Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four renal cell lines were derived from glomeruli, proximal, distal, and cortical collecting tubules microdissected from the kidneys of transgenic mice carrying the temperature-sensitive mutant of the simian virus 40 large T antigen under the control of the vimentin promoter. All four cell lines contained large T antigen in their nuclei, grew rapidly, and contained vimentin filaments when grown in serum-enriched medium at the permissive temperature of 33 degrees C. The glomerular cell line formed multiple layers of cells and contained smooth muscle actin and desmin filaments, features of mesangial cells. The three tubule cell lines formed monolayers of polarized cuboid cells separated by tight junctions and having a patchy distribution of cytokeratins K8-K18. A shift from 33 degrees C to the restrictive temperature (39.5 degrees C) stopped cell growth in all cell lines and caused profound changes in the content of intermediate filaments. Vimentin was still present in mesangial-like cells, but the proximal, distal, and collecting tubule cells contained uniform networks of cytokeratins K8-K18 and desmoplakin I and II around the cell peripheries. Potassium transport, mediated by Na+-K+ ATPase pumps and specific cAMP hormonal sensitivities, significantly increased in proximal, distal, and collecting tubule cells when shifted from 33 degrees C to 39.5 degrees C. Thus, the temperature-dependent inactivation of large T antigen, responsible for the arrest of cell growth, did not affect the phenotype of mesangial-like glomerular cells but induced some changes in the expression of intermediate filaments and restored, at least partially, the main parental cell-specific functions in proximal, distal, and collecting tubule cultured cells.
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PMID:Relationships between intermediate filaments and cell-specific functions in renal cell lines derived from transgenic mice harboring the temperature-sensitive T antigen. 869 37

Calpains are Ca-activated neutral proteases present in all cells together with an endogenous inhibitor, calpastatin. Proposed substrates are; cytoskeletal proteins like microtubules and actin, protein kinases such as PKC and membrane-bound enzymes like Ca-ATPase and the Ca-channel. In lenses from different species calpains have been detected in decreasing amounts from the epithelium to the cortex to the nucleus. Several substrates for calpain in the lens have been demonstrated: crystallins, vimentin, actin, beaded filaments and MP26 among others. Both studies on animal models and capsulorhexis indicate that calpains are mainly involved in cortical cataract.
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PMID:Calpains in the human lens: relations to membranes and possible role in cataract formation. 872 65

Intimal cells play an important role in the biology of the vascular wall. Variability in the metabolic activity of intimal smooth muscle cells (SMC), as well as the differential expression of cellular cytoskeletal proteins depend on factors such as degree of differentiation, aging, atherosclerosis, etc. Myosin ATPase activity and cytoskeletal proteins were studied in the intima of bovine femoral arteries and veins of mature animals. In some arteries the intima was thickened and two distinct layers--inner elastic hyperplastic (EHL) and outer, musculo-elastic (MEL) were observed. ATPase activity was well defined in endothelial cells (EC) as well as in SMC. However, differential enzymatic expression was observed in thickened intimas. SMC in the EHL were ATPase negative, while in the MEL they were ATPase positive. All EC and SMC in the "normal" intimas were vimentin positive, desmin and cytokeratin negative. In vessels with thickened intimas, the EHL showed intensive vimentin positivity; in the MEL desmin immunoreactive SMC were numerous as were as those in the media. Vimentin-positive SMC occupied their innermost part. Differences in the expression of ATPase activity and cytoskeletal proteins is discussed in terms of possible migration of medial SMC and/or morphological modulation observed in vessels with altered vascular walls.
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PMID:Expression of cytoskeletal proteins and ATPase activity in bovine femoral artery and vein intima. 886 55

A method has been developed that allows successful maintenance of secondary cell cultures derived from explants of the cochlear lateral wall of young adult gerbils. The secondary cultures were characterized morphologically with light and transmission electron microscopy and immunocytochemically with protein markers specific to various lateral wall cell types. Structural studies revealed fusiform-shaped cells with a paucity of cytoplasm surrounding the nucleus and slender processes. The cells showed little evidence of intercellular contact even when confluent. The cultures were immunopositive for vimentin, carbonic anhydrase isozyme II, creatine kinase isozyme BB and smooth endoplasmic reticulum Ca-ATPase, but lacked reactivity for cytokeratins and Na,K-ATPase. The results indicate that the cultures are comprised of type I fibrocytes from the spiral ligament. These findings are the first to demonstrate that inner ear spiral ligament cells can be isolated and maintained in secondary culture while retaining many of their in vivo characteristics. Based upon their location and content of ion transport enzymes, type I fibrocytes are thought to be involved in the recycling of potassium from perilymph into the stria vascularis. The establishment of this cell line provides a means to analyze the role of spiral ligament fibrocytes in maintenance of inner ear homeostasis.
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PMID:Characterization and development of an inner ear type I fibrocyte cell culture. 897 Aug 14

