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131.
132.
Budde BS Binner P Waldmüller S Höhne W Blankenfeldt W Hassfeld S Brömsen J Dermintzoglou A Wieczorek M May E Kirst E Selignow C Rackebrandt K Müller M Goody RS Vosberg HP Nürnberg P Scheffold T 《PloS one》2007,2(12):e1362
Noncompaction of the ventricular myocardium (NVM) is the morphological hallmark of a rare familial or sporadic unclassified heart disease of heterogeneous origin. NVM results presumably from a congenital developmental error and has been traced back to single point mutations in various genes. The objective of this study was to determine the underlying genetic defect in a large German family suffering from NVM. Twenty four family members were clinically assessed using advanced imaging techniques. For molecular characterization, a genome-wide linkage analysis was undertaken and the disease locus was mapped to chromosome 14ptel-14q12. Subsequently, two genes of the disease interval, MYH6 and MYH7 (encoding the alpha- and beta-myosin heavy chain, respectively) were sequenced, leading to the identification of a previously unknown de novo missense mutation, c.842G>C, in the gene MYH7. The mutation affects a highly conserved amino acid in the myosin subfragment-1 (R281T). In silico simulations suggest that the mutation R281T prevents the formation of a salt bridge between residues R281 and D325, thereby destabilizing the myosin head. The mutation was exclusively present in morphologically affected family members. A few members of the family displayed NVM in combination with other heart defects, such as dislocation of the tricuspid valve (Ebstein's anomaly, EA) and atrial septal defect (ASD). A high degree of clinical variability was observed, ranging from the absence of symptoms in childhood to cardiac death in the third decade of life. The data presented in this report provide first evidence that a mutation in a sarcomeric protein can cause noncompaction of the ventricular myocardium. 相似文献
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135.
Dingjiang Liu Melanie Cocco Masazumi Matsumura Da Ren Bridget Becker Richard L. Remmele Jr. David N. Brems 《Biomolecular NMR assignments》2007,1(1):93-94
Here we report the NMR resonance assignments for the reduced form of human IgG1 CH3 domain, a 26 kDa dimer in solution (residues 341–447). The assignments have been deposited in the BioMagResBank with a BMRB
accession number of 15204. 相似文献
136.
Melanie A. Murphy Katherine C. Kendall Andrew Robinson Lisette P. Waits 《Conservation Genetics》2007,8(5):1219-1224
To establish longevity of faecal DNA samples under varying summer field conditions, we collected 53 faeces from captive brown
bears (Ursus arctos) on a restricted vegetation diet. Each faeces was divided, and one half was placed on a warm, dry field site while the other
half was placed on a cool, wet field site on Moscow Mountain, Idaho, USA. Temperature, relative humidity, and dew point data
were collected on each site, and faeces were sampled for DNA extraction at <1, 3, 6, 14, 30, 45, and 60 days. Faecal DNA sample
viability was assessed by attempting PCR amplification of a mitochondrial DNA (mtDNA) locus (∼150 bp) and a nuclear DNA (nDNA)
microsatellite locus (180–200 bp). Time in the field, temperature, and dew point impacted mtDNA and nDNA amplification success
with the greatest drop in success rates occurring between 1 and 3 days. In addition, genotyping errors significantly increased
over time at both field sites. Based on these results, we recommend collecting samples at frequent transect intervals and
focusing sampling efforts during drier portions of the year when possible. 相似文献
137.
van Bueren AL Higgins M Wang D Burke RD Boraston AB 《Nature structural & molecular biology》2007,14(1):76-84
The ability of pathogenic bacteria to recognize host glycans is often essential to their virulence. Here we report structure-function studies of previously uncharacterized glycogen-binding modules in the surface-anchored pullulanases from Streptococcus pneumoniae (SpuA) and Streptococcus pyogenes (PulA). Multivalent binding to glycogen leads to a strong interaction with alveolar type II cells in mouse lung tissue. X-ray crystal structures of the binding modules reveal a novel fusion of tandem modules into single, bivalent functional domains. In addition to indicating a structural basis for multivalent attachment, the structure of the SpuA modules in complex with carbohydrate provides insight into the molecular basis for glycogen specificity. This report provides the first evidence that intracellular lung glycogen may be a novel target of pathogenic streptococci and thus provides a rationale for the identification of the streptococcal alpha-glucan-metabolizing machinery as virulence factors. 相似文献
138.
Manton KJ Haupt LM Vengadasalam K Nurcombe V Cool SM 《Journal of molecular histology》2007,38(5):415-424
Summary Understanding the complex mechanisms underlying bone remodeling is crucial to the development of novel therapeutics. Glycosaminoglycans
(GAGs) localised to the extracellular matrix (ECM) of bone are thought to play a key role in mediating aspects of bone development.
The influence of isolated GAGs was studied by utilising in vitro murine calvarial monolayer and organ culture model systems.
Addition of GAG preparations extracted from the cell surface of human osteoblasts at high concentrations (5 μg/ml) resulted
in decreased proliferation of cells and decreased suture width and number of bone lining cells in calvarial sections. When
we investigated potential interactions between the growth factors fibroblast growth factor-2 (FGF2), bone morphogenic protein-2
(BMP2) and transforming growth factor-β1 (TGFβ1) and the isolated cell surface GAGs, differences between the two model systems
emerged. The cell culture system demonstrated a potentiating role for the isolated GAGs in the inhibition of FGF2 and TGFβ1
actions. In contrast, the organ culture system demonstrated an enhanced stimulation of TFGβ1 effects. These results emphasise
the role of the ECM in mediating the interactions between GAGs and growth factors during bone development and suggest the
GAG preparations contain potent inhibitory or stimulatory components able to mediate growth factor activity.
Kerry J. Manton and Larisa M. Haupt—Co-first authors. 相似文献
139.
Alex A. Pollen Aparna Bhaduri Madeline G. Andrews Tomasz J. Nowakowski Olivia S. Meyerson Mohammed A. Mostajo-Radji Elizabeth Di Lullo Beatriz Alvarado Melanie Bedolli Max L. Dougherty Ian T. Fiddes Zev N. Kronenberg Joe Shuga Anne A. Leyrat Jay A. West Marina Bershteyn Craig B. Lowe Bryan J. Pavlovic Arnold R. Kriegstein 《Cell》2019,176(4):743-756.e17