182 research outputs found
Timing properties of gamma-ray bursts detected by SPI-ACS detector on board of INTEGRAL
We study timing properties of a large sample of gamma-ray bursts (GRB)
detected by the Anti-Coincidence Shield (ACS) of the SPI spectrometer of
INTEGRAL telescope. We identify GRB-like events in the SPI-ACS data. The data
set under investigation is the history of count rate of the SPI-ACS detector
recorded with a binning of 50 ms over the time span of ~10 yr. In spite of the
fact that SPI-ACS does not have imaging capability, it provides high statistics
signal for each GRB event, because of its large effective area. We classify all
isolated excesses in the SPI-ACS count rate into three types: short spikes
produced by cosmic rays, GRBs and Solar flare induced events. We find some
~1500 GRB-like events in the 10 yr exposure. A significant fraction of the
GRB-like events identified in SPI-ACS occur in coincidence with triggers of
other gamma-ray telescopes and could be considered as confirmed GRBs. We study
the distribution of durations of the GRBs detected by SPI-ACS and find that the
peak of the distribution of long GRBs is at ~ 20, i.e. somewhat shorter than
for the long GRBs detected by BATSE. Contrary to the BATSE observation, the
population of short GRBs does not have any characteristic time scale. Instead,
the distribution of durations extends as a powerlaw to the shortest time scale
accessible for SPI-ACS, < 50 ms. We also find that a large fraction of long
GRBs has a characteristic variability time scale of the order of 1 s. We
discuss the possible origin of this time scale.Comment: Accepted for publication in A&
A New Frequency-Luminosity Relation for Long GRBs?
We have studied power density spectra (PDS) of 206 long Gamma-Ray Bursts
(GRBs). We fitted the PDS with a simple power-law and extracted the exponent of
the power-law (alpha) and the noise-crossing threshold frequency (f_th). We
find that the distribution of the extracted alpha peaks around -1.4 and that of
f_th around 1 Hz. In addition, based on a sub-set of 58 bursts with known
redshifts, we show that the redshift-corrected threshold frequency is
positively correlated with the isotropic peak luminosity. The correlation
coefficient is 0.57 +/- 0.03.Comment: 9 pages, 17 figures, 1 table; Accepted for publication in MNRA
Translocation t(1;3)(p36;p21) and other aberrations in a case of AML secondary to MDS
Case report on a case of t(1;3)(p36;p21) and other aberrations in a case of AML secondary to MDS
Glycogen Synthase Kinase (GSK) 3β phosphorylates and protects nuclear myosin 1c from proteasome-mediated degradation to activate rDNA transcription in early G1 cells
Nuclear myosin 1c (NM1) mediates RNA polymerase I (pol I) transcription activation and cell cycle progression by facilitating PCAF-mediated H3K9 acetylation, but the molecular mechanism by which NM1 is regulated remains unclear. Here, we report that at early G1 the glycogen synthase kinase (GSK) 3β phosphorylates and stabilizes NM1, allowing for NM1 association with the chromatin. Genomic analysis by ChIP-Seq showed that this mechanism occurs on the rDNA as active GSK3β selectively occupies the gene. ChIP assays and transmission electron microscopy in GSK3β-/- mouse embryonic fibroblasts indicated that at G1 rRNA synthesis is suppressed due to decreased H3K9 acetylation leading to a chromatin state incompatible with transcription. We found that GSK3β directly phosphorylates the endogenous NM1 on a single serine residue (Ser-1020) located within the NM1 C-terminus. In G1 this phosphorylation event stabilizes NM1 and prevents NM1 polyubiquitination by the E3 ligase UBR5 and proteasome-mediated degradation. We conclude that GSK3β-mediated phosphorylation of NM1 is required for pol I transcription activation
Multi-wavelength observations of the energetic GRB 080810: detailed mapping of the broadband spectral evolution
GRB 080810 was one of the first bursts to trigger both Swift and the Fermi
Gamma-ray Space Telescope. It was subsequently monitored over the X-ray and
UV/optical bands by Swift, in the optical by ROTSE and a host of other
telescopes and was detected in the radio by the VLA. The redshift of z= 3.355
+/- 0.005 was determined by Keck/HIRES and confirmed by RTT150 and NOT. The
prompt gamma/X-ray emission, detected over 0.3-10^3 keV, systematically softens
over time, with E_peak moving from ~600 keV at the start to ~40 keV around 100
s after the trigger; alternatively, this spectral evolution could be identified
with the blackbody temperature of a quasithermal model shifting from ~60 keV to
~3 keV over the same time interval. The first optical detection was made at 38
s, but the smooth, featureless profile of the full optical coverage implies
that this originated from the afterglow component, not the pulsed/flaring
prompt emission.
