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PubMed2006

(Patho)physiological significance of the serum- and glucocorticoid-inducible kinase isoforms.

The serum- and glucocorticoid-inducible kinase-1 (SGK1) is ubiquitously expressed and under genomic control by cell stress (including cell shrinkage) and hormones (including gluco- and mineralocorticoids). Similar to its isoforms SGK2 and SGK3, SGK1 is activated by insulin and growth factors via phosphatidylinositol 3-kinase and the 3-phosphoinositide-dependent kinase PDK1. SGKs activate ion channels (e.g., ENaC, TRPV5, ROMK, Kv1.3, KCNE1/KCNQ1, GluR1, GluR6), carriers (e.g., NHE3, GLUT1, SGLT1, EAAT1-5), and the Na+-K+-ATPase. They regulate the activity of enzymes (e.g., glycogen synthase kinase-3, ubiquitin ligase Nedd4-2, phosphomannose mutase-2) and transcription factors (e.g., forkhead transcription factor FKHRL1, beta-catenin, nuclear factor kappaB). SGKs participate in the regulation of transport, hormone release, neuroexcitability, cell proliferation, and apoptosis. SGK1 contributes to Na+ retention and K+ elimination of the kidney, mineralocorticoid stimulation of salt appetite, glucocorticoid stimulation of intestinal Na+/H+ exchanger and nutrient transport, insulin-dependent salt sensitivity of blood pressure and salt sensitivity of peripheral glucose uptake, memory consolidation, and cardiac repolarization. A common ( approximately 5% prevalence) SGK1 gene variant is associated with increased blood pressure and body weight. SGK1 may thus contribute to metabolic syndrome. SGK1 may further participate in tumor growth, neurodegeneration, fibrosing disease, and the sequelae of ischemia. SGK3 is required for adequate hair growth and maintenance of intestinal nutrient transport and influences locomotive behavior. In conclusion, the SGKs cover a wide variety of physiological functions and may play an active role in a multitude of pathophysiological conditions. There is little doubt that further targets will be identified that are modulated by the SGK isoforms and that further SGK-dependent in vivo physiological functions and pathophysiological conditions will be defined.

Animals↗

PubMedDate not supplied

Detection of genetic structures at short distances in the Pisa area.

The genetic structure of the population of the urban and suburban area of the town of Pisa in Tuscany in Central Italy was studied in 1,174 adults residing in 4 zones in each of 3 sampling areas, using the phenotype and gene frequencies of 9 red cell enzymes. The area investigated has a surface of about 30 km2. The enzymes were: acid phosphatase (ACP1), adenosine deaminase (ADA), adenylate kinase (AK1), esterase D (ESD), glyoxalase I (GLOI), glutamic-pyruvic transaminase (GPT), 6-phosphogluconate dehydrogenase (6-PGD), phosphogluco-mutase 1 (PGM1), and phosphoglycollate phosphatase (PGP). For the analysis of the distributions of phenotype and gene frequencies, standardised variances, kinship profiles, analysis of correspondences and isonymy were used. It was found that in this area genetic differentiation (possibly due to recent immigration) can be perceived even at short geographic distances, indicated by the significant regression of kinship on distance, especially visible in the ADA and GPT systems.

Acid Phosphatase↗

PubMed1994

Developmental characteristics of trisomy 19 mice.

Trisomy 19 (Ts19), the only murine trisomy compatible with survival beyond birth, allows systematic studies on the effect of an additional chromosome upon postnatal development. In this review, developmental consequences of murine Ts19 are presented. In Ts19 mice, viability is limited to a few weeks postpartum. Body weight is markedly reduced. The occurrence of malformations of the cardiovascular, skeletal and central nervous systems depends on the parental genetic background. In all organ systems examined, development is delayed by 1-2 days. Ts19 hematopoietic cells exhibit the same survival rate in lethally irradiated hosts as controls. In the CNS, morphological and morphometric studies fail to detect cytoarchitectonic abnormalities: the orderly pattern of development is not disturbed in the visual cortex, cerebellum, locus coeruleus (LC), optic nerve and retina; but neurogenesis, gliogenesis, myelination and invasion of blood vessels are each delayed by 1-2 days. In addition, size and cell number of different brain regions are reduced to a variable degree: the telencephalon and the cerebellar vermis are markedly hypoplastic, whereas the LC, the optic nerve and the retina are hardly reduced in size. Choline acetyltransferase activity is selectively reduced in the Ts19 telencephalon, whereas the activity of the marker enzyme of the GABAergic system is decreased in all brain regions examined. In behavioral tests, visual capacities and orientation ability of Ts19 mice develop with a 2-day delay, while motor coordination is more severely retarded; there is no response to auditory stimulation. Fetal Ts19 ovaries show excessive oocyte degeneration. Development of the testes is only disturbed postnatally: differentiation of gonocytes to A spermatogonia and formation of B spermatogonia are severely disrupted, resulting in a striking reduction in germ cell number and a predominance of Sertoli cells. Histopathological changes exhibit marked intra- and interindividual variations. In addition, growth and lumen formation are impaired in the seminiferous tubules. The proliferative capacity of cultured Ts19 cells is not altered. The activities of glutamate oxaloacetate transaminase-1 and phosphoglycerate mutase-1 are increased by 50%, compatible with a gene dosage effect of these two enzymes. Ganglioside composition is altered in the Ts19 liver, but not in the brain, spleen and heart. Two-dimensional protein patterns show both chromosome-specific and chromosome-nonspecific changes, their frequency being far lower than expected from the number of proteins coded on chromosome 19. Possible pathogenetic mechanisms are discussed.

