238 research outputs found
Observation of a ppb mass threshoud enhancement in \psi^\prime\to\pi^+\pi^-J/\psi(J/\psi\to\gamma p\bar{p}) decay
The decay channel
is studied using a sample of events collected
by the BESIII experiment at BEPCII. A strong enhancement at threshold is
observed in the invariant mass spectrum. The enhancement can be fit
with an -wave Breit-Wigner resonance function with a resulting peak mass of
and a
narrow width that is at the 90% confidence level.
These results are consistent with published BESII results. These mass and width
values do not match with those of any known meson resonance.Comment: 5 pages, 3 figures, submitted to Chinese Physics
Signaling Mechanisms of Vav3, a Guanine Nucleotide Exchange Factor and Androgen Receptor Coactivator, in Physiology and Prostate Cancer Progression
The Rho GTPase guanine nucleotide exchange factor (GEF) Vav3 is the third member of the Vavfamily of GEFS and is activated by tyrosine phosphorylation. Through stimulation of Rho GTPaseactivity, Vav3 promotes cell migration, invasion, and other cellular processes. Work from our laboratory first established that Vav3 is upregulated in models of castration-resistant prostate cancer progression and enhances androgen receptor as well as androgen receptor splice variant activity. Recent analysis of clinical specimens supports Vav3 as a potential biomarker of aggressive prostate cancer. Consistent with a role in promoting castration-Βresistant disease, Vav3 is a versatile enhancer of androgen receptor by both ligand-dependent and ligand-independent mechanisms and as such impacts established pathways of androgen receptor reactivation in advanced prostate cancer. Distinct Vav3 domains and mechanisms participate in ligand-dependent and -independent androgen receptor coactivation. To provide a physiologic context, we review Vav3 actions elucidated by gene knockout studies. This chapter describes the pervasive role of Vav3 in progression of prostate cancer to castration resistance. We discuss the mechanisms by which prostate cancer cells exploit Vav3 signaling to promote androgen receptor activity under different hormonal milieus, which are relevant to clinical prostate cancer. Lastly, we review the data on the emerging role for Vav3 in other cancers ranging from leukemias to gliomas.https://nsuworks.nova.edu/hpd_medsci_faculty_books/1002/thumbnail.jp
Cathepsin S Deficiency Results in Abnormal Accumulation of Autophagosomes in Macrophages and Enhances Ang IIβInduced Cardiac Inflammation
BACKGROUND: Cathepsin S (Cat S) is overexpressed in human atherosclerotic and aneurysmal tissues and may contributes to degradation of extracellular matrix, especially elastin, in inflammatory diseases. We aimed to define the role of Cat S in cardiac inflammation and fibrosis induced by angiotensin II (Ang II) in mice. METHODS AND RESULTS: Cat S-knockout (Cat S(-/-)) and littermate wild-type (WT) C57BL/6J mice were infused continuously with Ang II (750 ng/kg/min) or saline for 7 days. Cat S(-/-) mice showed severe cardiac fibrosis, including elevated expression of collagen I and Ξ±-smooth muscle actin (Ξ±-SMA), as compared with WT mice. Moreover, macrophage infiltration and expression of inflammatory cytokines (tumor necrosis factor Ξ±, transforming growth factor Ξ² and interleukin 1Ξ²) were significantly greater in Cat S(-/-) than WT hearts. These Ang II-induced effects in Cat S(-/-) mouse hearts was associated with abnormal accumulation of autophagosomes and reduced clearance of damaged mitochondria, which led to increased levels of reactive oxygen species (ROS) and activation of nuclear factor-kappa B (NF-ΞΊB) in macrophages. CONCLUSION: Cat S in lysosomes is essential for mitophagy processing in macrophages, deficiency in Cat S can increase damaged mitochondria and elevate ROS levels and NF-ΞΊB activity in hypertensive mice, so it regulates cardiac inflammation and fibrosis
