temporary network from 1985 to 1994 was
 analyzed for focal mechanisms, stress tensor inversion, P-wave seismic attenuation and earthquake source parameters
 estimation. Fault plane solutions of selected events showed a variety of different mechanisms, even if
 a prevalence of normal dip-slip solutions with prevalent rupture orientations occurring along ca. NE-SW directions
 was observed. Stress tensor inversion analysis disclosed a region governed mainly by a NW-SE extensional
 stress regime with a nearly vertical ?1. These results are consistent with the structure movements affecting
 the studied area and with geodetic data.
 Furthermore, evaluation of P-waves seismic attenuation and earthquake source parameters of a subset of events
 highlighted a strong heterogeneity of the crust and the presence of fault segments and/or weakened zones where
 great stress accumulation or long-rupture propagation are hindered

Nuclear protein kinase C isoforms: key players in multiple cell functions?

Protein kinase C (PKC) isozymes are a family of serine/threonine protein kinases categorized into three subfamilies: classical, novel, and atypical. PKC isozymes, whose expression is cell type-specific and developmentally regulated, are key transducers in many agonist-induced signaling cascades. To date at least 10 different PKC isotypes have been identified and are believed to play distinct regulatory roles. PKC isoforms are catalytically activated by several lipid cofactors, including diacylglycerol. PKC is thought to reside in the cytoplasm in an inactive conformation and to translocate to the plasma membrane or cytoplasmic organelles upon cell activation by different stimuli. However, a sizable body of evidence collected over the last 15 years has shown PKC to be capable of translocating to the nucleus. Furthermore, PKC isoforms can reside within the nucleus. Studies from independent laboratories have to led to the identification of several nuclear proteins which act as PKC substrates as well as to the characterization of some nuclear PKC-binding proteins which may be of fundamental importance for finely tuning PKC function in this peculiar cell microenvironment. Most likely, nuclear PKC isozymes are involved in the regulation of several important biological processes such as cell proliferation and differentiation, neoplastic transformation, and apoptosis. In this review, we shall summarize the most intriguing evidence about the roles played by nuclear PKC isozymes

Nuclear diacylglycerol kinases: emerging downstream regulators in cell signaling networks

There exists an active lipid metabolism in the nucleus, which is regulated differentially from the lipid metabolism taking place elsewhere in the cell. Evidence has been accumulated that nuclear lipid metabolism is closely involved in a variety of cell responses, including proliferation, differentiation, and apoptosis. A fundamental lipid second messenger which is generated in the nucleus is diacylglycerol, that is mainly known for its role as an activator of some protein kinase C isoforms. Diacylglycerol kinases attenuate diacylglycerol signaling by converting this lipid to phosphatidic acid, which also has signaling functions. Ten mammalian diacylglycerol kinase isoforms have been cloned so far, and some of them are found also in the nucleus, either as resident proteins or after migration from cytoplasm in response to various agonists. Experiments using cultured cells have demonstrated that nuclear diacylglycerol kinases have prominent roles in cell cycle regulation and differentiation. In this review, the emerging roles played by diacylglycerol kinases in the nucleus, such as the control of G1/S phase transition, are discussed

Nuclear phosphoinositide specific phospholipase C (PI-PLC)-ß1: a central intermediary in nuclear lipid-dependent signal transduction

Several studies have demonstrated the existence of an autonomous intranuclear phosphoinositide cycle that involves the activation of nuclear PIPLC and the generation of diacylglycerol (DG) within the nucleus. Although several distinct isozymes of PIPLC have been detected in the nucleus, the isoform that has been most consistently highlighted as being nuclear is PI-PLC-ß1. Nuclear PI-PLC-ß1 has been linked with either cell proliferation or differentiation. Remarkably, the activation mechanism of nuclear PI-PLC-ß1 has been shown to be different from its plasma membrane counterpart, being dependent on phosphorylation effected by p44/42 mitogen activated protein (MAP) kinase. In this review, we report the most up-dated findings about nuclear PI-PLC-ß1, such as the localization in nuclear speckles, the activity changes during the cell cycle phases, and the possible involvement in the progression of myelodisplastic syndrome to acute myeloid leukemia