gebhart/patrepeval huggingface dataset:
Controlled Site-Selective Glycosylation of Proteins by a Combined Site-Directed Mutagenesis and Chemical Modification Approach (1998)

ADVERTISEMENT RETURN TO ISSUEPREVCommunicationNEXTControlled Site-Selective Glycosylation of Proteins by a Combined Site-Directed Mutagenesis and Chemical Modification ApproachBenjamin G. Davis, Richard C. Lloyd, and J. Bryan JonesView Author Information Department of Chemistry, University of Toronto, 80 St. George Street, Toronto, Ontario M5S 3H6, Canada Cite this: J. Org. Chem. 1998, 63, 26, 9614–9615Publication Date (Web):December 1, 1998Publication History Received17 August 1998Published online1 December 1998Published inissue 1 December 1998https://pubs.acs.org/doi/10.1021/jo9816461https://doi.org/10.1021/jo9816461rapid-communicationACS PublicationsCopyright © 1998 American Chemical SocietyRequest reuse permissionsArticle Views1838Altmetric-Citations76LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-AlertscloseSupporting Info (2)»Supporting Information Supporting Information SUBJECTS:Carbohydrates,Organic compounds,Peptides and proteins,Post-translational modification,Reagents Get e-Alerts
Ancestry of the 4-chlorobenzoate dehalogenase: analysis of amino acid sequence identities among families of acyl:adenyl ligases, enoyl-CoA hydratases/isomerases, and acyl-CoA thioesterases (1992)

We have deduced the nucleotide sequence of the genes encoding the three components of 4-chlorobenzoate (4-CBA) dehalogenase from Pseudomonas sp. CBS-3 and examined the origin of these proteins by homology analysis. Open reading frame 1 (ORF1) encodes a 30-kDa 4-CBA-coenzyme A dehalogenase related to enoyl-coenzyme A hydratases functioning in fatty acid beta-oxidation. ORF2 encodes a 57-kDa protein which activates 4-CBA by acyl adenylation/thioesterification. This 4-CBA:coenzyme A ligase shares significant sequence similarity with a large group of proteins, many of which catalyze similar chemistry in beta-oxidation pathways or in siderophore and antibiotic synthetic pathways. These proteins have in common a short stretch of sequence, (T,S)(S,G)G(T,S)(T,E)G(L,X)PK(G,-), which is particularly highly conserved and which may represent an important new class of "signature" sequence. We were unable to find any proteins homologous in sequence to the 16-kDa 4-hydroxybenzoate-coenzyme A thioesterase encoded by ORF3. Analysis of the chemistry and function of the proteins found to be structurally related to the 4-CBA:coenzyme A ligase and the 4-CBA-coenzyme A dehalogenase supports the proposal that they evolved from a beta-oxidation pathway.
Nuclear Localization Signal Receptor Affinity Correlates with in Vivo Localization in Saccharomyces cerevisiae (2006)

Nuclear localization signals (NLSs) target proteins into the nucleus through mediating interactions with nuclear import receptors. Here, we perform a quantitative analysis of the correlation between NLS receptor affinity and the steady-state distribution of NLS-bearing cargo proteins between the cytoplasm and the nucleus of live yeast, which reflects the relative import rates of various NLS sequences. We find that there is a complicated, but monotonic quantitative relationship between the affinity of an NLS for the import receptor, importin alpha, and the steady-state accumulation of the cargo in the nucleus. This analysis takes into consideration the impact of protein size. In addition, the hypothetical upper limit to an NLS affinity for the receptors is explored through genetic approaches. Overall, our results indicate that there is a correlation between the binding affinity of an NLS cargo for the NLS receptor, importin alpha, and the import rate for this cargo. This correlation, however, is not maintained for cargoes that bind to the NLS receptor with very weak or very strong affinity.
Mechanism of sympathetic neural regulation of insulin, somatostatin, and glucagon secretion (1990)

