1,967 research outputs found
In-cell NMR characterization of the secondary structure populations of a disordered conformation of α-Synuclein within E. coli cells
α-Synuclein is a small protein strongly implicated in the pathogenesis of Parkinsonâs disease and related neurodegenerative disorders. We report here the use of in-cell NMR spectroscopy to observe directly the structure and dynamics of this protein within E. coli cells. To improve the accuracy in the measurement of backbone chemical shifts within crowded in-cell NMR spectra, we have developed a deconvolution method to reduce inhomogeneous line broadening within cellular samples. The resulting chemical shift values were then used to evaluate the distribution of secondary structure populations which, in the absence of stable tertiary contacts, are a most effective way to describe the conformational fluctuations of disordered proteins. The results indicate that, at least within the bacterial cytosol, α-synuclein populates a highly dynamic state that, despite the highly crowded environment, has the same characteristics as the disordered monomeric form observed in aqueous solution
Cardiac Transcription Factor Nkx2.5 Is Downregulated under Excessive O-GlcNAcylation Condition
Post-translational modification of proteins with O-linked N-acetylglucosamine (O-GlcNAc) is linked the development of diabetic cardiomyopathy. We investigated whether Nkx2.5 protein, a cardiac transcription factor, is regulated by O-GlcNAc. Recombinant Nkx2.5 (myc-Nkx2.5) proteins were reduced by treatment with the O-GlcNAcase inhibitors STZ and O-(2-acetamido-2-deoxy-D-glucopyroanosylidene)-amino-N-phenylcarbamate; PUGNAC) as well as the overexpression of recombinant O-GlcNAc transferase (OGT-flag). Co-immunoprecipitation analysis revealed that myc-Nkx2.5 and OGT-flag proteins interacted and myc-Nkx2.5 proteins were modified by O-GlcNAc. In addition, Nkx2.5 proteins were reduced in the heart tissue of streptozotocin (STZ)-induced diabetic mice and O-GlcNAc modification of Nkx2.5 protein increased in diabetic heart tissue compared with non-diabetic heart. Thus, excessive O-GlcNAcylation causes downregulation of Nkx2.5, which may be an underlying contributing factor for the development of diabetic cardiomyopathy
Signaling of angiotensin II-induced vascular protein synthesis in conduit and resistance arteries in vivo
BACKGROUND: From in vitro studies, it has become clear that several signaling cascades are involved in angiotensin II-induced cellular hypertrophy. The aim of the present study was to determine some of the signaling pathways mediating angiotensin II (Ang II)-induced protein synthesis in vivo in large and small arteries. METHODS: Newly synthesized proteins were labeled during 4 hours with tritiated leucine in conscious control animals, or animals infused for 24 hours with angiotensin II (400 ng/kg/min). Hemodynamic parameters were measure simultaneously. Pharmacological agents affecting signaling cascades were injected 5 hours before the end of Ang II infusion. RESULTS: Angiotensin II nearly doubled the protein synthesis rate in the aorta and small mesenteric arteries, without affecting arterial pressure. The AT(1 )receptor antagonist Irbesartan antagonized the actions of Ang II. The Ang II-induced protein synthesis was associated with increased extracellular signal-regulated kinases (ERK)1/2 phosphorylation in aortic, but not in mesenteric vessels. Systemic administration of PD98059, an inhibitor of the ERK-1/2 pathway, produced a significant reduction of protein synthesis rate in the aorta, and only a modest decrease in mesenteric arteries. Rapamycin, which influences protein synthesis by alternative signaling, had a significant effect in both vessel types. Rapamycin and PD98059 did not alter basal protein synthesis and had minimal effects on arterial pressure. CONCLUSION: ERK1/2 and rapamycin-sensitive pathways are involved in pressure-independent angiotensin II-induced vascular protein synthesis in vivo. However, their relative contribution may vary depending on the nature of the artery under investigation
Study of Tau-pair Production in Photon-Photon Collisions at LEP and Limits on the Anomalous Electromagnetic Moments of the Tau Lepton
Tau-pair production in the process e+e- -> e+e-tau+tau- was studied using
data collected by the DELPHI experiment at LEP2 during the years 1997 - 2000.
