6 research outputs found
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