Database : MEDLINE
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[PMID]: 29524835
[Au] Autor:Chrzastek K; Lee DH; Gharaibeh S; Zsak A; Kapczynski DR
[Ad] Address:US National Poultry Research Center, Agricultural Research Service, US Department of Agriculture, 934 College Station Road, Athens, GA, 30605, USA.
[Ti] Title:Characterization of H9N2 avian influenza viruses from the Middle East demonstrates heterogeneity at amino acid position 226 in the hemagglutinin and potential for transmission to mammals.
[So] Source:Virology;518:195-201, 2018 Mar 07.
[Is] ISSN:1096-0341
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Next-generation sequencing (NGS) technologies are a valuable tool to monitor changes in viral genomes and determine the genetic heterogeneity of viruses. In this study, NGS was applied to clinical poultry samples from Jordan to detect eleven H9N2 low pathogenic avian influenza viruses (LPAIV). All of the viruses tested belonged to Middle East A genetic group of G1 lineage. Deep sequencing demonstrated a high degree of heterogeneity of glutamine and leucine residues at position 226 in the hemagglutinin (HA) gene, which increases specificity to either avian or mammalian-type receptors. Moreover, additional amino acid changes in PB1, PA, M1, M2, and NS1 were identified among the viruses tested. Compared to single gene amplification, application of NGS for surveillance and characterization of H9N2 LPAIV provides a complete genetic profile of emerging isolates and better understanding of the potential of zoonotic transmissions to mammals.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 46008 MEDLINE  
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[PMID]: 29524395
[Au] Autor:Hölzl G; Sohlenkamp C; Vences-Guzmán MA; Gisch N
[Ad] Address:Institute of Molecular Physiology and Biotechnology of Plants (IMBIO), University of Bonn, Karlrobert-Kreiten-Straße 13, 53115, Bonn, Germany.
[Ti] Title:Headgroup hydroxylation by OlsE occurs at the C4 position of ornithine lipid and is widespread in proteobacteria and bacteroidetes.
[So] Source:Chem Phys Lipids;, 2018 Mar 07.
[Is] ISSN:1873-2941
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Amino acid-containing acyloxyacyl lipids are composed of a 3-hydroxy fatty acid amide-bound to the α-amino group of an amino acid. A second fatty acid is ester-linked to the 3-hydroxy group of the first fatty acid. Most commonly, ornithine is the headgroup of these lipids, but glycine, serineglycine, glutamine and lysine have also been described in bacteria. Ornithine lipids (OL) can be synthesized by about 50% of the sequenced bacterial species, and several covalent modifications of its basic structure have been described. The OL hydroxylase OlsE is widespread in Rhizobium and Agrobacterium species and is responsible for introducing a hydroxyl group at a hence unknown position within the ornithine headgroup causing the formation of the OL named S2. Using NMR on purified OL S2, we show that the OlsE-mediated hydroxylation takes place at the C-4 position of the ornithine headgroup. Furthermore, we identify a hydroxylase in the genome of Pseudopedobacter saltans, distantly related to OlsE from α-proteobacteria, able to hydroxylate the headgroup of both ornithine lipids and lysine lipids. A homology search with the amino acid sequence of this hydroxylase allows us to predict that OL headgroup hydroxylation is not restricted to a few α-proteobacteria, but is apparently also common in many genera belonging to the Cytophaga-Flavobacterium-Bacteroidetes (CFB) group of bacteria.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 46008 MEDLINE  
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[PMID]: 29511334
[Au] Autor:White TL; Monnig MA; Walsh EG; Nitenson AZ; Harris AD; Cohen RA; Porges EC; Woods AJ; Lamb DG; Boyd CA; Fekir S
[Ad] Address:Center for Alcohol and Addiction Studies, Brown University, Providence, RI, USA. Tara_White@Brown.edu.
[Ti] Title:Psychostimulant drug effects on glutamate, Glx, and creatine in the anterior cingulate cortex and subjective response in healthy humans.
[So] Source:Neuropsychopharmacology;, 2018 Mar 06.