Abnormalities, Multiple↗

PubMed1990

Atrial natriuretic factor as a marker in congestive heart failure.

Cardiac overload is associated with an overexpression of the atrial natriuretic-factor (ANF) gene in experimental models and in man. Sites of ANF gene overexpression are the atria but also the ventricular myocardium. This recruitment phenomenon of the ventricle to synthesise and secrete ANF is directly dependent on the increase in stress-stretch relationship in each cardiocyte. Therefore, the levels of plasma ANF and its second messenger, cyclic glycophosphate mutase in plasma and urine appear as markers of congestive heart failure in animal models and in man. Particularly, plasma ANF has been recognized recently as independent prognostic factor in congestive heart failure.

Atrial Natriuretic Factor↗

PubMed1986

Erythrocyte enzymes in polycythemia vera: a comparison to erythrocyte enzyme activities of patients with iron deficiency anemia.

Fifteen cytoplasmic erythrocyte enzyme activities were determined in patients with polycythemia vera (PV), iron deficiency anemia (IDA), and a group of healthy volunteers. Among the PV patients, the erythrocyte enzyme activities were compared between 2 groups: patients treated solely with phlebotomy and patients treated with phlebotomy, Myleran (busulfan) and/or radioactive phosphorus 32P. Significant reduction in glutathione reductase activity was found in the PV group of patients. This activity was normalized by the addition of flavin adenine dinucleotide. In contrast to previous reports, no other enzyme activity was found to be significantly reduced. The activities of the enzymes known to be age-dependent were significantly elevated in all the groups tested except for phosphofructokinase and 3-phosphoglycerate mutase. The former was not elevated in any of the groups studied, while the latter was elevated only in the group of patients treated with Myleran and/or 32P. It was concluded that glutathione reductase (GR) deficiency is the only acquired enzyme deficiency in our group of PV patients and that radiation and chemotherapy did not induce further reduction in the activities of any of the enzymes tested. The possible involvement of GR deficiency in the etiology of the red cell life span shortening was discussed.

Anemia, Hypochromic↗

PubMed1988

Increase of enzyme activities following the in vitro peroxidation of normal human red blood cells.

Red blood cells (RBCs) from 15 normal human blood samples were incubated with different concentrations of hydrogen peroxide in sodium azide, and the effects of the peroxidation on several glycolytic and nucleotidic enzyme activities were investigated. The release of malonyl dialdehyde (MDA) and methemoglobin formation were used as indicators of RBC peroxidation. The increase of H2O2, final concentration from 0.1 to 5 mmol/l, resulted in a progressive rise of almost all glycolytic enzyme activities, especially those of aldolase (200% of normal at 1 mmol/l), phosphoglycerate kinase (140%), phosphoglycerate mutase (136%), pyruvate kinase (130%) and glutathione peroxidase (130%), and in a decrease of glucose-6-phosphate dehydrogenase (68%) and pyrimidine-5-nucleotidase (23%). The addition of beta-mercaptoethanol to the incubation medium abolished only the effect of 1 mmol/l H2O2 on glucose-6-phosphate dehydrogenase.

Azides↗

PubMed1970

The effects of deoxygenation of adult and fetal hemoglobin on the synthesis of red cell 2,3-diphosphoglycerate and its in vivo consequences.

