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:2.7.10.2 (focal adhesion kinase)
44,029 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mitochondria, besides playing a central role in energy metabolism within the cell, are involved in a cohort of other processes like cellular differentiation and apoptosis. Investigations during recent few years have shown that protein kinases, including PKA, PKB/Akt, PKC, Raf-1, p38 MAPK, JNK, ERK1/2, Src, Fyn and Csk, may directly interact with mitochondrial proteins. Their role mainly concentrates at phosphorylation of pro- and anti-apoptotic proteins (Bad, Bax, Bcl-2, Bcl-xL), phosphorylation/modification of electron transport chain proteins (complex I, COIV), MPTP forming proteins VDAC and ANT, proteins of mitochondrial ATP-sensitive potassium channel (mitoK(ATP)) and phospholipid scramblase 3 (PLSCR3). Many experimental data showed the presence of protein kinases in the outer and inner mitochondrial membranes as well as in the mitochondrial matrix during in vitro cell stimulations, in neurodegenerative diseases and in in vivo ischaemia heart preconditioning. These data show that translocation of protein kinases to mitochondria plays an important role especially during ischaemia/reperfusion in brain and heart.
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PMID:[Protein kinases in mitochondria]. 1880 32

The optimum conditions for drying primary-standard or SRM grade potassium dichromate have been further examined, and it has been established that if organic impurities are present in the material the drying temperature should not exceed 200. At higher temperatures the organic matter is decomposed oxidatively by the dichromate, with a resultant error when the dichromate is used for standardization purposes.
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PMID:Annotation: Drying conditions for potassium dichromate. 1896 39

The stability constants of the complexes of glycinate ion with copper(II), nickel(II) and hydrogen(I) and of nitrilotriacetate ion with calcium(II) and hydrogen(I) and the ionic product of water (K(w)) were determined potentiometrically. The measurements were carried out at 25.0 degrees C in four different ionic strengths up to I (= I(c)) = 2.50 and two different ionic media (KNO(3) and (CH(3))(4)NNO(3)). Extrapolation of equilibrium constants to zero ionic strength and ionic strength corrections to equilibrium constants were carried out with the data obtained from both media using the TEC (thermodynamic equilibrium constant) equation and computer program. The constants of the potassium complexes with nitrilotriacetic acid at low ionic strength are also given. Successful attempts to predict equilibrium constants for other ionic media using TEC parameters and the procedure of the specific ion-interaction theory (SIT) are given. The variations of equilibrium constants with the ionic strengths and ionic media are demonstrated.
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PMID:Extrapolation of molar equilibrium constants to zero ionic strength and parameters dependent on it. Copper(II), nickel(II), hydrogen(I) complexes with glycinate ion and calcium(II), hydrogen(I) complexes with nitrilotriacetate ion. 1896 30

Several procedures for the determination of Ca, Mg and Sr in soils have been compared on the basis of the accuracy of analysis of two NIST reference materials (Montana Soils SRM 2710 and SRM 2711). Samples were dissolved in a mixture of hydrofluoric and nitric acids in sealed vessels in a microwave oven and in teflon beakers on a hot plate. The digests obtained from both dissolution methods were evaporated to dryness in an attempt to remove silicon. Boric acid was added to prevent the precipitation of the lanthanum releasing agent (as lanthanum fluoride) and potassium was added as an ionization buffer. Determinations were made by flame atomic absorption spectrometry with both the nitrous oxide-acetylene flame and the air-acetylene flame, with calibration either by standard additions or against external standards matrix matched with respect to nitric acid, boric acid, lanthanum and potassium. The silicon remaining in the solution was also determined by external calibration. A single-line flow injection manifold was used to overcome any problems due to the presence of high dissolved solids. A volume of 300 mul was injected into a water carrier stream flowing at 8 ml min(-1). To determine Ca in the air-acetylene flame, it was necessary to remove silicon. Magnesium was determined in either flame without complete removal of the silicon, however, for the determination of Sr, it was necessary to remove the silicon and use the nitrous oxide-acetylene flame. The indicative value for Sr in SRM 2710 was too low: the value determined was 360+/-30 mug g(-1).
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PMID:Determination of calcium, magnesium and strontium in soils by flow injection flame atomic absorption spectrometry. 1896 85

