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  • Articles  (271)
  • Hindawi  (271)
  • American Meteorological Society
  • Blackwell Publishing Ltd
  • Copernicus
  • Elsevier
  • Institute of Electrical and Electronics Engineers
  • Institute of Physics
  • Molecular Diversity Preservation International
  • Springer Nature
  • Springer Science + Business Media
  • 2020-2022  (27)
  • 2010-2014  (244)
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  • 1960-1964
  • 2020  (27)
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  • Biochemistry Research International  (149)
  • 111724
  • Chemistry and Pharmacology  (271)
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  • Articles  (271)
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  • Hindawi  (271)
  • American Meteorological Society
  • Blackwell Publishing Ltd
  • Copernicus
  • Elsevier
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  • 2020-2022  (27)
  • 2010-2014  (244)
  • 1985-1989
  • 1960-1964
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  • Chemistry and Pharmacology  (271)
  • Law
  • Natural Sciences in General
  • Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition
  • Architecture, Civil Engineering, Surveying
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  • 1
    Publication Date: 2020-07-06
    Description: Aim. Adult growth hormone deficiency (AGHD) is associated with an increased risk of fractures. The interactions between various body composition and bone are known to be complex in nature. However, very few studies have examined this crosstalk in AGHD. In this study, we sought to investigate the relationship between various parameters of body composition and bone mineral density (BMD) as well as determine the role of visceral fat in determining the bone mass in patients with AGHD. Methods. We conducted a cross-sectional study on 57 patients with AGHD. Anthropometry, biochemistry, and analysis of body composition and BMD were performed according to standard protocols. Male and female patients were classified into those with osteoporosis and those without osteoporosis (normal subjects and patients with osteopenia). Further, we analyzed the correlation between the BMD and measurements obtained for various body composition parameters in male and female AGHD patients. Results. Our findings indicated that among female AGHD patients, those with osteoporosis had a significantly higher levels of fat mass (FM) and visceral adipose tissue mass (VATM) (both, P
    Print ISSN: 2090-2247
    Electronic ISSN: 2090-2255
    Topics: Biology , Chemistry and Pharmacology
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  • 2
    Publication Date: 2013-09-09
    Description: A quantitative structure-activity relationship (QSAR) and molecular docking study has been performed on a series of heteroaryl- and heterocyclyl-substituted imidazo[1,2-a]pyridine derivatives acting as acid pump antagonists in order to have a better understanding of the mechanism of H+/K+-ATPase inhibition. The QSAR study shows a significant correlation of activity with Global Topological Charge Indices (GTCI) of the compounds and the hydrophobic constant of some substituents, indicating that the charge transfer within the molecule and the hydrophobic property of some substituents will be the controlling factor of the activity of these compounds and that there can be dispersion interaction between the molecules and the receptor, where some substituents may have hydrophobic interaction, too. Based on this correlation some new compounds with higher potency have been predicted and their docking study has been performed to see if they can have better interaction with the receptor. The ADME properties of these predicted compounds have also been reported that follow Lipinski’s rule of five.
    Topics: Biology , Chemistry and Pharmacology
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  • 3
    Publication Date: 2013-09-19
    Description: In this theoretical study, the role of the side chain moiety of C-terminal residue in influencing the structural and molecular properties of dipeptides is analyzed by considering a series of seven dipeptides. The C-terminal positions of the dipeptides are varied with seven different amino acid residues, namely. Val, Leu, Asp, Ser, Gln, His, and Pyl while their N-terminal positions are kept constant with Sec residues. Full geometry optimization and vibrational frequency calculations are carried out at B3LYP/6-311++G(d,p) level in gas and aqueous phase. The stereo-electronic effects of the side chain moieties of C-terminal residues are found to influence the values of and dihedrals, planarity of the peptide planes, and geometry around the C7  -carbon atoms of the dipeptides. The gas phase intramolecular H-bond combinations of the dipeptides are similar to those in aqueous phase. The theoretical vibrational spectra of the dipeptides reflect the nature of intramolecular H-bonds existing in the dipeptide structures. Solvation effects of aqueous environment are evident on the geometrical parameters related to the amide planes, dipole moments, HOMOLUMO energy gaps as well as thermodynamic stability of the dipeptides.
    Topics: Biology , Chemistry and Pharmacology
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  • 4
    Publication Date: 2013-09-27
    Description: Introduction. Asymmetric dimethylarginine (ADMA) is a nonselective nitric oxide (NO) synthase inhibitor associated with cardiovascular and metabolic disorders. ADMA plays an important role in the regulation of vascular tone by acting as an endogenous inhibitor of NO synthesis. Objectives. This study aimed to investigate ADMA with respect to diabetes and its clinical relevance as an independent predictor of CAD (Coronary Artery Disease). Methodology. The present case control study includes two hundred and forty patients selected randomly. Serum ADMA was analyzed by using enzyme immunoassay for the quantitative determination of endogenous ADMA, and serum nitric oxide was estimated by the method of Cortes. Results. Elevated NO level levels was a strong predictor and significantly (: 9.86, ) associated with occurrence of CAD. Increased ADMA level was found to be another strong predictor and associated significantly (: 8.02, ) with CAD. On intra group analysis, the relationship between ADMA and NO in diseased group, is significant negative correlation (). (0.001) was found between ADMA and NO. Conclusion. ADMA level was found to be one of the strong predictors for CAD. ADMA is an emerging independent risk marker for future CVD (cardiovascular disease) events.
