University of Würzburg

About: University of Würzburg is a education organization based out in Wurzburg, Bayern, Germany. It is known for research contribution in the topics: Population & Gene. The organization has 31437 authors who have published 62203 publications receiving 2337033 citations. The organization is also known as: Julius-Maximilians-Universität Würzburg & Würzburg University.

Structure of coronavirus main proteinase reveals combination of a chymotrypsin fold with an extra alpha-helical domain.

Abstract: The key enzyme in coronavirus polyprotein processing is the viral main proteinase, M(pro), a protein with extremely low sequence similarity to other viral and cellular proteinases. Here, the crystal structure of the 33.1 kDa transmissible gastroenteritis (corona)virus M(pro) is reported. The structure was refined to 1.96 A resolution and revealed three dimers in the asymmetric unit. The mutual arrangement of the protomers in each of the dimers suggests that M(pro) self-processing occurs in trans. The active site, comprised of Cys144 and His41, is part of a chymotrypsin-like fold that is connected by a 16 residue loop to an extra domain featuring a novel alpha-helical fold. Molecular modelling and mutagenesis data implicate the loop in substrate binding and elucidate S1 and S2 subsites suitable to accommodate the side chains of the P1 glutamine and P2 leucine residues of M(pro) substrates. Interactions involving the N-terminus and the alpha-helical domain stabilize the loop in the orientation required for trans-cleavage activity. The study illustrates that RNA viruses have evolved unprecedented variations of the classical chymotrypsin fold.

Estimate of B(B̄→X s γ) at O(α s 2 )

Abstract: Combining our results for various $O({\ensuremath{\alpha}}_{s}^{2})$ corrections to the weak radiative $B$-meson decay, we are able to present the first estimate of the branching ratio at the next-to-next-to-leading order in QCD. We find $\mathcal{B}(\overline{B}\ensuremath{\rightarrow}{X}_{s}\ensuremath{\gamma})=(3.15\ifmmode\pm\else\textpm\fi{}0.23)\ifmmode\times\else\texttimes\fi{}{10}^{\ensuremath{-}4}$ for ${E}_{\ensuremath{\gamma}}g1.6\text{ }\text{ }\mathrm{GeV}$ in the $\overline{B}$-meson rest frame. The four types of uncertainties: nonperturbative (5%), parametric (3%), higher-order (3%), and ${m}_{c}$-interpolation ambiguity (3%) have been added in quadrature to obtain the total error.

Did the Indo-Asian collision alone create the Tibetan plateau?

Abstract: It is widely believed that the Tibetan plateau is a late Cenozoic feature produced by the Indo-Asian collision. However, because Tibet was the locus of continental accretion and subduction throughout the Mesozoic, crustal thickening during that time may also have contributed to growth of the plateau. This portion of the geologic history was investigated in a traverse through the central Lhasa block, southern Tibet. Together with earlier studies, our mapping and geochronological results show that the Lhasa block underwent little north-south shortening during the Cenozoic. Rather, our mapping shows that ∼60% crustal shortening, perhaps due to the collision between the Lhasa and Qiangtang blocks, occurred during the Early Cretaceous. This observation implies that a significant portion of southern Tibet was raised to perhaps 3–4 km elevation prior to the Indo-Asian collision.

Differential regulation of cell motility and invasion by FAK

Abstract: Cell migration and invasion are fundamental components of tumor cell metastasis. Increased focal adhesion kinase (FAK) expression and tyrosine phosphorylation are connected with elevated tumorigenesis. Null mutation of FAK results in embryonic lethality, and FAK−/− fibroblasts exhibit cell migration defects in culture. Here we show that viral Src (v-Src) transformation of FAK−/− cells promotes integrin-stimulated motility equal to stable FAK reexpression. However, FAK−/− v-Src cells were not invasive, and FAK reexpression, Tyr-397 phosphorylation, and FAK kinase activity were required for the generation of an invasive cell phenotype. Cell invasion was linked to transient FAK accumulation at lamellipodia, formation of a FAK–Src-p130Cas–Dock180 signaling complex, elevated Rac and c-Jun NH2-terminal kinase activation, and increased matrix metalloproteinase expression and activity. Our studies support a dual role for FAK in promoting cell motility and invasion through the activation of distinct signaling pathways.