Patients over 1 month of age with arterial oxygen pressures of less than 60 mm Hg were found to have elevated red cell 2,3-diphosphoglycerate (2,3-DPG) levels and blood with a decreased affinity for oxygen. The increase in 2,3-DPG was proportional to the degree of hypoxemia. In patients under 1 month of age this relationship was not observed. Red cells from adults, but not newborns, showed rapid increases in 2,3-DPG when incubated under nitrogen. Adult, but not fetal, deoxyhemoglobin was shown to facilitate in vitro synthesis of 2,3-DPG by binding this organic phosphate and relieving the product inhibition of 2,3-DPG mutase. Throughout a wide range change in oxygen affinity as measured by the P(50) is linear with respect to the 2,3-DPG concentration; a change of 430 mmumoles of 2,3-DPG/ml of red blood corpuscles (RBC) resulting in a change of the P(50) of 1 mm Hg. It appears that the 2,3-DPG of the adult's red cells responds rapidly to metabolic and environmental influences and in turn effects metabolism and the cellular environment. Many of these effects are not shared by the red cells of the newborn.

Adolescent↗

PubMed1970

Mechanism of action of thyroid hormones on erythrocyte 2,3-diphosphoglyceric acid synthesis.

Normal erythrocytes, when incubated with thyroid hormone, were found to have increased levels of 2,3-diphosphoglyceric acid. In addition, a partially purified enzyme preparation, when incubated with either a 1,3-diphosphoglyceric acid generating system or 1,3-diphosphoglyceric acid directly, showed increased levels of 2,3-diphosphoglyceric acid when exposed to thyroid hormone. The hormonal effect was biphasic and was witnessed after 5 min of incubation. Substitution on the 3 and 5 positions of the basic thyronine molecule was essential for hormonal effect. It appears that thyroid hormone acts by directly stimulating the diphosphoglycerate mutase enzyme. The hormonal effect on 2,3-DPG synthesis may offer a biochemical explanation for the shift in the oxyhemoglobin dissociation curve observed in thyroid disorders.

Adenosine Triphosphate↗

PubMed1984

Altered vitamin B12 metabolism in fibroblasts from a patient with megaloblastic anemia and homocystinuria due to a new defect in methionine biosynthesis.

Cultured fibroblasts from a recently described patient with homocystinuria and megaloblastic anemia of infancy without methylmalonic aciduria were previously shown to have normal cobalamin uptake and a specific decrease in the proportion of intracellular methylcobalamin. As in control cells but unlike in those from patients with combined homocystinuria and methylmalonic aciduria (cobalamin C and cobalamin D), accumulated 57Co-labeled cobalamin was bound in appropriate amounts and proportion to intracellular binders which are known to be the two vitamin B12-dependent enzymes, methionine synthetase and methylmalonyl-CoA mutase. Despite the association of a normal quantity of intracellular cobalamin with methionine synthetase, the proportion of intracellular cobalamin which was methyl-B12 was below normal and in the range observed in cobalamin C and D cells. This methyl-B12 was decreased by exposure of fibroblasts in culture to nitrous oxide as was observed with control cells. Exposure of control fibroblasts during culture, but not of fibroblasts from this patient, to nitrous oxide significantly reduced the holoenzyme activity of methionine synthetase assayed in cell extracts. In addition, although methionine synthetase activity in cell extracts of control and cells from the patient were similar in the presence of standard assay concentrations of thiols, at low thiol concentrations, methionine synthetase activity in extracts of cells from the patient was much lower than in control extracts. Mixing of control patient extracts corrected this decreased activity in excess of that explained by addition of the individual activities added. The defect of this patient appears to be in a reducing system required for methionine synthesis.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗

PubMed2005

Proteomic analysis of corticobasal degeneration: a case study of corticobasal degeneration at the proteome level.

Corticobasal degeneration (CBD) is an adult-onset progressive neurodegenerative disorder. However, its pathogenic mechanisms underlying this disorder remain poorly understood. The authors examined changes of proteome profiles between three nondemented comparison brains and a CBD brain based on two-dimensional gel electrophoresis. Two up-regulated proteins in the CBD brain were identified as protein-L-isoaspartate (D-aspartate) O-methyltransferase and cofilin 1 (non-muscle), and six down-regulated proteins were identified as carbonyl reductase [NADPH] 1, two of peptidyl-prolyl cis-trans isomerase A, ubiquitin carboxyl-terminal hydrolase isozyme L1, phosphoglycerate mutase 1 (brain) and chain A of human peroxiredoxin 5. Subsequently, the possible relevance of these changes was analyzed.

Aged↗

PubMed2005

Estrogen regulation of the rat anterior pituitary gland proteome.