The corresponding integrated luminosity is 650 pb^{-1}. The values of the
cross-section obtained are found to be in agreement with QED predictions.
Limits on the anomalous magnetic and electric dipole moments of the tau lepton
are deduced.Comment: 20 pages, 9 figures, Accepted by Eur. Phys. J.
Energy dependence of Cronin momentum in saturation model for and collisions
We calculate dependence of Cronin momentum for and
collisions in saturation model. We show that this dependence is consistent with
expectation from formula which was obtained using simple dimentional
consideration. This can be used to test validity of saturation model (and
distinguish among its variants) and measure dependence of saturation
momentum from experimental data.Comment: LaTeX2e, 12 pages, 8 figure
CP asymmetry in in a general two-Higgs-doublet model with fourth-generation quarks
We discuss the time-dependent CP asymmetry of decay in an
extension of the Standard Model with both two Higgs doublets and additional
fourth-generation quarks. We show that although the Standard Model with
two-Higgs-doublet and the Standard model with fourth generation quarks alone
are not likely to largely change the effective from the decay of
, the model with both additional Higgs doublet and
fourth-generation quarks can easily account for the possible large negative
value of without conflicting with other experimental
constraints. In this model, additional large CP violating effects may arise
from the flavor changing Yukawa interactions between neutral Higgs bosons and
the heavy fourth generation down type quark, which can modify the QCD penguin
contributions. With the constraints obtained from processes
such as and , this model can lead to the
effective to be as large as in the CP asymmetry of .Comment: 13 pages, 5 figures, references added, to appear in Eur.Phys.J.
A Precise Measurement of the Tau Lifetime
The tau lepton lifetime has been measured with the e+e- -> tau+tau- events
collected by the DELPHI detector at LEP in the years 1991-1995. Three different
methods have been exploited, using both one-prong and three-prong tau decay
channels. Two measurements have been made using events in which both taus decay
to a single charged particle. Combining these measurements gave tau_tau (1
prong) = 291.8 +/- 2.3 (stat) +/- 1.5 (sys) fs. A third measurement using taus
which decayed to three charged particles yielded tau_tau (3 prong) = 288.6 +/-
2.4 (stat) +/- 1.3 (sys) fs. These were combined with previous DELPHI results
to measure the tau lifetime, using the full LEP1 data sample, to be tau_tau =
290.9 +/- 1.4 (stat) +/- 1.0 (sys) fs.Comment: 27 pages, 7 figure
Measurement of the branching fraction
The branching fraction is measured in a data sample
corresponding to 0.41 of integrated luminosity collected with the LHCb
detector at the LHC. This channel is sensitive to the penguin contributions
affecting the sin2 measurement from The
time-integrated branching fraction is measured to be . This is the most precise measurement to
date
Differential branching fraction and angular analysis of the decay B0âKâ0ÎŒ+ÎŒâ
The angular distribution and differential branching fraction of the decay B 0â K â0 ÎŒ + ÎŒ â are studied using a data sample, collected by the LHCb experiment in pp collisions at sâ=7 TeV, corresponding to an integrated luminosity of 1.0 fbâ1. Several angular observables are measured in bins of the dimuon invariant mass squared, q 2. A first measurement of the zero-crossing point of the forward-backward asymmetry of the dimuon system is also presented. The zero-crossing point is measured to be q20=4.9±0.9GeV2/c4 , where the uncertainty is the sum of statistical and systematic uncertainties. The results are consistent with the Standard Model predictions
Opposite-side flavour tagging of B mesons at the LHCb experiment
The calibration and performance of the oppositeside
flavour tagging algorithms used for the measurements
of time-dependent asymmetries at the LHCb experiment
are described. The algorithms have been developed using
simulated events and optimized and calibrated with
B
+ âJ/ÏK
+, B0 âJ/ÏK
â0 and B0 âD
ââ
Ό
+
ΜΌ decay
modes with 0.37 fbâ1 of data collected in pp collisions
at
â
s = 7 TeV during the 2011 physics run. The oppositeside
tagging power is determined in the B
+ â J/ÏK
+
channel to be (2.10 ± 0.08 ± 0.24) %, where the first uncertainty
is statistical and the second is systematic
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