Phosphorylation of Kif26b Promotes Its Polyubiquitination and Subsequent Proteasomal Degradation during Kidney Development
Kif26b, a member of the kinesin superfamily proteins (KIFs), is essential for kidney development. Kif26b expression is restricted to the metanephric mesenchyme, and its transcription is regulated by a zinc finger transcriptional regulator Sall1. However, the mechanism(s) by which Kif26b protein is regulated remain unknown. Here, we demonstrate phosphorylation and subsequent polyubiquitination of Kif26b in the developing kidney. We find that Kif26b interacts with an E3 ubiquitin ligase, neural precursor cell expressed developmentally down-regulated protein 4 (Nedd4) in developing kidney. Phosphorylation of Kif26b at Thr-1859 and Ser-1962 by the cyclin-dependent kinases (CDKs) enhances the interaction of Kif26b with Nedd4. Nedd4 polyubiquitinates Kif26b and thereby promotes degradation of Kif26b via the ubiquitin-proteasome pathway. Furthermore, Kif26b lacks ATPase activity but does associate with microtubules. Nocodazole treatment not only disrupts the localization of Kif26b to microtubules but also promotes phosphorylation and polyubiquitination of Kif26b. These results suggest that the function of Kif26b is microtubule-based and that Kif26b degradation in the metanephric mesenchyme via the ubiquitin-proteasome pathway may be important for proper kidney development
Higher-order multipole amplitude measurement in Ο β²βΞ³Ο c2
Using 106Γ106 Ο β² events collected with the BESIII detector at the BEPCII storage ring, the higher-order multipole amplitudes in the radiative transition Ο β²βΞ³Ο c2βΞ³Ο +Ο -/Ξ³K +K - are measured. A fit to the Ο c2 production and decay angular distributions yields M2=0.046Β±0. 010Β±0.013 and E3=0.015Β±0.008Β±0.018, where the first errors are statistical and the second systematic. Here M2 denotes the normalized magnetic quadrupole amplitude and E3 the normalized electric octupole amplitude. This measurement shows evidence for the existence of the M2 signal with 4.4Ο statistical significance and is consistent with the charm quark having no anomalous magnetic moment. Β© 2011 American Physical Society.published_or_final_versio
Study of a00(980)-f0(980) mixing
Using samples of 2.25Γ108 J/Ο events and 1.06Γ108 Ο β² events collected with the BES III detector, we study the f 0(980)βa00(980) and a00(980)βf 0(980) transitions in the processes J/ΟβΟf 0(980) βΟa00(980) and Ο c1βΟ0a00(980)βΟ0f 0(980), respectively. Evidence for f 0(980)βa00(980) is found with a significance of 3.4Ο, while in the case of a00(980)βf 0(980) transition, the significance is 1.9Ο. Measurements and upper limits of both branching ratios and mixing intensities are determined. Β© 2011 American Physical Society.published_or_final_versio
Two-photon widths of the Ο c0,2 states and helicity analysis for Ο c2βΞ³Ξ³
Based on a data sample of 106Γ106 Ο β² events collected with the BESIII detector, the decays Ο β²βΞ³Ο c0,2, Ο c0,2βΞ³Ξ³ are studied to determine the two-photon widths of the Ο c0,2 states. The two-photon decay branching fractions are determined to be B(Ο c0βΞ³Ξ³)=(2. 24Β±0.19Β±0.12Β±0.08)Γ10 -4 and B(Ο c2βΞ³Ξ³)=(3.21Β±0.18Β±0. 17Β±0.13)Γ10 -4. From these, the two-photon widths are determined to be Ξ Ξ³Ξ³(Ο c0)=(2. 33Β±0.20Β±0.13Β±0.17)keV, Ξ Ξ³Ξ³(Ο c2)=(0.63Β±0.04Β±0. 04Β±0.04)keV, and R=Ξ Ξ³Ξ³(Ο c2)/ Ξ Ξ³Ξ³(Ο c0)=0.271Β±0. 029Β±0.013Β±0.027, where the uncertainties are statistical, systematic, and those from the PDG B(Ο β²βΞ³Ο c0,2) and Ξ(Ο c0,2) errors, respectively. The ratio of the two-photon widths for helicity Ξ»=0 and helicity Ξ»=2 components in the decay Ο c2βΞ³Ξ³ is measured for the first time to be f 0/2=ΞΞ³Ξ³Ξ»= 0(Ο c2)/ΞΞ³Ξ³Ξ»=2(Ο c2)=0. 00Β±0.02Β±0.02. Β© 2012 American Physical Society.published_or_final_versio
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