11 research outputs found
Isotype-specific activation of cystic fibrosis transmembrane conductance regulator-chloride channels by cGMP-dependent protein kinase II
Type II cGMP-dependent protein kinase (cGKII) isolated from pig intestinal
brush borders and type I alpha cGK (cGKI) purified from bovine lung were
compared for their ability to activate the cystic fibrosis transmembrane
conductance regulator (CFTR)-Cl- channel in excised, inside-out membrane
patches from NIH-3T3 fibroblasts and from a rat intestinal cell line
(IEC-CF7) stably expressing recombinant CFTR. In both cell models, in the
presence of cGMP and ATP, cGKII was found to mimic the effect of the
catalytic subunit of cAMP-dependent protein kinase (cAK) on opening
CFTR-Cl-channels, albeit with different kinetics (2-3-min lag time,
reduced rate of activation). By contrast, cGKI or a monomeric cGKI
catalytic fragment was incapable of opening CFTR-Cl- channels and also
failed to potentiate cGKII activation of the channels. The cAK activation
but not the cGKII activation was blocked by a cAK inhibitor peptide. The
slow activation by cGKII could not be ascribed to counteracting protein
phosphatases, since neither calyculin A, a potent inhibitor of phosphatase
1 and 2A, nor ATP gamma S (adenosine 5'-O-(thiotriphosphate)), producing
stable thiophosphorylation, was able to enhance the activation kinetics.
Channels preactivated by cGKII closed instantaneously upon removal of ATP
and kinase but reopened in the presence of ATP alone. Paradoxically,
immunoprecipitated CFTR or CF-2, a cloned R domain fragment of CFTR (amino
acids 645-835) could be phosphorylated to a similar extent with only minor
kinetic differences by both isotypes of cGK. Phosphopeptide maps of CF-2
and CFTR, however, revealed very subtle differences in site-specificity
between the cGK isoforms. These results indicate that cGKII, in contrast
to cGKI alpha, is a potential activator of chloride transport in
CFTR-expressing cell types
How Rural Physicians Compare on Cost and Quality Measures for Medicaid Ambulatory Care Episodes
High speed double torsion tests on tough polymers. II: Nonlinear elastic dynamic analysis
Interpretation of gravity and magnetic anomalies at Lake Rotomahana: Geological and hydrothermal implications
Hiperidricidade: uma desordem metabólica Hyperhydricity: a metabolic disorder
A hiperidricidade, anteriormente chamada vitrificação, é considerada uma desordem fisiológica, bioquímica e morfológica decorrente do acúmulo anormal de água no interior das células e tecidos. As plantas cultivadas in vitro estão, indubitavelmente, sob contínua condição de estresse, os quais resultam em alterações metabólicas características do estresse oxidativo. Anatomicamente, plantas ou brotos afetados frequentemente apresentam-se inchados, com coloração verde claro, folhas translúcidas e com aparência de vidro, baixa relação número de células/área celular e hipolignificação. Alterações fisiológicas que ocorrem nas principais vias metabólicas, incluindo fotossíntese, respiração e transpiração, resultam em redução de eficiência dessas vias metabólicas. Os distúrbios morfológicos, fisiológicos e bioquímicos são desencadeados por fatores físicos, relacionados ao ambiente dos recipientes de cultivo e consistência do meio de cultura ou por fatores químicos como os componentes do meio de cultura, em especial dos reguladores de crescimento em altas concentrações. A hiperidricidade ocorre em vários níveis de severidade, chegando a resultar na perda irreversível da capacidade morfogênica e o estabelecimento de um estado neoplásico das células, no entanto, na maioria dos casos, a hiperidricidade é considerada reversível. Esta revisão foca o conhecimento atual sobre o fenômeno da hiperidricidade abordando aspectos morfológicos, fisiológicos, bioquímicos e a reversibilidade do processo.<br>The hyperhydricity, formerly called vitrification, is considered a physiological, biochemistry and morfologic disorder due to abnormal accumulation of water inside the cells and tissues. Plants grown in vitro are undoubtedly under continuous stress condition which results in metabolic changes characteristic of oxidative stress. Anatomically plants or shoots affected often become swollen, with pale green, translucent sheets, glass-like, low relative number of cells / cell area and hipolignification. Physiological changes occur in major metabolic pathways including photosynthesis, respiration and transpiration resulting in reduced efficiency of these metabolic pathways. Morphological, physiological and biochemical disorders are triggered by physical factors related to the environment of cultivation vessels and consistency of the culture medium or by chemical factors such as culture medium components, especially the growth regulators in high concentrations. The hyperhydricity occurs at various levels of severity, reaching result in irreversible loss of morphogenic capacity and the establishment of a state of neoplastic cells, however, in most cases hyperhydricity is considered reversible. This review focuses on the current knowledge about the phenomenon of hyperhydricity addressing morphological, physiological, biochemical, and reversibility of the process