    Topics: Biology , Chemistry and Pharmacology
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  • 5
    Publication Date: 2012-12-10
    Description: Background. SOCS proteins are known to negatively regulate insulin signaling by inhibiting insulin receptor substrate-1 (IRS1). IRS1 has been reported to be a substrate for ubiquitin-dependent proteasomal degradation. Given that SOCS proteins can function as substrate receptor subunits of Cullin-5 E3 ubiquitin ligases, we examined whether Cullin-5 dependent ubiquitination is involved in the regulation of basal IRS1 protein stability and signal-induced IRS1 degradation. Findings. Our results indicate that basal IRS1 stability varies between cell types. However, the Cullin-5 E3 ligase does not play a major role in mediating IRS1 ubiquitination under basal conditions. Protein kinase C activation triggered pronounced IRS1 destabilization. However, this effect was also independent of the function of Cullin-5 E3 ubiquitin ligases. Conclusions. In conclusion, SOCS proteins do not exert a negative regulatory effect on IRS1 by functioning as substrate receptors for Cullin-5-based E3 ubiquitin ligases both under basal conditions and when IRS1 degradation is induced by protein kinase C activation.
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  • 6
    Publication Date: 2013-03-07
    Topics: Biology , Chemistry and Pharmacology
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  • 7
    Publication Date: 2013-03-07
    Topics: Biology , Chemistry and Pharmacology
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  • 8
    Publication Date: 2013-03-07
    Description: Protein homeostasis, proteostasis, is essential to understand cell function. Protein degradation is a crucial component of the proteostatic mechanisms of the cell. Experiments on protein degradation are nowadays present in many investigations in the field of molecular and cell biology. In the present paper, we focus on the different experimental approaches to study protein degradation and present a critical appraisal of the results derived from steady-state and kinetic experiments using detection of unlabelled and labelled protein methodologies with a proteostatic perspective. This perspective allows pinpointing the limitations in interpretation of results and the need of further experiments and/or controls to establish “definitive evidence” for the role of protein degradation in the proteostasis of a given protein or the entire proteome. We also provide a spreadsheet for simple calculations of mRNA and protein decays for mimicking different experimental conditions and a checklist for the analysis of experiments dealing with protein degradation studies that may be useful for researchers interested in the area of protein turnover.
    Topics: Biology , Chemistry and Pharmacology
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  • 9
    Publication Date: 2013-03-07
    Description: Previous studies of cardiomyopathy-related mutations in cardiac troponin C (cTnC)—L29Q and G159D—have shown diverse findings. The link between such mutant effects and their divergent impact on cardiac phenotypes has remained elusive due to lack of studies on contractile dynamics. We hypothesized that a cTnC mutant-induced change in the thin filament will affect global myofilament mechanodynamics because of the interactions of thin filament kinetics with both Ca2+ binding and crossbridge (XB) cycling kinetics. We measured pCa-tension relationship and contractile dynamics in detergent-skinned rat cardiac papillary muscle fibers reconstituted with the recombinant wild-type rat cTnC (cTnCWT), cTnCL29Q, and cTnCG159D mutants. cTnCL29Q fibers demonstrated a significant decrease in Ca2+ sensitivity, but cTnCG159D fibers did not. Both mutants had no effect on Ca2+-activated maximal tension. The rate of XB recruitment dynamics increased in cTnCL29Q (26%) and cTnCG159D (25%) fibers. The rate of XB distortion dynamics increased in cTnCG159D fibers (15%). Thus, the cTnCL29Q mutant modulates the equilibrium between the non-cycling and cycling pool of XB by affecting the on/off kinetics of the regulatory units (Tropomyosin-Troponin); whereas, the cTnCG159D mutant increases XB cycling rate. Different effects on contractile dynamics may offer clue regarding how cTnCL29Q and cTnCG159D cause divergent effects on cardiac phenotypes.
    Topics: Biology , Chemistry and Pharmacology
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  • 10
    Publication Date: 2013-03-07
    Description: In metazoans, proteins of the arrestin family are key players of G-protein-coupled receptors (GPCRS) signaling and trafficking. Following stimulation, activated receptors are phosphorylated, thus allowing the binding of arrestins and hence an “arrest” of receptor signaling. Arrestins act by uncoupling receptors from G proteins and contribute to the recruitment of endocytic proteins, such as clathrin, to direct receptor trafficking into the endocytic pathway. Arrestins also serve as adaptor proteins by promoting the recruitment of ubiquitin ligases and participate in the agonist-induced ubiquitylation of receptors, known to have impact on their subcellular localization and stability. Recently, the arrestin family has expanded following the discovery of arrestin-related proteins in other eukaryotes such as yeasts or fungi. Surprisingly, most of these proteins are also involved in the ubiquitylation and endocytosis of plasma membrane proteins, thus suggesting that the role of arrestins as ubiquitin ligase adaptors is at the core of these proteins' functions. Importantly, arrestins are themselves ubiquitylated, and this modification is crucial for their function. In this paper, we discuss recent data on the intricate connections between arrestins and the ubiquitin pathway in the control of endocytosis.
    Topics: Biology , Chemistry and Pharmacology
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