Biliary epithelial cells (cholangiocytes) modulate bile fluidity and alkalinity absorbing and/or secreting fluid and electrolytes, particularly HCO3- and Cl-. Mechanisms responsible for transepithelial H+/HCO3- secretion in human cholangiocytes are largely unknown. Human cholangiocytes isolated by enzymatic digestion and immunomagnetic purification from normal liver tissue obtained from reduced grafts used for pediatric liver transplantation were cultured in the presence of human hepatocyte growth factor. Maintenance of cholangiocyte phenotypic features was assessed using markers such as cytokeratin 19, gamma-glutamyltranspeptidase, vimentin, factor VIII-related antigen, desmin, epithelial membrane antigen (EMA), and human epithelial antigen (HEA) 125. Intracellular pH (pHi) transients were measured microfluorimetrically 2'7'-Bis(2-carboxyethyl)-5,6, carboxyfluorescein-acetossimethylester (BCECF). In the absence of HCO3-, pHi recovery from an intracellular acid load (ammonia pre-pulse technique) was Na(+)-dependent and amiloride-inhibitable. No Na(+)-independent recovery was recorded even after stimulation with agents raising intracellular cyclic adenosine monophosphate (cAMP) concentrations. In the presence of HCO3-, recovery from an intracellular acid load required Na+, but was only partly inhibited by amiloride. In these conditions H+ extrusion was inhibited by 4,4-diisothiocyan atostilben-2,2-disulfonic acid (DIDS) and by intracellular Cl- depletion. Acute removal of extracellular Cl induced a pHi alkalinization that was inhibited by DIDS. pHi recovery from an intracellular alkaline load (isohydric CO2 changes) was Cl(-)-dependent and DIDS-inhibitable. Administration of agents raising intracellular cAMP concentrations increased both Na(+)-dependent and Na(+)-independent Cl-/HCO-3 exchange activity. Stimulation of Cl-/HCO3- exchange activity was not prevented by the Cl- channel inhibitor 5'-nitro-2(2)-phenylpropyl-amino-benzoate(NPPB). In conclusion, human cholangiocytes possess two acid extruders (Na+/H+exchanger and Na(+)-dependent Cl-/HCO3- exchange) and an acid loader (Cl-/HCO3- exchange), whereas no evidence was found for cAMP activated H(+)-ATPase. Bicarbonate influx is thus mainly mediated by Na-dependent Cl-/HCO3- exchange, whereas Na+:HCO-3 cotransport is not active in the physiological range of pHi. Stimulation of Na(+)-independent Cl-/HCO3- exchanger by cAMP does not require activation of Cl- conductances. These mechanisms may underlay hormone-regulated biliary HCO3- secretion in the human biliary tree.
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PMID:Na(+)-dependent and -independent Cl-/HCO-3 exchange mediate cellular HCO3- transport in cultured human intrahepatic bile duct cells. 909 7

