Expansion of the Gene Ontology knowledgebase and resources

The Gene Ontology (GO) is a comprehensive resource of computable knowledge regarding the functions of genes and gene products. As such, it is extensively used by the biomedical research community for the analysis of -omics and related data. Our continued focus is on improving the quality and utility of the GO resources, and we welcome and encourage input from researchers in all areas of biology. In this update, we summarize the current contents of the GO knowledgebase, and present several new features and improvements that have been made to the ontology, the annotations and the tools. Among the highlights are 1) developments that facilitate access to, and application of, the GO knowledgebase, and 2) extensions to the resource as well as increasing support for descriptions of causal models of biological systems and network biology. To learn more, visit http://geneontology.org/

Radical defects modulate the photocatalytic response in 2D-graphitic carbon nitride

Graphitic carbon nitride (gCN) is an important heterogeneous metal-free catalytic material. Thermally induced post-synthetic modifications, such as amorphization and/or reduction, were recently used to enhance the photocatalytic response of these materials for certain classes of organic transformations, with structural defects possibly playing an important role. The knowledge of how these surface modifications modulate the photocatalytic response of gCN is therefore not only interesting from a fundamental point of view, but also necessary for the development and/or tuning of metal-free gCN systems with superior photo-catalytic properties. Herein, employing density functional theory calculations and combining both the periodic and molecular approaches, in conjunction with experimental EPR measurements, we demonstrate that different structural defects on the gCN surface generate distinctive radical defect states localized within the electronic bandgap, with only those correlated with amorphous and reduced gCN structures being photo-active. To this end, we (i) model defective gCN surfaces containing radical defect states; (ii) assess the interactions of these defects with the radical precursors involved in the photo-driven alkylation of electron-rich aromatic compounds (namely perfluoroalkyl iodides); and (iii) describe the photo-chemical processes triggering the initial step of that reaction at the gCN surface. We provide a coherent structure/photo-catalytic property relationship on defective gCN surfaces, elaborating how only specific defect types act as binding sites for the perfluoroalkyl iodide reagent and can favor a photo-induced charge transfer from the gCN surface to the molecule, thus triggering the perfluoroalkylation reaction

The Pervasive Effects of ER Stress on a Typical Endocrine Cell: Dedifferentiation, Mesenchymal Shift and Antioxidant Response in the Thyrocyte

none13noThe endoplasmic reticulum stress and the unfolded protein response are triggered following an imbalance between protein load and protein folding. Until recently, two possible outcomes of the unfolded protein response have been considered: life or death. We sought to substantiate a third alternative, dedifferentiation, mesenchymal shift, and activation of the antioxidant response by using typical endocrine cells, i.e. thyroid cells. The thyroid is a unique system both of endoplasmic reticulum stress (a single protein, thyroglobulin represents the majority of proteins synthesized in the endoplasmic reticulum by the thyrocyte) and of polarized epithelium (the single layer of thyrocytes delimiting the follicle). Following endoplasmic reticulum stress, in thyroid cells the folding of thyroglobulin was disrupted. The mRNAs of unfolded protein response were induced or spliced (X-box binding protein-1). Differentiation was inhibited: mRNA levels of thyroid specific genes, and of thyroid transcription factors were dramatically downregulated, at least in part, transcriptionally. The dedifferentiating response was accompanied by an upregulation of mRNAs of antioxidant genes. Moreover, cadherin-1, and the thyroid (and kidney)-specific cadherin-16 mRNAs were downregulated, vimentin, and SNAI1 mRNAs were upregulated. In addition, loss of cortical actin and stress fibers formation were observed. Together, these data indicate that ER stress in thyroid cells induces dedifferentiation, loss of epithelial organization, shift towards a mesenchymal phenotype, and activation of the antioxidant response, highlighting, at the same time, a new and wide strategy to achieve survival following ER stress, and, as a sort of the other side of the coin, a possible new molecular mechanism of decline/loss of function leading to a deficit of thyroid hormones formation.openUlianich L.; Mirra P.; Garbi C.; Cali G.; Conza D.; Treglia A.S.; Miraglia A.; Punzi D.; Miele C.; Raciti G.A.; Beguinot F.; Consiglio E.; Di Jeso B.Ulianich, L.; Mirra, P.; Garbi, C.; Cali, G.; Conza, D.; Treglia, A. S.; Miraglia, A.; Punzi, D.; Miele, C.; Raciti, G. A.; Beguinot, F.; Consiglio, E.; Di Jeso, B