The effects of electrical stimulation of the left splanchnic nerve on insulin, somatostatin, and glucagon secretion from the isolated perfused rat pancreas were investigated. Electrical splanchnic nerve stimulation (SNS), performed by square-wave impulses, produced a 25% decrease in effluent flow and a 10-fold increase in perfusate norepinephrine. Both insulin and somatostatin output in the presence of 16.7 mM glucose were inhibited during SNS by 85 and 56% of the basal value, respectively. Glucagon output in the presence of 5.5 mM glucose was stimulated 20-fold by SNS. Perfusion with 10(-6) M propranolol further decreased insulin and somatostatin output during SNS, when expressed as the total decrement beneath basal during stimulation. The glucagon response to SNS tended to be enhanced, although not significantly, by simultaneous infusion of 10(-6) M propranolol. However, 10(-6) M phentolamine (Phe) attenuated the SNS-induced inhibition of insulin and somatostatin output by 50 and 40%, respectively. However, insulin output remained decreased after SNS with Phe. The SNS-induced glucagon response was completely abolished by 10(-6) M Phe alone or by 10(-6) M Phe plus 10(-6) M propranolol. With 10(-6) M Phe plus 10(-6) M propranolol, insulin and somatostatin output remained decreased after SNS. These results suggest that insulin and somatostatin secretions induced by glucose are inhibited during SNS through the alpha-adrenergic mechanism and also that the beta-adrenergic mechanism exerts a stimulatory action. SNS-induced glucagon secretion occurs mainly through alpha-adrenergic activation.(ABSTRACT TRUNCATED AT 250 WORDS)
Intracellular trafficking of photoreceptors during light-induced signal transduction in plants (2001)

Plants monitor changes in the ambient light environment by highly specialised photoreceptors, which include the red/far-red photoreversible phytochromes, the blue-light-absorbing cryptochromes and phototropin and the so-far-unidentified UVB photoreceptor(s). Light easily penetrates plant organs/tissues and reaches even the subcellular compartments of various cell types. Therefore, it is not surprising that the determination of the intracellular localisation of photoreceptors has been, for many years, a major, and often controversial, subject of plant photobiology and cell biology research. Phototropin, one of the blue-light photoreceptors of higher plants, controls phototropism by monitoring the direction of light, and it is localised in or at the plasmalemma. In contrast, the subcellular localisation of phytochromes changes dynamically and exhibits a very complex pattern. These photoreceptors are localised in the cytosol in dark- grown tissues. Irradiation, however, induces import of phytochromes into the nucleus. The import occurs in a light-quality- and light-quantity-dependent fashion and, as such, seems to be unique to higher plants. Light-induced accumulation of phytochromes in the nuclei correlates well with various physiological responses mediated by these photoreceptors. These observations indicate that light-dependent intracellular redistribution of phytochrome photoreceptors is one of the major regulatory steps in photomorphogenesis.
Aza analogs of lucanthone: synthesis and antitumor and bactericidal properties (1983)

Three types of aza analogues of lucanthone were synthesized for evaluation as antitumor drugs. None of the compounds was found to have significant cytotoxic effects either on Friend tumor cells or on L1210 leukemia cells. However, one of the target compounds, 5,10-dihydro-10-oxo-1-[[3-(diethylamino)propyl]amino]-3-methylpyrido [4,3-b]quinoline, was shown to have noticeable antibiotic properties.
Intracellular and surface distribution of a membrane protein (CD8) derived from a single nucleus in multinucleated myotubes. (1989)

We have investigated the contribution of an individual nucleus to intracellular and surface membranes in multinucleated muscle fibers. Using a retroviral vector, we introduced the gene encoding the human T-lymphocyte antigen CD8 into C2 mouse muscle cells to form a stable line expressing the human protein on its surface. The intracellular and surface distributions of the protein were then investigated by immunocytochemistry in hybrid myotubes containing a single nucleus expressing CD8. We show that the intracellular distribution of CD8 is limited to a local area surrounding the nucleus encoding it and several neighboring nuclei. On the cell surface, however, the protein is distributed over the entire myotube. Widespread distribution of a surface membrane protein in multinucleated myotubes can thus result from localized synthesis and processing.
Charge Photogeneration in Donor–Acceptor Conjugated Materials: Influence of Excess Excitation Energy and Chain Length (2013)

