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Pagina 1 a partire dal 102 risultati
Acidosis-induced protein tyrosine phosphorylation depends on Ca2+ influx via voltage-dependent Ca2+ channels in SHR aorta.
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The contractile response to acidosis in isolated aorta from spontaneously hypertensive rat (SHR) depends upon tyrosine phosphorylation of phosphatidylinositol 3 kinase (PI3-kinase) and Ca2+ influx via voltage-dependent Ca2+ channels (VDCC). In this study, verapamil, a VDCC inhibitor, was shown to
Hypercapnic Acidosis Regulates Mer Tyrosine Kinase Receptor Shedding and Activity.
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The binding of zinc and copper ions to nerve growth factor is differentially affected by pH: implications for cerebral acidosis.
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It has recently been shown that transition metal cations Zn2+ and Cu2+ bind to histidine residues of nerve growth factor (NGF) and other neurotrophins (a family of proteins important for neuronal survival) leading to their inactivation. Experimental data and theoretical considerations indicate that
Effect of acute acidosis on protein and amino acid metabolism in rats.
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OBJECTIVE
Metabolic acidosis is a common finding in critical illness. The aim of the present study was to evaluate acute acidosis as a signal that induces changes in protein metabolism.
METHODS
In the first study, Wistar rats were infused for 6h with HCl or saline resulting in blood pH7.30+/-0.03
Whole-exome sequencing as a diagnostic tool for distal renal tubular acidosis.
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OBJECTIVE
Distal renal tubular acidosis (dRTA) is characterized by metabolic acidosis due to impaired renal acid excretion. The aim of this study was to demonstrate the genetic diagnosis of four children with dRTA through use of whole-exome sequencing.
METHODS
Two unrelated families were selected; a
Acidosis impairs insulin receptor substrate-1-associated phosphoinositide 3-kinase signaling in muscle cells: consequences on proteolysis.
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Chronic acidosis is a stimulus for proteolysis in muscle in vivo, but the mechanism of this response is unknown. We tested the hypothesis that acidosis or TNF-alpha, a cytokine whose production increases in acidosis, regulates proteolysis by inhibiting insulin signaling through phosphoinositide
Prolactin-Stat5 signaling in breast cancer is potently disrupted by acidosis within the tumor microenvironment.
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BACKGROUND
Emerging evidence in estrogen receptor-positive breast cancer supports the notion that prolactin-Stat5 signaling promotes survival and maintenance of differentiated luminal cells, and loss of nuclear tyrosine phosphorylated Stat5 (Nuc-pYStat5) in clinical breast cancer is associated with
Cholestasis in late metabolic acidosis of prematurely born infants.
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Serum concentrations of bile acids and tyrosine were determined in 14 premature infants with late metabolic acidosis and in 13 comparable controls without acidosis (protein intake 2 g/kg X d). At the same time the bile acids and the catalytic activity concentrations of lipase and trypsin were
Acidic stress facilitates tyrosine phosphorylation of HLJ1 to associate with actin cytoskeleton in lung cancer cells.
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Acidosis is a common stress in solid tumours and is also a major determinant of tumour growth, metabolism, and metastasis. During cellular stress, heat shock proteins play an important role in actin cytoskeleton stability. HLJ1, a member of the DnaJ-like heat shock protein 40, has been characterised
Regions of human kidney anion exchanger 1 (kAE1) required for basolateral targeting of kAE1 in polarised kidney cells: mis-targeting explains dominant renal tubular acidosis (dRTA).
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Distal renal tubular acidosis (dRTA) is characterised by defective acid secretion by kidney alpha-intercalated cells. Some dominantly inherited forms of dRTA result from anion exchanger 1 (AE1) mutations. We have developed a stably transfected cell model for the expression of human kidney AE1 (kAE1)
Effects of tyrphostins and genistein on the circulatory failure and organ dysfunction caused by endotoxin in the rat: a possible role for protein tyrosine kinase.
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1 Here we compared the effects of various inhibitors of the activity of protein tyrosine kinase on (i) the expression of the activity of the inducible isoform of nitric oxide (NO) synthase (iNOS) caused by endotoxin (lipopolysaccharide, LPS) in cultured macrophages, (ii) the induction of iNOS and
Effect of acute acid-base disturbances on ErbB1/2 tyrosine phosphorylation in rabbit renal proximal tubules.
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The renal proximal tubule (PT) is a major site for maintaining whole body pH homeostasis and is responsible for reabsorbing ∼80% of filtered HCO3(-), the major plasma buffer, into the blood. The PT adapts its rate of HCO3(-) reabsorption (JHCO3(-)) in response to acute acid-base disturbances. Our
A new form of prolonged transient tyrosinemia presenting with severe metabolic acidosis.
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Yet another form of tyrosinemia is described, in a young baby who developed metabolic acidosis and ceased to grow when weaned from breast milk onto a higher protein formula. Severe tyrosyluria and mild tyrosinemia cleared on a low-protein diet which also corrected the acidosis. However, restoration
Defective kidney anion-exchanger 1 (AE1, Band 3) trafficking in dominant distal renal tubular acidosis (dRTA).
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dRTA (distal renal tubular acidosis) results from the failure of the a-intercalated cells in the distal tubule of the nephron to acidify the urine. A truncated form of AE1 (anion-exchanger 1; Band 3), kAE1 (kidney isoform of AE1), is located in the basolateral membrane of the intercalated cell.
Regulation of apoA1 gene expression with acidosis: requirement for a transcriptional repressor.
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Serum apolipoprotein A(1) (apoA(1)) concentration is inversely correlated with the risk of premature atherosclerosis. Serum apoA(1) concentrations are regulated, in part, at the transcriptional level. ApoA(1) mRNA is synthesized primarily in the liver and small intestine, under the direction of a
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