Total mercury in biological samples was determined by flow injection (FI) cold vapour atomic absorption spectrometry (CVAAS) following tissue solubilization with formic acid. A mixture of potassium bromide and potassium bromate was used to decompose organomercury compounds prior to their reduction with sodium borohydride. A gold amalgam system was used to achieve lower detection limits when required. National Research Council Canada certified reference materials dogfish liver (DOLT-3), dogfish flesh (DORM-2) and lobster hepatopancreas (TORT-2), as well as oyster tissue (NIST SRM 1566b) and mussel tissue (NIST SRM 2976) were used to assess the accuracy of the method. The method of standard additions provided the most accurate results. Limit of detection (LOD) for Hg in the solid sample of 0.001 and 0.01mugg(-1) were achieved with and without amalgamation, respectively. The precision of measurement for 1.6ngml(-1) methylmercury was 2.7% using the amalgam system.
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PMID:Determination of total mercury in biological samples using flow injection CVAAS following tissue solubilization in formic acid. 1897 Apr 58

Aldosterone synthesis is primarily regulated by angiotensin II and potassium ions. In addition, endothelial cell-secreted factors have been shown to regulate mineralocorticoid release. We analyzed the pathways that mediate endothelial cell-factor-induced aldosterone release from adrenocortical cells, NCI-H295R using endothelial cell-conditioned medium (ECM). The cAMP antagonist Rp-cAMP caused a 44% decrease in the ECM-induced aldosterone release but inhibition of cAMP-dependent PKA had no effect on aldosterone release. Interestingly, inhibition of cAMP-regulated guanine nucleotide exchange factor Epac with brefeldin-A decreased the ECM-induced aldosterone release by 45%. Similarly, inhibition of p38 MAP-kinase; PI-3-kinase and PKB significantly reduced the ECM-induced aldosterone release whereas inhibition of ERK1/2 and PKC did not decrease aldosterone release. These results provide evidence for the existence of a cAMP-dependent but PKA-independent pathway in mediating the ECM-induced aldosterone release and the significant influence of more than one signaling mechanism.
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PMID:Endothelial factors mediate aldosterone release via PKA-independent pathways. 1907 32

KCl (40 mM) caused reproducible relaxations in frog esophagus. N(G)-nitro-L-arginine (L-NOARG; 1-100 microM), a steriospecific inhibitor of nitric oxide synthase (NOS), completely inhibited the relaxations induced by KCl but not those induced by vasoactive intestinal polypeptide (VIP) antagonist. The inhibitory effect of L-NOARG was prevented by L-arginine (L-ARG; 0.1-1 mM), the precursor of nitric oxide (NO) biosynthesis, but not by D-arginine (D-ARG; 0.1-0.5 mM), the enantiomer of L-arginine. L-ARG or D-ARG alone did not significantly modify the effect of KCl. The relaxations to KCl were significantly inhibited by omega conotoxin (omega-conotoxin; 0.1 microM), a selective blocker of N-type calcium channels. Propranolol (0.1-1 microM), a nonselective blocker of beta-adrenergic receptors, prazosine (0.01-0.1 microM), a selective blocker of alpha(1)-adrenergic receptors, phentolamine (0.1-1 microM), a nonselective blocker of adrenergic receptors, atropine, a selective blocker of muscarinic cholinergic receptors, and lidocaine (1-10 microM), a blocker of sodium channels, had no effect on KCl-evoked relaxations. Caffeine (500 microM), an intracellular calcium releasing agent, did not significantly modify the effect of KCl. In contrast, ruthenium red (100 microM), a selective blocker of ryanodine receptors (intracellular Ca(2+) channels), significantly inhibited these relaxations. Similarly, potassium channel blockers such as 4-aminopyridine (4-AP; 100 microM) and tetraethylammonium (TEA; 100 microM) caused a significant inhibition on relaxations to KCl. In addition, ouabain (100 microM), a specific blocker of Na(+)-K(+)-ATPase, also caused a significant inhibition on these relaxations. The results suggest that NO, Na(+)-K(+)-ATPase and potassium channels may have a role on relaxations induced by 40 mM KCl in the frog esophagus.
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PMID:Molecular mechanism of KCl-induced relaxation of the esophagus. 1917 Nov 33