Estrogen is known to affect the regulation of all six of the established anterior pituitary gland (AP) hormones, but little is known of the specifics of its regulation of the AP hormones, their isoforms, and nonhormonal AP proteins. We used difference gel electrophoresis in conjunction with matrix-assisted laser desorption/ionization time-of-flight mass spectrometry and peptide mass fingerprinting to quantify the effects of estrogen on the AP-soluble protein fraction in rats. Two-month-old rats were ovariectomized and used at 6 months of age. They were injected subcutaneously with sesame oil vehicle or 50 mug estradiol valerate in vehicle and studied 48 hrs later, approximately 3 hrs before the time of the anticipated onset of the estrogen-induced surges of gonadotropins in blood. The APs were pooled, and the soluble protein fraction was examined in replicate analyses. After DeCyder software analysis, we identified 26 protein spots that had a 1.5-fold or greater average increase in the experimental group relative to the controls. Nineteen showed a 1.5-fold or greater decrease. Estrogen increased levels of the more acidic isoforms of growth hormone and prolactin and of proteins involved in protein synthesis, folding, and secretion (e.g., eukaryotic translation elongation factor 2, ERp57, ERp29, Hsc70-ps1, calreticulin, coatomer delta subunit, and secretogranin II) and of some metabolic enzymes (e.g., arginosuccinate synthetase, enolase 1, creatine kinase B, phosphoglycerate mutase, malate dehydrogenase, pyruvate kinase, and aldolase A). The majority of the downregulated proteins were involved in RNA or DNA interactions (e.g., five heterogeneous nuclear ribonucleoproteins, DEAD-box proteins 17 and 48, ssDNA binding protein PUR-alpha, PTB-associated splicing factor, and Pigpen protein), but isovaleryl coenzyme A dehydrogenase, mitochondrial aldehyde dehydrogenase, stathmin 1, vinculin, radixin, and secretogranin III were also reduced. Our results indicate that estrogen acts in vivo within 48 hrs to modulate levels of a significant number of AP proteins.

Animals↗

PubMed2026

Programmed cell death and risk of diabetic retinopathy: a Mendelian randomization study.

BACKGROUND: Programmed cell death (PCD) plays an important role in diabetic retinopathy (DR); however, the underlying genetic mechanisms remain unclear. We used Mendelian randomization (MR) to investigate the causal relationships between PCD-related genes and DR. This study aimed to investigate the effects of PCD on the risk of DR by conducting MR analysis. METHODS: Summary statistics from gene expression quantitative trait loci (eQTL) studies (31,684 Europeans) were analyzed. Genetic instrumental variables were selected using cis-eQTL single-nucleotide polymorphisms (SNPs; P < 5 × 10- 8). Summary data-based MR (SMR) was employed to assess causal associations between PCD-related genes and DR, with three additional MR methods used for sensitivity testing. Bayesian colocalization was used to examine the shared regulatory mechanisms between PCD QTLs and DR risk loci. RESULTS: Sensitivity and colocalization analyses revealed six genes that affected DR: cathepsin H (CTSH), NAD(P)H: quinone oxidoreductase 1 (NQO1), tribbles pseudokinase 3 (TRIB3), and phosphoglycerate mutase 5 (PGAM5), which increased DR risk, and iron-responsive element binding protein 2 (IREB2) and tumor necrosis factor (TNF), which exhibited protective effects. Multivariate MR confirmed significant causal effects for CTSH, IREB2, and PGAM5 (p < 0.050). Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis (including 10 STRING-derived genes) revealed that 13 genes were enriched in necroptosis, apoptosis, mitophagy, and TNF signaling pathways in DR. CONCLUSIONS: This MR study supports the causal involvement of PCD in DR and identifies candidate genes (CTSH, IREB2, PGAM5, NQO1, TRIB3, and TNF) for therapeutic targeting or biomarker development in DR prevention or diagnosis.

Humans↗

PubMed1979

Inhibition of the glycine cleavage system by branched-chain amino acid metabolites.

The effects of 18 normally occurring and 11 patalogical metabolites of the branched-chain amino acids on the glycine cleavage system were investigated on intact rat liver mitochondria. It was demonstrated, that 2-oxo-isovaleric acid, 2-methyl-butyric acid, and isobutyric acid significantly inhibited the glycine cleavage system in intact mitochondria. Further studies on the solubilized glycine cleavage system demonstrated that the inhibitory effect was due to 2-methyl-butyryl-CoA (linear noncompetitive inhibition, ki: 0.1--0.15 mM) and isobutyryl-CoA (S-hyperbolic, I-linear noncompetitive inhibition, ki: 0.2--0.3 mM). Both 2-methyl-butyric acid and isobutyric acid exhibited less inhibition (2-methyl-butyric acid: competitive inhibition, ki: 5.5 mM, isobutyric acid: competitive inhibition, ki: 16 mM), while 2-oxo-isovaleric acid was without inhibitory effect, and probably affects intact mitochondria through transformation to isobutyryl-CoA. It is suggested that the inhibitory action of 2-methyl-butyryl-CoA and isobutyryl-CoA may explain the hyperglycinemia seen in propionyl-CoA carboxylase deficiency, methyl-malonyl-CoA mutase deficiency and beta-ketothiolase deficiency.