[Is] ISSN:1740-634X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Prescription psychostimulants produce rapid changes in mood, energy, and attention. These drugs are widely used and abused. However, their effects in human neocortex on glutamate and glutamine (pooled as Glx), and key neurometabolites such as N-acetylaspartate (tNAA), creatine (tCr), choline (Cho), and myo-inositol (Ins) are poorly understood. Changes in these compounds could inform the mechanism of action of psychostimulant drugs and their abuse potential in humans. We investigated the acute impact of two FDA-approved psychostimulant drugs on neurometabolites using magnetic resonance spectroscopy ( H MRS). Single clinically relevant doses of d-amphetamine (AMP, 20 mg oral), methamphetamine (MA, 20 mg oral; Desoxyn®), or placebo were administered to healthy participants (n = 26) on three separate test days in a placebo-controlled, double-blinded, within-subjects crossover design. Each participant experienced all three conditions and thus served as his/her own control. H MRS was conducted in the dorsal anterior cingulate cortex (dACC), an integrative neocortical hub, during the peak period of drug responses (140-150 m post ingestion). D-amphetamine increased the level of Glu (p = .0001), Glx (p = .003), and tCr (p = .0067) in the dACC. Methamphetamine increased Glu in females, producing a significant crossover interaction pattern with gender (p = .02). Drug effects on Glu, tCr, and Glx were positively correlated with subjective drug responses, predicting both the duration of AMP liking (Glu: r = +.49, p = .02; tCr: r = +.41, p = .047) and the magnitude of peak drug high to MA (Glu: r = +.52, p = .016; Glx: r = +.42, p = .049). Neither drug affected the levels of tNAA, Cho, or Ins after correction for multiple comparisons. We conclude that d-amphetamine increased the concentration of glutamate, Glx, and tCr in the dACC in male and female volunteers 2 / hours after drug consumption. There was evidence that methamphetamine differentially affects dACC Glu levels in women and men. These findings provide the first experimental evidence that specific psychostimulants increase the level of glutamatergic compounds in the human brain, and that glutamatergic changes predict the extent and magnitude of subjective responses to psychostimulants.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1038/s41386-018-0027-7

  4 / 46008 MEDLINE  
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[PMID]: 29506576
[Au] Autor:Söbbeler FJ; Carrera I; Pasloske K; Ranasinghe MG; Kircher P; Kästner SBR
[Ad] Address:Small Animal Clinic (Söbbeler, Kästner), University of Veterinary Medicine Hanover Foundation, Bünteweg 9, 30559, Hannover, Germany. franz.josef.soebbeler@tiho-hannover.de.
[Ti] Title:Effects of isoflurane, sevoflurane, propofol and alfaxalone on brain metabolism in dogs assessed by proton magnetic resonance spectroscopy ( H MRS).
[So] Source:BMC Vet Res;14(1):69, 2018 Mar 05.
[Is] ISSN:1746-6148
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: The purpose of this study was to determine the effects of isoflurane, sevoflurane, propofol and alfaxalone on the canine brain metabolite bioprofile, measured with single voxel short echo time proton magnetic resonance spectroscopy at 3 Tesla. Ten adult healthy Beagle dogs were assigned to receive isoflurane, sevoflurane, propofol and alfaxalone at 3 different dose rates each in a randomized cross-over study design. Doses for isoflurane, sevoflurane, propofol and alfaxalone were F 'Iso 1.7 vol%, 2.1 vol%, 2.8 vol%, F 'Sevo 2.8 vol%, 3.5 vol% and 4.7 vol%, 30, 45 and 60 mg kg h and 10, 15 and 20 mg kg h respectively. A single voxel Point Resolved Spectroscopy Sequence was performed on a 3 T MRI scanner in three brain regions (basal ganglia, parietal and occipital lobes). Spectral data were analyzed with LCModel. Concentration of total N-acetylaspartate (tNAA), choline, creatine, inositol and glutamine and glutamate complex (Glx) relative to water content was obtained. Plasma concentration of lactate, glucose, triglycerides, propofol and alfaxalone were determined. Statistics were performed using repeated measures ANOVA or Wilcoxon Sign Rank test with alpha = 5%. RESULTS: Plasma glucose increased with isoflurane, sevoflurane and alfaxalone but decreased with propofol. Plasma lactate increased with all anesthetics (isoflurane > sevoflurane > propofol > alfaxalone). Cerebral lactate could not be detected. Only minor changes in cerebral metabolite concentrations of tNAA, choline, inositol, creatine and Glx occurred with anesthetic dose changes. CONCLUSION: The metabolomic profile detected with proton magnetic resonance spectroscopy at 3 Tesla of canine brain showed only minor differences between doses and anesthetics related to tNAA, choline, creatine, inositol and Glx.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1186/s12917-018-1396-1

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[PMID]: 29506554
[Au] Autor:Vizuete AFK; Hansen F; Negri E; Leite MC; de Oliveira DL; Gonçalves CA
[Ad] Address:Department of Biochemistry, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos, 2600-Anexo, Porto Alegre, RS, 90035-003, Brazil. adrianavizuete@gmail.com.
