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31.
Nucleotide sequence of a chicken vitellogenin gene and derived amino acid sequence of the encoded yolk precursor protein 总被引:7,自引:0,他引:7
F D van het Schip J Samallo J Broos J Ophuis M Mojet M Gruber G AB 《Journal of molecular biology》1987,196(2):245-260
The gene encoding the major vitellogenin from chicken has been completely sequenced and its exon-intron organization has been established. The gene is 20,342 base-pairs long and contains 35 exons with a combined length of 5787 base-pairs. They encode the 1850-amino acid pre-peptide of vitellogenin, which is the precursor of the mature yolk proteins, the serine-rich and heavily phosphorylated phosvitin and the lipovitellin. The 217-amino acid phosvitin polypeptide occupies an internal position (residue 1112 through 1328) within the vitellogenin molecule. The 125,000 and 30,000 Mr lipovitellin polypeptides are encoded by the sequences at the N-terminal and the C-terminal sides of the phosvitin section, respectively. The main features of the gene and protein sequences, and the evolutionary implications, are discussed. 相似文献
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33.
Diercks T AB E Daniels MA de Jong RN Besseling R Kaptein R Folkers GE 《Journal of molecular biology》2008,383(5):1156-1170
The MutS1 protein recognizes unpaired bases and initiates mismatch repair, which are essential for high-fidelity DNA replication. The homologous MutS2 protein does not contribute to mismatch repair, but suppresses homologous recombination. MutS2 lacks the damage-recognition domain of MutS1, but contains an additional C-terminal extension: the small MutS-related (Smr) domain. This domain, which is present in both prokaryotes and eukaryotes, has previously been reported to bind to DNA and to possess nicking endonuclease activity. We determine here the solution structure of the functionally active Smr domain of the Bcl3-binding protein (also known as Nedd4-binding protein 2), a protein with unknown function that lacks other domains present in MutS proteins. The Smr domain adopts a two-layer α-β sandwich fold, which has a structural similarity to the C-terminal domain of IF3, the R3H domain, and the N-terminal domain of DNase I. The most conserved residues are located in three loops that form a contiguous, exposed, and positively charged surface with distinct sequence identity for prokaryotic and eukaryotic Smr domains. NMR titration experiments and DNA binding studies using Bcl3-binding protein-Smr domain mutants suggested that these most conserved loop regions participate in DNA binding to single-stranded/double-stranded DNA junctions. Based on the observed DNA-binding-induced multimerization, the structural similarity with both subdomains of DNase I, and the experimentally identified DNA-binding surface, we propose a model for DNA recognition by the Smr domain. 相似文献
34.
Claire J Greenhill Gareth W Jones Mari A Nowell Zarabeth Newton Ann K Harvey Abdul N Moideen Fraser L Collins Anja C Bloom Rebecca C Coll Avril AB Robertson Matthew A Cooper Marcela Rosas Philip R Taylor Luke A O’Neill Ian R Humphreys Anwen S Williams Simon A Jones 《Arthritis research & therapy》2014,16(4)
Introduction
Activation of the inflammasome has been implicated in the pathology of various autoinflammatory and autoimmune diseases. While the NLRP3 inflammasome has been linked to arthritis progression, little is known about its synovial regulation or contribution to joint histopathology. Regulators of inflammation activation, such as interleukin (IL)-10, may have the potential to limit the inflammasome-driven arthritic disease course and associated structural damage. Hence, we used IL-10-deficient (IL-10KO) mice to assess NLRP3 inflammasome-driven arthritic pathology.Methods
Antigen-induced arthritis (AIA) was established in IL-10KO mice and wild-type controls. Using histological and radiographic approaches together with quantitative real-time PCR of synovial mRNA studies, we explored the regulation of inflammasome components. These were combined with selective blocking agents and ex vivo investigative studies in osteoclast differentiation assays.Results
In AIA, IL-10KO mice display severe disease with increased histological and radiographic joint scores. Here, focal bone erosions were associated with increased tartrate-resistant acid phosphatase (TRAP)-positive cells and a localized expression of IL-1β. When compared to controls, IL-10KO synovium showed increased expression of Il1b, Il33 and NLRP3 inflammasome components. Synovial Nlrp3 and Casp1 expression further correlated with Acp5 (encoding TRAP), while neutralization of IL-10 receptor signaling in control mice caused increased expression of Nlrp3 and Casp1. In ex vivo osteoclast differentiation assays, addition of exogenous IL-10 or selective blockade of the NLRP3 inflammasome inhibited osteoclastogenesis.Conclusions
These data provide a link between IL-10, synovial regulation of the NLRP3 inflammasome and the degree of bone erosions observed in inflammatory arthritis.Electronic supplementary material
The online version of this article (doi:10.1186/s13075-014-0419-y) contains supplementary material, which is available to authorized users. 相似文献35.