Pion radii in nonlocal chiral quark model

The electromagnetic radius of the charged pion and the transition radius of the neutral pion are calculated in the framework of the nonlocal chiral quark model. It is shown in this model that the contributions of vector mesons to the pion radii are noticeably suppressed in comparison with a similar contribution in the local Nambu--Jona-Lasinio model. The form-factor for the process gamma*pi+pi- is calculated for the -1 GeV^2<q^2<1.6 GeV^2. Our results are in satisfactory agreement with experimental data.Comment: 7 pages, 7 figure

Multiplicity correlations of intermediate-mass fragments with pions and fast protons in 12C + 197Au

Low-energy pi+ (E < 35 MeV) from 12C+197Au collisions at incident energies from 300 to 1800 MeV per nucleon were detected with the Si-Si(Li)-CsI(Tl) calibration telescopes of the INDRA multidetector. The inclusive angular distributions are approximately isotropic, consistent with multiple rescattering in the target spectator. The multiplicity correlations of the low-energy pions and of energetic protons (E > 150 MeV) with intermediate-mass fragments were determined from the measured coincidence data. The deduced correlation functions 1 + R \approx 1.3 for inclusive event samples reflect the strong correlations evident from the common impact-parameter dependence of the considered multiplicities. For narrow impact-parameter bins (based on charged-particle multiplicity), the correlation functions are close to unity and do not indicate strong additional correlations. Only for pions at high particle multiplicities (central collisions) a weak anticorrelation is observed, probably due to a limited competition between these emissions. Overall, the results are consistent with the equilibrium assumption made in statistical multifragmentation scenarios. Predictions obtained with intranuclear cascade models coupled to the Statistical Multifragmentation Model are in good agreement with the experimental data.Comment: 9 pages, 11 figures, subm. to EPJ

GRP78 Mediates Cell Growth and Invasiveness in Endometrial Cancer.

Abstract Recent studies have indicated that endoplasmic reticulum stress, the unfolded protein response activation and altered GRP78 expression can play an important role in a variety of tumors development and progression. Very recently we reported for the first time that GRP78 is increased in endometrial tumors. However, whether GRP78 could play a role in the growth and/or invasiveness of endometrial cancer cells is still unknown. Here we report that the silencing of GRP78 expression affects both cell growth and invasiveness of Ishikawa and AN3CA cells, analyzed by the (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) and transwell migration assay, respectively. At variance with Ishikawa cells, AN3CA cells showed, besides an endoplasmic reticulum, also a plasma membrane GRP78 localization, evidenced by both immunofluorescence and cell membrane biotinylation experiments. Intriguingly, flow cytometry experiments showed that the treatment with a specific antibody targeting GRP78 C-terminal domain caused apoptosis in AN3CA but not in Ishikawa cells. Induction of apoptosis in AN3CA cells was not mediated by the p53 pathway activation but was rather associated to reduced AKT phosphorylation. Interestingly, immunofluorescence analysis evidenced that endometrioid adenocarcinoma tissues displayed, similarly to AN3CA cells, also a GRP78 plasma membrane localization. These data suggest that GRP78 and its plasma membrane localization, might play a role in endometrial cancer development and progression and might constitute a novel target for the treatment of endometrial cancer

Time Scales in Spectator Fragmentation

Proton-proton correlations and correlations of p-alpha, d-alpha, and t-alpha from spectator decays following Au + Au collisions at 1000 AMeV have been measured with an highly efficient detector hodoscope. The constructed correlation functions indicate a moderate expansion and low breakup densities similar to assumptions made in statistical multifragmentation models. In agreement with a volume breakup rather short time scales were deduced employing directional cuts in proton-proton correlations. PACS numbers: 25.70.Pq, 21.65.+f, 25.70.MnComment: 8 pages, with 5 included figures; To appear in the proceedings of the CRIS 2000 conference; Also available from http://www-kp3.gsi.de/www/kp3/aladin_publications.htm