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931.
Cell fusions are important to fertilization, placentation, development of skeletal muscle and bone, calcium homeostasis and
the immune defense system. Additionally, cell fusions participate in tissue repair and may be important to cancer development
and progression. A large number of factors appear to regulate cell fusions, including receptors and ligands, membrane domain
organizing proteins, proteases, signaling molecules and fusogenic proteins forming alpha-helical bundles that bring membranes
close together. The syncytin family of proteins represent true fusogens and the founding member, syncytin-1, has been documented
to be involved in fusions between placental trophoblasts, between cancer cells and between cancer cells and host cells. We
review the literature with emphasis on the syncytin family and propose that syncytins may represent universal fusogens in
primates and rodents, which work together with a number of other proteins to regulate the cell fusion machinery. 相似文献
932.
Allister EM Pal S Thomson AM Helmerhorst E Mamo JC 《Journal of biomedical science》2004,11(6):789-798
We compared the acute effect of insulin on the human colonic intestinal epithelial cell line CaCo-2 and the transformed human hepatic cell line HepG2. Over 24 h, 100 nM and 10 µM insulin significantly inhibited the secretion of apolipoprotein (apo) B-100 from HepG2 cells to 63 and 49% of control, respectively. Insulin had no effect on the secretion of apoB-48 from CaCo-2 cells. There was no effect of insulin on the cholesterol ester or free cholesterol concentrations in HepG2 or CaCo-2 cells. HepG2 and CaCo-2 cells bound insulin with high affinity, leading to similar stimulation of insulin receptor protein tyrosine kinase activation. Protein kinase C or mitogen-activated protein kinase activity in the presence or absence of insulin was not correlated with apoB-48 production in CaCo-2 cells. Therefore, insulin acutely decreases the secretion of apoB-100 in hepatic HepG2 cells, but does not acutely modulate the production or secretion of apoB-48 from CaCo-2 intestinal cells. 相似文献
933.
Alcántara-Sánchez F Reynaga-Peña CG Salcedo-Hernández R Ruiz-Herrera J 《Antonie van Leeuwenhoek》2004,86(4):301-311
The effects of the Ca2+/H+ exchanger A23187 and the K+/H+ exchanger nigericin on the growth of Neurospora crassa were analyzed. Both ionophores had the same effects on the fungus. They both inhibited growth in liquid media, apical extension
being more affected than protein synthesis. A sudden challenge to either ionophore on solid media rapidly stopped hyphal extension.
Additionally, both ionophores induced profuse mycelium branching and upward hyphal growth. Hyphae growing on nigericin-containing
media also burst at the apex. Both ionophores caused a rapid inhibition in the apically-occurring synthesis of structural
wall polysaccharides, but they did not affect mitochondrial energy conservation. With the use of DiBAC, a membrane-potential
sensitive fluorophore, it was excluded that their effects were due to depletion of the plasma membrane potential. Considering
that both ionophores exchange H+ for different metallic ions, we concluded that their effect was due to dissipation of a proton gradient, which is directly
or indirectly involved in the apical growth of the fungus.
This revised version was published online in June 2006 with corrections to the Cover Date. 相似文献
934.
Background
Insertions and deletions of DNA segments (indels) are together with substitutions the major mutational processes that generate genetic variation. Here we focus on recent DNA insertions and deletions in protein coding regions of the human genome to investigate selective constraints on indels in protein evolution. 相似文献935.
Han Hu Kshitij Khatri Joshua Klein Nancy Leymarie Joseph Zaia 《Glycoconjugate journal》2016,33(3):285-296
Despite the publication of several software tools for analysis of glycopeptide tandem mass spectra, there remains a lack of consensus regarding the most effective and appropriate methods. In part, this reflects problems with applying standard methods for proteomics database searching and false discovery rate calculation. While the analysis of small post-translational modifications (PTMs) may be regarded as an extension of proteomics database searching, glycosylation requires specialized approaches. This is because glycans are large and heterogeneous by nature, causing glycopeptides to exist as multiple glycosylated variants. Thus, the mass of the peptide cannot be calculated directly from that of the intact glycopeptide. In addition, the chemical nature of the glycan strongly influences product ion patterns observed for glycopeptides. As a result, glycopeptidomics requires specialized bioinformatics methods. We summarize the recent progress towards a consensus for effective glycopeptide tandem mass spectrometric analysis. 相似文献
936.