[Ti] Title:Effects of dexamethasone on the Li-pilocarpine model of epilepsy: protection against hippocampal inflammation and astrogliosis.
[So] Source:J Neuroinflammation;15(1):68, 2018 Mar 05.
[Is] ISSN:1742-2094
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Temporal lobe epilepsy (TLE) is the most common form of partial epilepsy and is accompanied, in one third of cases, by resistance to antiepileptic drugs (AED). Most AED target neuronal activity modulated by ionic channels, and the steroid sensitivity of these channels has supported the use of corticosteroids as adjunctives to AED. Assuming the importance of astrocytes in neuronal activity, we investigated inflammatory and astroglial markers in the hippocampus, a key structure affected in TLE and in the Li-pilocarpine model of epilepsy. METHODS: Initially, hippocampal slices were obtained from sham rats and rats subjected to the Li-pilocarpine model of epilepsy, at 1, 14, and 56 days after status epilepticus (SE), which correspond to the acute, silent, and chronic phases. Dexamethasone was added to the incubation medium to evaluate the secretion of S100B, an astrocyte-derived protein widely used as a marker of brain injury. In the second set of experiments, we evaluated the in vivo effect of dexamethasone, administrated at 2 days after SE, on hippocampal inflammatory (COX-1/2, PGE2, and cytokines) and astroglial parameters: GFAP, S100B, glutamine synthetase (GS) and water (AQP-4), and K (Kir 4.1) channels. RESULTS: Basal S100B secretion and S100B secretion in high-K medium did not differ at 1, 14, and 56 days for the hippocampal slices from epileptic rats, in contrast to sham animal slices, where high-K medium decreased S100B secretion. Dexamethasone addition to the incubation medium per se induced a decrease in S100B secretion in sham and epileptic rats (1 and 56 days after SE induction). Following in vivo dexamethasone administration, inflammatory improvements were observed, astrogliosis was prevented (based on GFAP and S100B content), and astroglial dysfunction was partially abrogated (based on Kir 4.1 protein and GSH content). The GS decrease was not prevented by dexamethasone, and AQP-4 was not altered in this epileptic model. CONCLUSIONS: Changes in astroglial parameters emphasize the importance of these cells for understanding alterations and mechanisms of epileptic disorders in this model. In vivo dexamethasone administration prevented most of the parameters analyzed, reinforcing the importance of anti-inflammatory steroid therapy in the Li-pilocarpine model and possibly in other epileptic conditions in which neuroinflammation is present.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1186/s12974-018-1109-5

  6 / 46008 MEDLINE  
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[PMID]: 29506475
[Au] Autor:Siddiqui JK; Baskin E; Liu M; Cantemir-Stone CZ; Zhang B; Bonneville R; McElroy JP; Coombes KR; Mathé EA
[Ad] Address:Department of Biomedical Informatics, College of Medicine, The Ohio State University, Columbus, OH, USA.
[Ti] Title:IntLIM: integration using linear models of metabolomics and gene expression data.
[So] Source:BMC Bioinformatics;19(1):81, 2018 Mar 05.