We investigate the role of excess excitation energy on the nature of photoexcitations in donor-acceptor π-conjugated materials. We compare the polymer poly(2,6-(4,4-bis(2-ethylhexyl)-4H-cyclopenta[1,2-b;3,4-b']dithiophene)-4,7-benzo[2,1,3]thiadiazole) (PCPDTBT) and a short oligomer with identical constituents at different excitation wavelengths, from the near-infrared up to the ultraviolet spectral region. Ultrafast spectroscopic measurements clearly show an increased polaron pair yield for higher excess energies directly after photoexcitation when compared to the exciton population. This effect, already observable in the polymer, is even more pronounced for the shorter oligomer. Supported by quantum chemical simulations, we show that excitation in high-energy states generates electron and hole wave functions with reduced overlap, which likely act as precursors for the polaron pairs. Interestingly, in the oligomer we observe a lifetime of polaron pairs which is one order of magnitude longer. We suggest that this behavior results from the intermolecular nature of polaron pairs in oligomers. The study excludes the presence of carrier multiplication in these materials and highlights new aspects in the photophysics of donor-acceptor small molecules when compared to polymers. The former are identified as promising materials for efficient organic photovoltaics.
Progressive multiple sclerosis (2015)

PMS represents a significant challenge, as the pathogenesis of the disease is not well understood, no validated outcome metrics have been established and clinical trial experience to date has been disappointing. Advances in the understanding of the disease and lessons learned in previous clinical trials are paving the way for successful development of disease-modifying agents for this disease.
Trilayer hybrid polymer-quantum dot light-emitting diodes (2004)

We report a trilayer hybrid polymer-quantum-dot light-emitting diode fabricated by sandwiching a CdSe-ZnS core–shell quantum-dot (QD) layer, a few monolayers thick, between films of polyvinylcarbazole (PVK) and an oxadiazole derivative (butyl-PBD). All the layers have been deposited by a controlled spin-coating technique. Stable aqueous dispersion of QDs has been prepared to make possible the spin coating of multiple layers without affecting the layer underneath. Our device shows 20 times the quantum efficiency (0.2%) and less than half the threshold voltage (5 V) of a single-layer device made from the PVK-QD-PBD blend. This is attributed to balanced carrier conduction, enhanced recombination, and reduced quenching of emission due to a better electro-optical device design.
Heparin- and sulfatide-binding peptides from the type I repeats of human thrombospondin promote melanoma cell adhesion. (1992)

Peptides from the three type I repeats of human endothelial cell thrombospondin, containing the consensus sequence-Trp-Ser-Xaa-Trp-, bind to sulfated glycoconjugates including heparin and sulfatide. The peptides are potent inhibitors for the binding of thrombospondin, laminin, or apolipoprotein E to these ligands. The thrombospondin peptides that inhibit heparin binding, but not adjacent peptides from the thrombospondin sequence containing the previously identified adhesive motif Val-Thr-Cys-Gly, promote melanoma cell adhesion when immobilized on plastic. Melanoma cell adhesion to the immobilized peptides is inhibited by soluble recombinant heparin-binding fragment of thrombospondin. The peptides also inhibit heparin-dependent binding of thrombospondin or laminin to human melanoma cells. The active peptides lack any previously identified heparin-binding consensus sequences and most do not contain any basic amino acids. Studies with homologous peptides showed that the tryptophan residues are required for binding. Adjacent basic residues in the second type I repeat enhance binding to heparin but not to sulfatide. Thus the type I peptides of thrombospondin define a distinct class of heparin-binding peptides.
Differential regulation of cyclin B1 RNA and protein expression during hepatocyte growth in vivo. (1996)