The selective catalytic reduction (SCR) of NO(x) with C3H6 was studied in the presence of oxygen. The double wash-coat monolith catalysts for SCR comprised a lower layer of Au (or Pt)/Al2O3 and a upper layer of zeolites. The catalytic performance of the double wash-coated catalyst was remarkably improved to broaden the temperature window. The Au and Pt particles were dispersed uniformly on the monolith with particle sizes range of 3 approximately 5 nm and 5 approximately 10 nm, respectively. The catalyst binders used were colloidal silica, potassium silicate and tetraethyl orthosilicate, and the best catalyst activity was achieved with using colloidal silica as a binder. The zeolites used for the catalyst upper layer were MCM-41, FER, Y5.3-Zeolite and ZSM5, among which the NH4-ZSM5-coated catalyst showed the highest activity. The experimental results confirmed the promising potential of the double wash-coat, monolith catalyst for SCR of NO(x) with C3H6 due to the effective combination of noble metal monolith catalyst with zeolite for the removal of NO(x) by SCR with hydrocarbons.
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PMID:Activity of double wash-coat monolith catalyst with noble metals and zeolites in selective catalytic reduction of NO(x) with C3H6. 1919 44

Large-conductance Ca(2+)-activated potassium channels, located on the inner mitochondrial membrane, have recently been implicated in cytoprotection. Therefore, the primary aim of this study was to determine the role of large-conductance Ca(2+)-activated potassium channels in adenosine A(1) receptor-induced pharmacological preconditioning in the rat embryonic cardiomyoblast-derived cell line H9c2. For pharmacological preconditioning, H9c2 cells were exposed to the adenosine A(1) receptor agonist N(6)-cyclopentyladenosine (100 nM) or the Ca(2+)-activated potassium channel opener NS1619 (10 microM) for 30 min prior to 6 h hypoxia (0.5% O(2)) in glucose-free and serum-free media. Where appropriate cells were treated (15 min) before pharmacological preconditioning with the Ca(2+)-activated potassium channels blockers paxilline (1 microM) or iberiotoxin (100 nM). Cell viability following 6 h hypoxia was assessed by monitoring lactate dehydrogenase (LDH) release and caspase-3 activation. Ca(2+)-activated potassium channel subunit protein expression and cell survival protein kinase (ERK1/2 and PKB/Akt) activation were assessed by Western blotting. The results demonstrate that the adenosine A(1) receptor is functionally expressed in H9c2 cells and when activated protects against hypoxia-induced LDH release and caspase-3 activation. Treatment with paxilline or iberiotoxin attenuated adenosine A(1) receptor and NS1619-induced pharmacological preconditioning. Large-conductance Ca(2+)-activated potassium channel alpha and beta4 protein subunits were detected in mitochondrial fractions isolated from H9c2 cells. NS1619 (10 microM) induced no significant changes in ERK1/2 or PKB phosphorylation. These results have shown for the first time that large-conductance Ca(2+)-activated potassium channels are involved in adenosine A(1) receptor-induced pharmacological preconditioning in a cell model system.
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PMID:Role of large-conductance Ca(2+) -activated potassium channels in adenosine A(1) receptor-mediated pharmacological preconditioning in H9c2 cells. 1961 21

Bone morphogenetic proteins (BMPs) have been implicated in the generation and postnatal differentiation of cerebellar granule cells (CGCs). Here, we examined the eventual role of BMPs on the survival of these neurons. Lack of depolarization causes CGC death by apoptosis in vivo, a phenomenon that is mimicked in vitro by deprivation of high potassium in cultured CGCs. We have found that BMP-6, but not BMP-7, is able to block low potassium-mediated apoptosis in CGCs. The neuroprotective effect of BMP-6 is not accompanied by an increase of Smad translocation to the nucleus, suggesting that the canonical pathway is not involved. By contrast, activation of the MEK/ERK/CREB pathway by BMP-6 is necessary for its neuroprotective effect, which involves inhibition of caspase activity and an increase in Bcl-2 protein levels. Other pathways involved in the regulation of CGC survival, such as the c-Jun terminal kinase and the phosphatidylinositol 3-kinase (PI3K)-Akt/PKB, were not affected by BMP-6. Moreover, failure of BMP-7 to activate the MEK/ERK/CREB pathway could explain its inability to protect CGCs from low potassium-mediated apoptosis. Thus, this study demonstrates that BMP-6 acting through the noncanonical MEK/ERK/CREB pathway plays a crucial role on CGC survival.
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PMID:Bone morphogenetic protein-6 promotes cerebellar granule neurons survival by activation of the MEK/ERK/CREB pathway. 1984 61


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