[Is] ISSN:1471-2105
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Integration of transcriptomic and metabolomic data improves functional interpretation of disease-related metabolomic phenotypes, and facilitates discovery of putative metabolite biomarkers and gene targets. For this reason, these data are increasingly collected in large (> 100 participants) cohorts, thereby driving a need for the development of user-friendly and open-source methods/tools for their integration. Of note, clinical/translational studies typically provide snapshot (e.g. one time point) gene and metabolite profiles and, oftentimes, most metabolites measured are not identified. Thus, in these types of studies, pathway/network approaches that take into account the complexity of transcript-metabolite relationships may neither be applicable nor readily uncover novel relationships. With this in mind, we propose a simple linear modeling approach to capture disease-(or other phenotype) specific gene-metabolite associations, with the assumption that co-regulation patterns reflect functionally related genes and metabolites. RESULTS: The proposed linear model, metabolite ~ gene + phenotype + gene:phenotype, specifically evaluates whether gene-metabolite relationships differ by phenotype, by testing whether the relationship in one phenotype is significantly different from the relationship in another phenotype (via a statistical interaction gene:phenotype p-value). Statistical interaction p-values for all possible gene-metabolite pairs are computed and significant pairs are then clustered by the directionality of associations (e.g. strong positive association in one phenotype, strong negative association in another phenotype). We implemented our approach as an R package, IntLIM, which includes a user-friendly R Shiny web interface, thereby making the integrative analyses accessible to non-computational experts. We applied IntLIM to two previously published datasets, collected in the NCI-60 cancer cell lines and in human breast tumor and non-tumor tissue, for which transcriptomic and metabolomic data are available. We demonstrate that IntLIM captures relevant tumor-specific gene-metabolite associations involved in known cancer-related pathways, including glutamine metabolism. Using IntLIM, we also uncover biologically relevant novel relationships that could be further tested experimentally. CONCLUSIONS: IntLIM provides a user-friendly, reproducible framework to integrate transcriptomic and metabolomic data and help interpret metabolomic data and uncover novel gene-metabolite relationships. The IntLIM R package is publicly available in GitHub ( https://github.com/mathelab/IntLIM ) and includes a user-friendly web application, vignettes, sample data and data/code to reproduce results.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1186/s12859-018-2085-6

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[PMID]: 29491345
[Au] Autor:Wang C; Deng Y; Yue Y; Chen W; Zhang Y; Shi G; Wu Z
[Ad] Address:Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital and Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China (mainland).
[Ti] Title:Glutamine Enhances the Hypoglycemic Effect of Insulin in L6 Cells via Phosphatidylinositol-3-Kinase (PI3K)/Protein Kinase B (AKT)/Glucose Transporter 4 (GLUT4) Signaling Pathway.
[So] Source:Med Sci Monit;24:1241-1250, 2018 Mar 01.
[Is] ISSN:1643-3750
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND Diabetes mellitus (DM) is characterized by a decreased blood level of glutamine (Gln), which may contribute to the disturbance in the effect of insulin on skeletal muscle. Therefore, it is crucial to study how to improve the effect of insulin on skeletal muscle by increasing Gln. In the present study, we investigated the effect of Gln on the hypoglycemic action of insulin in skeletal muscle L6 cells at high glucose levels through the insulin signaling pathway and glycogen synthesis pathway. MATERIAL AND METHODS The L6 cells were cultured in and stimulated by Gln and insulin. The glutamine analogue, L-Gamma-Glutamyl-p-nitroanilide (GPNA), was used for verifying the effect of Gln. The expression of insulin signaling molecules, including phosphatidylinositol-3-kinase (PI3K), 3-phosphoinositide-dependent protein kinase-1 (PDK1), protein kinase B (AKT), protein kinase C zeta (PKCz), and glucose transporter 4 (GLUT4), were detected by real-time PCR and Western blot analysis, GLUT4 translocation was observed by immunofluorescence staining, glycogen synthase kinase (GSK) was analyzed by Western blotting, and glucose uptake was measured by glucose oxidase method (GOD). RESULTS The results demonstrated that Gln combined with insulin remarkably up-regulated PI3K and PDK1 and also increased AKT and PKCz phosphorylation. The present study shows that Gln enhanced the impact of insulin on GLUT4 and its translocation. The results of glucose uptake and GSK phosphorylation further confirmed the hypoglycemic effect of Gln accompanied with insulin. The hypoglycemic effect of Gln was reversed by GPNA. CONCLUSIONS These findings suggest that Gln enhances the hypoglycemic role of insulin through the PI3K/AKT/GLUT4 signaling pathway and glycogen synthesis pathway.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process

  8 / 46008 MEDLINE  
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[PMID]: 29423830
[Au] Autor:Waisbren SE; Cuthbertson D; Burgard P; Holbert A; McCarter R; Cederbaum S; Members of the Urea Cycle Disorders Consortium
[Ad] Address:Division of Genetics and Genomics, Boston Children's Hospital and Department of Medicine, Harvard Medical School, 1 Autumn Street #525, Boston, MA, 02115, USA. Susan.waisbren@childrens.harvard.edu.
[Ti] Title:Biochemical markers and neuropsychological functioning in distal urea cycle disorders.
[So] Source:J Inherit Metab Dis;, 2018 Feb 08.