Cyclin genes and their products are important regulatory participants in the eukaryotic cell cycle. It is well established that cyclin B1 protein forms a complex with cyclin-dependent kinase 1 (CDK1), which, when activated, initiates mitosis. We have previously established that cyclin B1 gene expression is posttranscriptionally regulated in regenerating rat liver after 70% partial hepatectomy (PH). We now report further characterization of cyclin B1 gene expression, as well as that of CDK1 and cdc25B, in this unique in vivo model of cell proliferation. Cyclin B1 transcripts were detected by RNase protection through 96 h of liver regeneration and exhibited dramatic changes in steady-state levels. Peak expressions occurred at 24-30 h, more significantly at 42-48, and at 72 h. By Northern blot analysis, single transcripts for CDK1 and cdc25B were detected, and the temporal expression of both transcripts during liver regeneration mirrored that of cyclin B1. By Western blot and immunohistochemical analyses, cyclin B1 protein levels did not change significantly in either nuclear or cytoplasmic fractions, whereas CDK1 protein levels paralleled their associated RNA expression. Cdc25B protein levels steadily decreased from 0 to 96 h after PH. In addition, cytoplasmic protein levels of cyclin B1 exhibited a constant distribution in subfractions of microsome- and polysome-associated and free proteins. Cyclin B1 RNA also localized to these three cytoplasmic subfractions. Finally, the apparent translational activity of cyclin B1 transcripts was very similar at both 24 and 48 h after PH, in contrast to their respective mRNA half-lives. In a peroxisome proliferation model of hepatocyte growth and apoptosis, cyclin B1 and CDK1 proteins were induced in the absence of transcript up-regulation. Our results demonstrate that cyclin B1 mRNA steady-state levels are regulated posttranscriptionally in regenerating rat liver. Furthermore, the pattern of cyclin B1 transcript expression is paralleled by that of the CDK1 gene, whereas their respective protein steady-state levels provide a striking contrast. Finally, cyclin B1 is differentially regulated by an uncoupling of transcript abundance and translational processing in two in vivo models of hepatocyte growth. The abundance of cyclin B1 protein in nonreplicating cells suggests that cyclin B1 may be available for other cellular pathways in the hepatocyte.
Nucleophilicities of amino acids and peptides (2007)

The kinetics of the reactions of amino acids with stabilized diarylcarbenium ions (Ar(2)CH(+)) have been studied photometrically in aqueous solution at variable pH. In the range of 10.5 < pH < 12, the amino acids react much faster than the competing nucleophiles hydroxide and water. Though the pK(aH) values of the amino acids vary by almost four units, the nucleophilic reactivities of all primary amino groups differ by less than a factor of 4. The secondary amino group of proline is 10(2) times more reactive, and the thiolate site in cysteine exceeds the reactivities of the primary amino groups by a factor of 10(4). Nucleophilicity parameters N as defined by the correlation log k(20 degrees C) = s(N + E) have been determined in order to include amino acids into the most comprehensive nucleophilicity scales presently available, which provide a direct comparison of n-, pi-, and sigma-nucleophiles.
Platelets and stroke (1999)

Platelets are anucleate cells with little or no capacity for de novo protein synthesis. Their potential haemostatic reactivity is established at or before thrombopoiesis by their precursor cell, the bone marrow megakaryocyte. In some pathologic conditions, the megakaryocyte-platelet-haemostatic axis (MPHA) becomes perturbed, resulting in the formation of hyperfunctional platelets which may contribute to the development of vascular disease or an acute thrombotic event such as ischaemic stroke or myocardial infarction. Laboratory measurements of platelet function have established that platelet reactivity is accentuated in acute ischaemic stroke, particularly following cortical rather than lacunar infarction. Whether accentuated platelet function is a cause or a consequence of stroke is not yet clear, but it is likely that patients with certain risk factor profiles have some degree of platelet activation preceding the stroke. Further work into the MPHA is required to establish whether enhanced post-stroke platelet reactivity can be referred to the megakaryocyte. The antiplatelet agents tested to date are effective in secondary but not primary prevention of stroke. This probably reflects the diverse pathophysiology of stroke: accentuated platelet function is only likely to be a significant factor in cortical stroke.
Adaptive camera-based color mapping for mixed-reality applications (2011)

We present a novel adaptive color mapping method for virtual objects in mixed-reality environments. In several mixed-reality applications, added virtual objects should be visually indistinguishable from real objects. Recent mixed-reality methods use global-illumination algorithms to approach this goal. However, simulating the light distribution is not enough for visually plausible images. Since the observing camera has its very own transfer function from real-world radiance values to RGB colors, virtual objects look artificial just because their rendered colors do not match with those of the camera. Our approach combines an on-line camera characterization method with a heuristic to map colors of virtual objects to colors as they would be seen by the observing camera. Previous tone-mapping functions were not designed for use in mixed-reality systems and thus did not take the camera-specific behavior into account. In contrast, our method takes the camera into account and thus can also handle changes of its parameters during runtime. The results show that virtual objects look visually more plausible than by just applying tone-mapping operators.
An activity specified by the osteosarcoma line U2OS can substitute functionally for ICP0, a major regulatory protein of herpes simplex virus type 1 (1995)