During the past 10 years, our teams developed long-term primary cultures of ependymal cells derived from ventricular walls of telencephalon and hypothalamus or choroidal cells (modified ependymal cells) derived from plexuses dissected out of fetal or newborn mouse or rat brains. Cultures were established in serum-supplemented or chemically defined media after seeding on serum-, fibronectin-, or collagen-laminin-coated plastic dishes or semipermeable inserts. To identify and characterize cell types growing in our cultures, we used morphological features provided by phase contrast, scanning, and transmission electron microscopy. We used antibodies against intermediate filament proteins (vimentin, glial fibrillary acidic protein, cytokeratin, desmin, neurofilament proteins), actin, myosin, ciliary rootlets, laminin, and fibronectin in single or double immunostaining, and monoclonal antibodies against epitopes of ependymal or endothelial cells, to recognize ventricular wall cell types with immunological criteria. Ciliated or nonciliated ependymal cells in telencephalic cultures, tanycytes and ciliated and nonciliated ependymal cells in hypothalamic cultures always exceeded 75% of the cultured cells under the conditions used. These cells were characterized by their cell shape and epithelial organization, by their apical differentiations observed by scanning and transmission electron microscopy, and by specific markers (e.g., glial fibrillary acidic protein, ciliary rootlet proteins, DARPP 32) detected by immunofluorescence. All these cultured ependymal cell types remarkably resembled in vivo ependymocytes in terms of molecular markers and ultrastructural features. Choroidal cells were also maintained for several weeks in culture, and abundantly expressed markers were detected in both choroidal tissue and culture (Na+-K+-dependent ATPase, DARPP 32, G proteins, ANP receptors). In this review, the culture models we developed (defined in terms of biological material, media, substrates, duration, and subculturing) are also compared with those developed by other investigators during the last 10 years. Focusing on morphological and functional approaches, we have shown that these culture models were suitable to investigate and provide new insights on (1) the gap junctional communication of ependymal, choroidal, and astroglial cells in long-term primary cultures by freeze-fracture or dye transfer of Lucifer Yellow CH after intracellular microinjection; (2) some ionic channels; (3) the hormone receptors to tri-iodothyronine or atrial natriuretic peptides; (4) the regulatory effect of tri-iodothyronine on glutamine synthetase expression; (5) the endocytosis and transcytosis of proteins; and (6) the morphogenetic effects of galactosyl-ceramide. We also discuss new insights provided by recent results reported on in vitro ependymal and choroidal expressions of neuropeptide-processing enzymes and neurosecretory proteins or choroidal expression of transferrin regulated through serotoninergic activation.
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PMID:Ependymal and choroidal cells in culture: characterization and functional differentiation. 957 99

The immunohistochemical study of chamois (Rupicapra rupicapra L.) skin showed that a limited number of available monoclonal and polyclonal antibodies expressed reactivity with skin cell components. These included cytokeratins, vimentin, desmin, neuron-specific enolase and S-100 protein with almost the same distribution pattern as already described in the skin of humans and animals. Antibodies used for labelling skin-associated lymphoid tissues and other cells with the immunologic function in human skin failed to demonstrate these cells in the chamois skin with the exception of LCA and OKT6 antibodies. Epidermal Langerhans cells were reliably demonstrated only by the enzyme histochemical method for adenosine triphosphatase, while the majority of mononuclear cells in dermal infiltrates showed a strong immunoreaction with OKT6 antibody. The histologic and histochemical analysis showed that the dermal infiltrations in infested skin consisted of macrophages, lymphocytes, granulocytes, mastocytes and fibroblasts. The chamois skin affected with sarcoptes mange showed a significant loss of cytokeratins in the epidermis and its derivatives. Particular keratinocytes showing nonspecific staining with several antibodies were also described and discussed in this paper.
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PMID:Immunohistochemical study of normal and mange (S. scabiei var. rupicaprae) infested chamois (Rupicapra rupicapra L.) skin. 965 47

Numerous muscular dystrophies, such as dystrophinopathies, sarcoglycanopathies, and emerino- and laminopathies, are marked by the absence or reduction of mutant transsarcolemmal or nuclear proteins. In addition to these recently identified minus-proteinopathies, there are a growing number of plus-proteinopathies among neuromuscular disorders marked by a surplus or excess of endogenous proteins within muscle fibers of different, i.e., nontranssarcolemmal and nonnuclear types. These proteins are often filamentous; for example, desmin and actin accrue in respective desmin-related myopathies, among which are entities marked by mutant desmin, true desminopathies, and actinopathy, the latter often seen as a subgroup in nemaline myopathies. Desmin-related myopathies consist largely of those marked by desmin-containing inclusions and those characterized by desmin-containing granulofilamentous material. When mutations in the desmin gene can be identified, the mutant desmin is thought to form the major myopathological lesion. Together with desmin, other proteins often accumulate. The spectrum of these proteins is quite diverse and encompasses such proteins as dystrophin, nestin, vimentin, alphaB-crystallin, ubiquitin, amyloid precursor protein, and beta-amyloid epitopes, as well as gelsolin and alpha(1)-antichymotrypsin. Among these associated proteins, one, alphaB-crystallin, has been found mutant in one large family, justifying the term alphaB-crystallinopathy as a separate condition among the desmin-related myopathies. Other proteins accruing with desmin have not yet been identified as mutant in desmin-related myopathies. Mutations in the desmin gene entail missense mutations and small deletions. The formation of mutant actin may lead to aggregates of actin filaments which may or may not be associated with formation of sarcoplasmic and/or intranuclear nemaline bodies. A considerable number of missense mutations in the sarcomeric actin gene ACTA1 have been discovered in patients with nemaline myopathy and also in a few patients without myopathological evidence of nemaline bodies in biopsied skeletal muscle fibres. Apart from alphaB-crystallin, no other proteins coaggregating with actin in actin filament aggregates of actinopathy or the actin mutation type of nemaline myopathy have so far been identified. Two further candidates for protein surplus myopathies are hyaline body myopathy, which is marked by accumulation of granular nonfilamentous material within muscle fibers that is rich in myosin and adenosine triphosphatase activities, and hereditary inclusion body myopathies, which are marked by accumulation of tubulofilaments similar to the helical filaments of Alzheimer neurofibrillary tangles. These tubulofilaments consist of diverse proteins as well, though no mutant protein has yet been discovered. So far, no genes responsible for familial hyaline body and hereditary inclusion body myopathies have been identified. The discovery of mutant proteins, desmin, alphaB-crystallin, and actin, as components of surplus or excess proteins accumulating in muscle fibers in certain neuromuscular conditions is responsible for the recent emergence of this new concept of gene-related protein surplus myopathies.
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PMID:Gene-related protein surplus myopathies. 1100 21