[Is] ISSN:1573-2665
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Urea cycle disorders often present as devastating metabolic conditions, resulting in high mortality and significant neuropsychological damage, despite treatment. The Urea Cycle Disorders Longitudinal Study is a natural history study that collects data from regular clinical follow-up and neuropsychological testing. This report examines links between biochemical markers (ammonia, glutamine, arginine, citrulline) and primary neuropsychological endpoints in three distal disorders, argininosuccinic acid synthetase deficiency (ASD or citrullinemia type I), argininosuccinic acid lyase deficiency (ASA or ALD), and arginase deficiency (ARGD). Laboratory results and test scores from neuropsychological evaluations were assessed in 145 study participants, ages 3 years and older, with ASD (n = 64), ASA (n = 65) and ARGD (n = 16). Mean full scale IQ was below the population mean of 100 ± 15 for all groups: (ASD = 79 ± 24; ASA = 71 ± 21; ARGD = 65 ± 19). The greatest deficits were noted in visual performance and motor skills for all groups. While ammonia levels remain prominent as prognostic biomarkers, other biomarkers may be equally valuable as correlates of neuropsychological functioning. Cumulative exposure to the biomarkers included in the study proved to be highly sensitive indicators of neuropsychological outcomes, even when below the cut-off levels generally considered toxic. Blood levels of biomarkers obtained on the day of neuropsychological evaluations were not correlated with measures of functioning for any disorder in any domain. The importance of cumulative exposure supports early identification and confirms the need for well-controlled management of all biochemical abnormalities (and not just ammonia) that occur in urea cycle disorders.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1007/s10545-017-0132-5

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[PMID]: 29316436
[Au] Autor:Gwinn DM; Lee AG; Briones-Martin-Del-Campo M; Conn CS; Simpson DR; Scott AI; Le A; Cowan TM; Ruggero D; Sweet-Cordero EA
[Ad] Address:Division of Hematology and Oncology, Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305, USA; Division of Hematology and Oncology, Department of Pediatrics, University of California San Francisco, San Francisco, CA 94158, USA.
[Ti] Title:Oncogenic KRAS Regulates Amino Acid Homeostasis and Asparagine Biosynthesis via ATF4 and Alters Sensitivity to L-Asparaginase.
[So] Source:Cancer Cell;33(1):91-107.e6, 2018 Jan 08.
[Is] ISSN:1878-3686
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:KRAS is a regulator of the nutrient stress response in non-small-cell lung cancer (NSCLC). Induction of the ATF4 pathway during nutrient depletion requires AKT and NRF2 downstream of KRAS. The tumor suppressor KEAP1 strongly influences the outcome of activation of this pathway during nutrient stress; loss of KEAP1 in KRAS mutant cells leads to apoptosis. Through ATF4 regulation, KRAS alters amino acid uptake and asparagine biosynthesis. The ATF4 target asparagine synthetase (ASNS) contributes to apoptotic suppression, protein biosynthesis, and mTORC1 activation. Inhibition of AKT suppressed ASNS expression and, combined with depletion of extracellular asparagine, decreased tumor growth. Therefore, KRAS is important for the cellular response to nutrient stress, and ASNS represents a promising therapeutic target in KRAS mutant NSCLC.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review

  10 / 46008 MEDLINE  
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[PMID]: 29524280
[Au] Autor:Banda-Vázquez J; Shanmugaratnam S; Rodríguez-Sotres R; Torres-Larios A; Höcker B; Sosa-Peinado A
[Ad] Address:UNAM, Mexico.
[Ti] Title:Redesign of LAOBP to bind novel L-amino acid ligands.
[So] Source:Protein Sci;, 2018 Mar 10.
[Is] ISSN:1469-896X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Computational protein design is still a challenge for advancing structure-function relationships. While recent advances in this field are promising, more information for genuine predictions is needed. Here, we discuss different approaches applied to install novel glutamine (Gln) binding into the Lysine/Arginine/Ornithine binding protein (LAOBP) from Salmonella typhimurium. We studied the ligand binding behaviour of two mutants: a binding pocket grafting design based on a structural superposition of LAOBP to the Gln binding protein QBP from Escherichia coli and a design based on statistical coupled positions. The latter showed the ability to bind Gln even though the protein was not very stable. Comparison of both approaches highlighted a non-conservative shared point mutation between LAOBP_graft and LAOBP_sca. This context dependent L117K mutation in LAOBP turned out to be sufficient for introducing Gln binding, as confirmed by different experimental techniques. Moreover, the crystal structure of LAOBP_L117K in complex with its ligand is reported. This article is protected by copyright. All rights reserved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1002/pro.3403


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