Some remarks on animal population dynamics 总被引:5,自引:0,他引:5
MORAN PA 《Biometrics》1950,6(3):250-258
36.
37.
Salvador Casares Eiso AB Henk Eshuis Obdulio Lopez-Mayorga Nico AJ van Nuland Francisco Conejero-Lara 《BMC structural biology》2007,7(1):22
Background
SH3 domains are small protein modules of 60–85 amino acids that bind to short proline-rich sequences with moderate-to-low affinity and specificity. Interactions with SH3 domains play a crucial role in regulation of many cellular processes (some are related to cancer and AIDS) and have thus been interesting targets in drug design. The decapeptide APSYSPPPPP (p41) binds with relatively high affinity to the SH3 domain of the Abl tyrosine kinase (Abl-SH3), while it has a 100 times lower affinity for the α-spectrin SH3 domain (Spc-SH3). 相似文献38.
REBECCA MORAN IAN HARVEY BRIAN MOSS HEIDRUN FEUCHTMAYR KEITH HATTON TOM HEYES DAVID ATKINSON 《Freshwater Biology》2010,55(2):315-325
1. Shallow lakes and their ectothermic inhabitants are particularly vulnerable to the effects of climatic warming. These impacts are likely to depend on nutrient loading, especially if the combination of warming and eutrophication leads to severe hypoxia. 2. To investigate effects of realistic warming and nutrient loading on a fish species with high tolerance of warming and hypoxia, we observed population changes and timing of reproduction of three‐spined sticklebacks in 24 outdoor shallow freshwater ecosystems with combinations of temperature (ambient and ambient +4 °C) and three nutrient treatments over 16 months. 3. Warming reduced stickleback population biomass by 60% (population size by 76%) and nutrient‐addition reduced biomass by about 80% (population size 95%). Nutrients and warming together resulted in extinction of the stickleback populations. These losses were mainly attributed to the increased likelihood of severe hypoxia in heated and nutrient‐addition mesocosms. 4. Warming of nutrient‐rich waters can thus have dire consequences for freshwater ectotherm populations. The loss even of a hardy fish suggests a precarious future for many less tolerant species in such eutrophic systems under current climate change predictions. 相似文献
39.
Theo S Plantinga Jaap Fransen Nozomi Takahashi Rinke Stienstra Piet L van Riel Wim B van den Berg Mihai G Netea Leo AB Joosten 《Arthritis research & therapy》2010,12(1):1-10
Introduction
We have previously demonstrated that ex vivo inhibition of costimulatory molecules on antigen-pulsed dendritic cells (DCs) can be useful for induction of antigen-specific immune deviation and suppression of autoimmune arthritis in the collagen induced arthritis (CIA) model. The current study evaluated a practical method of immune modulation through temporary systemic inhibition of the costimulatory molecule CD40.Methods
Mice with collagen II (CII)-induced arthritis (CIA) were administered siRNA targeting the CD40 molecule. Therapeutic effects were evaluated by clinical symptoms, histopathology, Ag-specific T cell and B cell immune responses.Results
Systemic administration of CD40-targeting siRNA can inhibit antigen-specific T cell response to collagen II, as well as prevent pathogenesis of disease in both a pre- and post-immunization manner in the CIA model. Disease amelioration was associated with suppression of Th1 cytokines, attenuation of antibody production, and upregulation of T regulatory cells.Conclusions
These studies support the feasibility of transient gene silencing at a systemic level as a mechanism of resetting autoreactive immunity. 相似文献40.
Masakazu Kobayashi Eiso AB Alexander M. J. J. Bonvin Gregg Siegal 《The Journal of biological chemistry》2010,285(13):10087-10097
BRCA1 C-terminal domain (BRCT)-containing proteins are found widely throughout the animal and bacteria kingdoms where they are exclusively involved in cell cycle regulation and DNA metabolism. Whereas most BRCT domains are involved in protein-protein interactions, a small subset has bona fide DNA binding activity. Here, we present the solution structure of the BRCT region of the large subunit of replication factor C bound to DNA and a model of the structure-specific complex with 5′-phosphorylated double-stranded DNA. The replication factor C BRCT domain possesses a large basic patch on one face, which includes residues that are structurally conserved and ligate the phosphate in phosphopeptide binding BRCT domains. An extra α-helix at the N terminus, which is required for DNA binding, inserts into the major groove and makes extensive contacts to the DNA backbone. The model of the protein-DNA complex suggests 5′-phosphate recognition by the BRCT domains of bacterial NAD+-dependent ligases and a nonclamp loading role for the replication factor C complex in DNA transactions. 相似文献