Silin Wu Ye Gu Yuying Huang Tyh-Chai Wong Hailin Ding Tengfei Liu Yu Zhang Xiaobiao Zhang 《Biochemical genetics》2017,55(3):253-267
The microRNAs (miRNAs) are involved in multiple pathological processes among various types of tumors. However, the functions of miRNAs in benign brain tumors are largely unexplored. In order to explore the pathogenesis of the invasiveness in non-functional pituitary adenoma (NFPA), the miRNAs expression profile was analyzed between invasive and non-invasive non-functional pituitary adenoma by miRNAs microarray. Six most significant differentially expressed miRNAs were identified including four upregulated miRNAs hsa-miR-181b-5p, hsa-miR-181d, hsa-miR-191-3p, and hsa-miR-598 and two downregulated miRNAs hsa-miR-3676-5p and hsa-miR-383. The functions and corresponding signaling pathways of differentially expressed miRNAs were investigated by bioinformatics techniques, including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. The result of GO analysis indicates regulation of voltage-gated potassium channel activity, positive regulation of sodium ion transport, positive regulation of GTPase activity, negative regulation of Notch signaling pathway, etc. KEGG pathway reveals a series of biological processes, including prolactin signaling pathway, endocrine and other factor-regulated calcium reabsorption, fatty acid metabolism, neuroactive ligand-receptor interaction, etc. The miRNAs hsa-miR-181a-5p was verified by quantitative real-time PCR, and the expression level was in accordance with the microarray result. Our result can provide the evidence on featured miRNAs which play a prominent role in pituitary adenoma as effective biomarkers and therapeutic targets in the future. 相似文献
937.
Liqian Sun Manman Zhao Aihua Liu Ming Lv Jingbo Zhang Youxiang Li Xinjian Yang Zhongxue Wu 《Cellular and molecular neurobiology》2018,38(2):541-548
Phenotypic modulation of vascular smooth muscle cells (VSMCs) is involved in the pathophysiological processes of the intracranial aneurysms (IAs). Although shear stress has been implicated in the proliferation, migration, and phenotypic conversion of VSMCs, the molecular mechanisms underlying these events are currently unknown. In this study, we investigated whether shear stress(SS)-induced VSMC phenotypic modulation was mediated by autophagy involved in adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR)/Unc-51-like kinase 1 (ULK1) pathway. The results show that shear stress could inhibit the expression of key VSMC contractile genes and induce pro-inflammatory/matrix-remodeling genes levels, contributing to VSMCs phenotypic switching from a contractile to a synthetic phenotype. More importantly, Shear stress also markedly increased the levels of the autophagy marker microtubule-associated protein light chain 3-II (LC3II), Beclin-1, and p62 degradation. The autophagy inhibitor 3-methyladenine (3-MA) significantly blocked shear-induced phenotypic modulation of VSMCs. To further explore the molecular mechanism involved in shear-induced autophagy, we found that shear stress could activate AMPK/mTOR/ULK1 signaling pathway in VSMCs. Compound C, a pharmacological inhibitor of AMPK, significantly reduced the levels of p-AMPK and p-ULK, enhanced p-mTOR level, and finally decreased LC3II and Beclin-1 level, which suggested that activated AMPK/mTOR/ULK1 signaling was related to shear-mediated autophagy. These results indicate that shear stress promotes VSMC phenotypic modulation through the induction of autophagy involved in activating the AMPK/mTOR/ULK1 pathway. 相似文献
938.
