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101.
Rhodopsin is a prototypical G protein-coupled receptor (GPCR) - a member of the superfamily that shares a similar structural architecture consisting of seven-transmembrane helices and propagates various signals across biological membranes. Rhodopsin is embedded in the lipid bilayer of specialized disk membranes in the outer segments of retinal rod photoreceptor cells where it transmits a light-stimulated signal. Photoactivated rhodopsin then activates a visual signaling cascade through its cognate G protein, transducin or Gt, that results in a neuronal response in the brain. Interestingly, the lipid composition of ROS membranes not only differs from that of the photoreceptor plasma membrane but is critical for visual transduction. Specifically, lipids can modulate structural changes in rhodopsin that occur after photoactivation and influence binding of transducin. Thus, altering the lipid organization of ROS membranes can result in visual dysfunction and blindness. 相似文献
102.
A naturally occurring mutation of the opsin gene (T4R) in dogs affects glycosylation and stability of the G protein-coupled receptor 总被引:1,自引:0,他引:1
Zhu L Jang GF Jastrzebska B Filipek S Pearce-Kelling SE Aguirre GD Stenkamp RE Acland GM Palczewski K 《The Journal of biological chemistry》2004,279(51):53828-53839
Rho (rhodopsin; opsin plus 11-cis-retinal) is a prototypical G protein-coupled receptor responsible for the capture of a photon in retinal photoreceptor cells. A large number of mutations in the opsin gene associated with autosomal dominant retinitis pigmentosa have been identified. The naturally occurring T4R opsin mutation in the English mastiff dog leads to a progressive retinal degeneration that closely resembles human retinitis pigmentosa caused by the T4K mutation in the opsin gene. Using genetic approaches and biochemical assays, we explored the properties of the T4R mutant protein. Employing immunoaffinity-purified Rho from affected RHO(T4R/T4R) dog retina, we found that the mutation abolished glycosylation at Asn(2), whereas glycosylation at Asn(15) was unaffected, and the mutant opsin localized normally to the rod outer segments. Moreover, we found that T4R Rho(*) lost its chromophore faster as measured by the decay of meta-rhodopsin II and that it was less resistant to heat denaturation. Detergent-solubilized T4R opsin regenerated poorly and interacted abnormally with the G protein transducin (G(t)). Structurally, the mutation affected mainly the "plug" at the intradiscal (extracellular) side of Rho, which is possibly responsible for protecting the chromophore from the access of bulk water. The T4R mutation may represent a novel molecular mechanism of degeneration where the unliganded form of the mutant opsin exerts a detrimental effect by losing its structural integrity. 相似文献
103.
Schwarzenbacher R Canaves JM Brinen LS Dai X Deacon AM Elsliger MA Eshaghi S Floyd R Godzik A Grittini C Grzechnik SK Guda C Jaroszewski L Karlak C Klock HE Koesema E Kovarik JS Kreusch A Kuhn P Lesley SA McMullan D McPhillips TM Miller MA Miller MD Morse A Moy K Ouyang J Robb A Rodrigues K Selby TL Spraggon G Stevens RC van den Bedem H Velasquez J Vincent J Wang X West B Wolf G Hodgson KO Wooley J Wilson IA 《Proteins》2003,53(1):142-145
104.
Heine A Canaves JM von Delft F Brinen LS Dai X Deacon AM Elsliger MA Eshaghi S Floyd R Godzik A Grittini C Grzechnik SK Guda C Jaroszewski L Karlak C Klock HE Koesema E Kovarik JS Kreusch A Kuhn P Lesley SA McMullan D McPhillips TM Miller MA Miller MD Morse A Moy K Ouyang J Page R Robb A Rodrigues K Schwarzenbacher R Selby TL Spraggon G Stevens RC van den Bedem H Velasquez J Vincent J Wang X West B Wolf G Hodgson KO Wooley J Wilson IA 《Proteins》2004,56(2):387-391
105.