Among the five immediate-early regulatory proteins of herpes simplex virus (HSV) type 1, only ICP0 is capable of activating all kinetic classes of viral genes. Consistent with its broad transactivating activity, ICP0 plays a major role in enhancing the reactivation of HSV from latency both in vivo and in vitro. Although not essential for viral replication, ICP0 confers a significant growth advantage on the virus, especially at low multiplicities of infection. In this report we describe the expression of a novel activity by the osteosarcoma cell line U2OS that can substitute functionally for ICP0. Compared with Vero cells, both U2OS cells and cells of the ICP0-expressing line 0-28 significantly enhanced the plating efficiency of an ICP0 null mutant, 7134. In contrast, the plating efficiencies of the wild-type virus in all three cell types were similar. Single-step growth experiments demonstrated that the yield of 7134 in U2OS cells was severalfold higher than that in 0-28 cells and about 100-fold higher than that in Vero cells. In order to identify the viral genes whose expression is enhanced by the activity in U2OS cells, levels of expression of selected viral proteins in extracts of Vero and U2OS cells were compared by Western blot (immunoblot) analysis following low-multiplicity infection. At a multiplicity of 0.1 PFU per cell, the levels of expression of the immediate-early protein ICP4 and the early protein gD in 7134-infected U2OS cells were significantly higher than those in 7134-infected Vero cells. When infections were carried out at a multiplicity of 1 PFU per cell, however, no major differences in the levels of expression of these proteins in U2OS and Vero cells were observed. Cycloheximide reversal experiments demonstrated that the cellular activity expressed in U2OS cells that promotes high-level expression of ICP4 is not synthesized de novo but appears to exist as a preformed protein(s). To confirm this observation and to determine whether, like immediate-early genes, early, delayed-early, and late viral genes are also responsive to the cellular activity, transient-expression assays were performed. The results of these tests demonstrated that basal levels of expression from immediate-early, early, and delayed-early promoters, but not that from a late promoter, were significantly higher in U2OS cells than in Vero cells and that this enhancement occurred in the absence of viral proteins.(ABSTRACT TRUNCATED AT 400 WORDS)
Endothelial nitric oxide synthase overexpression attenuates myocardial reperfusion injury (2004)

Previous studies indicate that deficiency of endothelial nitric oxide (NO) synthase (eNOS)-derived NO exacerbates myocardial reperfusion injury. We hypothesized that overexpression of eNOS would reduce the extent of myocardial ischemia-reperfusion (MI/R) injury. We investigated two distinct strains of transgenic (TG) mice overexpressing the eNOS gene (eNOS TG). Bovine eNOS was overexpressed in one strain (eNOS TG-Kobe), whereas the human eNOS gene was overexpressed in the other strain (eNOS TG-RT). Non-TG (NTG) and eNOS TG mice were subjected to 30 min of coronary artery occlusion followed by 24 h of reperfusion, and the extent of myocardial infarction was determined. Myocardial infarct size was reduced by 33% in the eNOS TG-Kobe strain (P < 0.05 vs. NTG) and by 32% in the eNOS TG-RT strain (P < 0.05 vs. NTG). However, postischemic cardiac function (cardiac output, fractional shortening) was not improved in the eNOS TG-Kobe mouse at 24 h of reperfusion [P = not significant (NS) vs. NTG]. In additional studies, eNOS TG-Kobe mice were subjected to 30 min of myocardial infarction and 7 days of reperfusion. Fractional shortening and the first derivative of left ventricular pressure were measured in eNOS TG-Kobe and NTG mice, and no significant differences in contractility were observed (P = NS) between the eNOS TG mice and NTG controls. Left ventricular end-diastolic pressure was significantly (P < 0.05 vs. NTG) reduced in the eNOS TG-Kobe strain at 7 days of reperfusion. The cardioprotective effects of eNOS overexpression on myocardial infarct size were ablated by Nomega-nitro-l-arginine methyl ester (300 mg/kg) pretreatment. Thus genetic overexpression of eNOS in mice attenuates myocardial infarction after MI/R but fails to significantly protect against postischemic myocardial contractile dysfunction in mice.