The localized surface plasmon resonances of multilayered nanostructures are studied using finite difference time domain simulations and plasmon hybridization method. Concentric metal–dielectric–metal (MDM) structure with metal core and nanoshell separated by a thin dielectric layer exhibits a strong coupling between the core and nanoshell plasmon resonance modes. The coupled resonance mode wavelengths show dependence on the dielectric layer thickness and composition of core and outer layer metal. The aluminum-based MDM structures show lower plasmon wavelength compared with Ag- and Au-based MDM nanostructures. The calculated refractive index sensitivity (RIS) factor is in the order Ag–Air–Ag>Au–Air–Au>Al–Air–Al for monometallic multilayered nanostructures. Bimetallic multilayered nanostructures support strong and tunable plasmon resonance wavelengths as well as high RIS factor of 510 nm/refractive index unit (RIU) and 470 nm/RIU for Al–Air–Au and Ag-Air-Au, respectively. The MDM structures not only exhibit higher index sensitivity but also cover a wide ultraviolet–near-infrared wavelengths, making these structures very promising for index sensing, biomolecule sensing, and surface-enhanced Raman spectroscopy. 相似文献
939.
Preparation of cross-linked carboxymethyl chitosan for repairing sciatic nerve injury in rats 总被引:1,自引:0,他引:1
A successful nerve regeneration process was achieved with nerve repair tubes made up of 1-ethyl-3(3-dimethylaminopropyl) carbodiimide
hydrochloride (EDC) cross-linked carboxymethyl chitosan (CM-chitosan) with improved biodegradability. Chitosan has a very
slow degradation rate, while the EDC cross-linked CM-chitosan tubes degraded to 30% of original weight during 8 weeks of incubation
in lysozyme solution. In vitro cell culture indicated that the CM-chitosan films presented no cytotoxicity to Schwann cells.
From in vivo studies using a 10 mm rat sciatic nerve defect model investigated by histomorphometry analysis, the average diameter
of the fibers and the average thickness of myelin sheath in the CM-chitosan tubes were 3.7 ± 0.33 and 0.33 ± 0.04 μm, respectively,
which demonstrated equivalence to nerve autografts (the current “gold” standard); furthermore, the average fiber density in
the CM-chitosan tubes was 20.5 × 103/mm2, which was similar to that of autografts (21 × 103/mm2) and significantly higher than that of common chitosan tubes (15.3 × 103/mm2). 相似文献
940.
Alessia Carocci Alessia Catalano Maria Stefania Sinicropi Giuseppe Genchi 《Biometals》2018,31(5):715-735
Many evidences indicate that oxidative stress plays a significant role in a variety of human disease states, including neurodegenerative diseases. Iron is an essential metal for almost all living organisms due to its involvement in a large number of iron-containing proteins and enzymes, though it could be also toxic. Actually, free iron excess generates oxidative stress, particularly in brain, where anti-oxidative defences are relatively low. Its accumulation in specific regions is associated with pathogenesis in a variety of neurodegenerative diseases (i.e., Parkinson’s disease, Alzheimer’s disease, Huntington’s chorea, Amyotrophic Lateral Sclerosis and Neurodegeneration with Brain Iron Accumulation). Anyway, the extent of toxicity is dictated, in part, by the localization of the iron complex within the cell (cytosolic, lysosomal and mitochondrial), its biochemical form, i.e., ferritin or hemosiderin, as well as the ability of the cell to prevent the generation and propagation of free radical by the wide range of antioxidants and cytoprotective enzymes in the cell. Particularly, ferrous iron can act as a catalyst in the Fenton reaction that potentiates oxygen toxicity by generating a wide range of free radical species, including hydroxyl radicals (·OH). The observation that patients with neurodegenerative diseases show a dramatic increase in their brain iron content, correlated with the production of reactive oxigen species in these areas of the brain, conceivably suggests that disturbances in brain iron homeostasis may contribute to the pathogenesis of these disorders. The aim of this review is to describe the chemical features of iron in human beings and iron induced toxicity in neurodegenerative diseases. Furthermore, the attention is focused on metal chelating drugs therapeutic strategies. 相似文献