Schwarzenbacher R Jaroszewski L von Delft F Abdubek P Ambing E Biorac T Brinen LS Canaves JM Cambell J Chiu HJ Dai X Deacon AM DiDonato M Elsliger MA Eshagi S Floyd R Godzik A Grittini C Grzechnik SK Hampton E Karlak C Klock HE Koesema E Kovarik JS Kreusch A Kuhn P Lesley SA Levin I McMullan D McPhillips TM Miller MD Morse A Moy K Ouyang J Page R Quijano K Robb A Spraggon G Stevens RC van den Bedem H Velasquez J Vincent J Wang X West B Wolf G Xu Q Hodgson KO Wooley J Wilson IA 《Proteins》2004,55(3):768-771
106.
Spraggon G Schwarzenbacher R Kreusch A Lee CC Abdubek P Ambing E Biorac T Brinen LS Canaves JM Cambell J Chiu HJ Dai X Deacon AM DiDonato M Elsliger MA Eshagi S Floyd R Godzik A Grittini C Grzechnik SK Hampton E Jaroszewski L Karlak C Klock HE Koesema E Kovarik JS Kuhn P Levin I McMullan D McPhillips TM Miller MD Morse A Moy K Ouyang J Page R Quijano K Robb A Stevens RC van den Bedem H Velasquez J Vincent J von Delft F Wang X West B Wolf G Xu Q Hodgson KO Wooley J Lesley SA Wilson IA 《Proteins》2004,55(4):1078-1081
107.
Gérard Cros Jean-Pierre Gies Dominique Cahard Pascale Cohen Barbara Filipek Jean-Jacques Mongold Jean-Jacques Serrano 《Molecular and cellular biochemistry》1992,109(2):181-183
Evolution of cholinergic response of rat isolated trachea was determined after various durations of diabetes (17, 40, 90, 150 and 210 days). Long-term diabetes was associated with both impairment of contractility and supersensitivity to cholinergic stimulation. However, the mechanism of these alterations remains to be determined, as response to field stimulation was not specifically altered while electron microscopy studies could not detect any significant change in the aspect of nerves, smooth muscle or epithelium. As well, binding studies of lung cholinergic receptors using the antagonist ligand [3H]-quinuclidinyl benzylate and the agonist carbachol did not detect any change in diabetic animals. 相似文献
108.
Thouverey C Malinowska A Balcerzak M Strzelecka-Kiliszek A Buchet R Dadlez M Pikula S 《Journal of Proteomics》2011,74(7):1123-1134
Matrix vesicles (MVs), released by budding from apical microvilli of osteoblasts during bone formation and development, are involved in the initiation of mineralization by promoting the formation of hydroxyapatite in their lumen. To gain additional insights into MV biogenesis and functions, MVs and apical microvilli were co-isolated from mineralizing osteoblast-like Saos-2 cells and their proteomes were characterized using LC-ESI-MS/MS and compared. In total, 282 MV and 451 microvillar proteins were identified. Of those, 262 were common in both preparations, confirming that MVs originate from apical microvilli. The occurrence of vesicular trafficking molecules (e.g. Rab proteins) and of the on-site protein synthetic machinery suggests that cell polarization and apical targeting are required for the incorporation of specific lipids and proteins at the site of MV formation. MV release from microvilli may be driven by actions of actin-severing proteins (gelsolin, cofilin 1) and contractile motor proteins (myosins). In addition to the already known proteins involved in MV-mediated mineralization, new MV residents were detected, such as inorganic pyrophosphatase 1, SLC4A7 sodium bicarbonate cotransporter or sphingomyelin phosphodiesterase 3, providing additional insights into MV functions. 相似文献
109.
Sgt1 was originally identified in yeast as a suppressor of the Skp1 protein. Later, it was found that Sgt1 is present in plant and mammalian organisms and that it binds other ligands such as S100A6, a calcium-binding protein. In this work we show that in HEp-2 cells Sgt1 translocates to the nucleus due to heat shock. We also found that in HEp-2 cells with diminished level of S100A6, due to stable transfection with siRNA against S100A6, such translocation occurred at a much smaller scale in comparison with cells expressing a normal level of S100A6. Moreover, translocation of Sgt1 was observed in HEp-2 cells treated with thapsigargin instead of heat shock. In contrast thapsigargin was ineffective in cells with diminished level of S100A6. Thus, our results suggest that increase in intracellular concentration of Ca2+, transduced by S100A6, is necessary for nuclear translocation of the Sgt1 protein. 相似文献
110.