Broadband optical and X-ray coverage of the afterglow at the start of the
final X-ray decay (~8 ks) reveals a spectral break between the optical and
X-ray bands in the range 10^15 - 2x10^16 Hz. The decay profiles of the X-ray
and optical bands show that this break initially migrates blueward to this
frequency and then subsequently drifts redward to below the optical band by
~3x10^5 s. GRB 080810 was very energetic, with an isotropic energy output for
the prompt component of 3x10^53 erg and 1.6x10^52 erg for the afterglow; there
is no evidence for a jet break in the afterglow up to six days following the
burst.Comment: 15 pages, 9 figures, 4 in colour. Accepted for publication in MNRA
A Genome-Wide RNAi Screen Identifies Regulators of Cholesterol-Modified Hedgehog Secretion in Drosophila
Hedgehog (Hh) proteins are secreted molecules that function as organizers in animal development. In addition to being palmitoylated, Hh is the only metazoan protein known to possess a covalently-linked cholesterol moiety. The absence of either modification severely disrupts the organization of numerous tissues during development. It is currently not known how lipid-modified Hh is secreted and released from producing cells. We have performed a genome-wide RNAi screen in Drosophila melanogaster cells to identify regulators of Hh secretion. We found that cholesterol-modified Hh secretion is strongly dependent on coat protein complex I (COPI) but not COPII vesicles, suggesting that cholesterol modification alters the movement of Hh through the early secretory pathway. We provide evidence that both proteolysis and cholesterol modification are necessary for the efficient trafficking of Hh through the ER and Golgi. Finally, we identified several putative regulators of protein secretion and demonstrate a role for some of these genes in Hh and Wingless (Wg) morphogen secretion in vivo. These data open new perspectives for studying how morphogen secretion is regulated, as well as provide insight into regulation of lipid-modified protein secretion
Discovery and progress in our understanding of the regulated secretory pathway in neuroendocrine cells
In this review we start with a historical perspective beginning with the early morphological work done almost 50 years ago. The importance of these pioneering studies is underscored by our brief summary of the key questions addressed by subsequent research into the mechanism of secretion. We then highlight important advances in our understanding of the formation and maturation of neuroendocrine secretory granules, first using in vitro reconstitution systems, then most recently biochemical approaches, and finally genetic manipulations in vitro and in vivo
Proteomic Analysis of the Dysferlin Protein Complex Unveils Its Importance for Sarcolemmal Maintenance and Integrity
Dysferlin is critical for repair of muscle membranes after damage. Mutations in dysferlin lead to a progressive muscular dystrophy. Recent studies suggest additional roles for dysferlin. We set out to study dysferlin's protein-protein interactions to obtain comprehensive knowledge of dysferlin functionalities in a myogenic context. We developed a robust and reproducible method to isolate dysferlin protein complexes from cells and tissue. We analyzed the composition of these complexes in cultured myoblasts, myotubes and skeletal muscle tissue by mass spectrometry and subsequently inferred potential protein functions through bioinformatics analyses. Our data confirm previously reported interactions and support a function for dysferlin as a vesicle trafficking protein. In addition novel potential functionalities were uncovered, including phagocytosis and focal adhesion. Our data reveal that the dysferlin protein complex has a dynamic composition as a function of myogenic differentiation. We provide additional experimental evidence and show dysferlin localization to, and interaction with the focal adhesion protein vinculin at the sarcolemma. Finally, our studies reveal evidence for cross-talk between dysferlin and its protein family member myoferlin. Together our analyses show that dysferlin is not only a membrane repair protein but also important for muscle membrane maintenance and integrity
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