The lateral wall of the dog cochlear duct was investigated by classical staining and immunohistochemistry for NaK/ATPase beta2 isoform, cytokeratins (Cks), vimentin, nestin, and S100A6 during the postnatal cochlear maturation, i.e., from birth to postnatal day 110. The dog stria vascularis was immature at birth. Fine melanin granules were evident in the stria from the second week of life, and melanin concentration increased drastically beyond the first month. The marginal cells were NaK/ATPase- and Ck-positive; intermediate cells were either nestin- and S100A6-positive or vimentin-positive; the basal cells were vimentin-positive; the capillary endothelium showed vimentin and nestin labeling; the cell layer underlying the stria was nestin-positive. The fibrocytes of the spiral ligament and spiral prominence expressed nestin and vimentin. The epithelial cells overlaying the spiral prominence and the external sulcus were Ck-positive, and transiently nestin- and vimentin-positive. Double immunolabeling, for S100A6 and either nestin, vimentin, or NaK/ATPase, and for nestin and vimentin suggested the presence of two distinct intermediate cell types. The results enabled us to differentiate the cell types forming the lateral wall of the dog cochlear duct, and to follow their postnatal maturation. This study may form a basis for future investigations about spontaneous cochleosaccular degeneration in dogs. This species is an important companion animal, and a possible model for the study of comparable diseases in humans.
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PMID:Postnatal maturation of the dog stria vascularis-- an immunohistochemical study. 1249 92

Previous studies have demonstrated that functional interaction between endothelin (ET)-1 and nitric oxide (NO) involves changes in Ca(2+) mobilization and cytoskeleton in human brain microvascular endothelial cells. The focus of this investigation was to examine the possible existence of analogous interplay between these vasoactive substances and elucidate their signal transduction pathways in human brain capillary endothelial cells. The results indicate that ET-1-stimulated Ca(2+) mobilization in these cells is dose-dependently inhibited by NOR-1 (an NO donor). This inhibition was prevented by ODQ (an inhibitor of guanylyl cyclase) or Rp-8-CPT-cGMPS (an inhibitor of protein kinase G). Treatment of endothelial cells with 8-bromo-cGMP reduced ET-1-induced Ca(2+) mobilization in a manner similar to that observed with NOR-1 treatment. In addition, NOR-1 or cGMP reduced Ca(2+) mobilization induced by mastoparan (an activator of G protein), inositol 1,4,5-trisphosphate, or thapsigargin (an inhibitor of Ca(2+)-ATPase). Interestingly, alterations in endothelial cytoskeleton (actin and vimentin) were associated with these effects. The data indicate for the first time that the cGMP-dependent protein kinase colocalizes with actin. These changes were accompanied by altered levels of phosphorylated vasodilator-stimulated phosphoprotein, which were elevated in endothelial cells incubated with NOR-1 and significantly reduced by ODQ or Rp-8-CPT-cGMPS. The findings indicate a potential mechanism by which the functional interrelationship between ET-1 and NO plays a role in regulating capillary tone, microcirculation, and blood-brain barrier function.
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PMID:ET-1- and NO-mediated signal transduction pathway in human brain capillary endothelial cells. 1252 47


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