Amino Acids, Branched-Chain↗

PubMed1991

Accumulation of odd-numbered long-chain fatty acids in fetuses and neonates with inherited disorders of propionate metabolism.

Fetuses affected with propionic acidemia incorporate great amounts of odd-numbered long-chain fatty acids (OLCFA) into their body lipids. This is due to abundant supply with precursor amino acids of propionyl-CoA throughout pregnancy. After birth, the lower provision of precursor amino acids during dietary treatment compared with fetal life results in a decline of propionyl-CoA production and therefore OLCFA synthesis. However, the observed decrease of OLCFA may also partly reflect the recovery from acute ketoacidotic episodes that the patients experienced soon after birth as long as they were undiagnosed. In a patient with vitamin B12-responsive methylmalonic aciduria treated prenatally with large doses of vitamin B12 given to the mother, the cord plasma lipids contained normal amounts of OLCFA. This indicates that prenatal therapy led to an increased flux of propionyl-CoA through the defective methylmalonyl-CoA mutase step. Thus, in addition to the quantification of a decline in methylmalonic acid in maternal urine, OLCFA in cord blood lipids might be a further parameter for evaluating prenatal treatment in patients with vitamin B12-responsive methylmalonic aciduria.

Acyl Coenzyme A↗

PubMed1997

A genetic screen reveals a role for the late G1-specific transcription factor Swi4p in diverse cellular functions including cytokinesis.

The transcription factor Swi4p plays a crucial role in the control of the initiation of the cell cycle in budding yeast. To further understand Swi4p function, we set up a synthetic lethal screen for genes interacting with SWI4. Fourteen conditional mutations which resulted in lethality only in the absence of SWI4 have been isolated. Only two of them were suppressed by ectopic expression of CLN2, indicating that Swi4p is involved in diverse cellular processes in addition to its requirement for CLN1,2 regulation. In most of the mutants a cell cycle phenotype was observed, including defects in G1 progression, budding, the G2/M transition and cytokinesis. In addition, four of the mutations resulted in massive cell lysis at the restrictive temperature, indicating that Swi4p is involved in the maintenance of cell integrity. One of the mutants, rsf1 swi4delta, was characterized in detail and it is defective in cytokinesis at the restrictive temperature. Staining with Calcofluor revealed that the rsf1 swi4delta mutant is impaired in chitin biosynthesis. rsf1 is allelic to the AGM1 gene, coding for N-acetylglucosamine-phosphate mutase, an enzyme involved in the biosynthesis of chitin. A single copy of SWI4 suppressed the cytokinesis defect. The above data suggest that Swi4p has a role in cytokinesis and becomes essential in this process when chitin biosynthesis is compromised. As overexpression or ectopic expression of CLN did not suppress the rsf1 swi4delta mutant phenotype, Swi4p must control some other gene(s) involved in cytokinesis.

Alleles↗

PubMed2003

Analysis of glycolytic enzyme co-localization in Drosophila flight muscle.

In Drosophila flight muscles, glycolytic enzymes are co-localized along sarcomeres at M-lines and Z-discs and co-localization is required for normal flight. We have extended our analysis of this phenomenon to include a set of six glycolytic enzymes that catalyze consecutive reactions along the glycolytic pathway: aldolase, glycerol-3-phosphate dehydrogenase (GPDH), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), triose phosphate isomerase, phosphoglycerate kinase and phosphoglycerol mutase (PGLYM). Each of these enzymes has an identical pattern of localization. In mutants null for GPDH, localization of none of the other enzymes occurs and therefore is interdependent. In optimally fixed preparations of myofibrils, accumulation of the enzymes at M-lines is much greater than at Z-discs. However, localization at M-lines is more labile, as shown by loss of localization when fixation is delayed. We have begun to analyze the protein-protein interaction involved in glycolytic enzyme co-localization using the yeast two-hybrid system. We have identified two pair-wise interactions. One is between GPDH and GAPDH and another is between GPDH and PGLYM.

Animals↗

PubMed2000

An efficient method for production of uridine 5'-diphospho-N-acetylglucosamine.

Uridine 5'-diphospho-N-acetylglucosamine (UDP-GlcNAc) has been synthesized by a yeast-based method from 5'-UMP and glucosamine, in which yeast cells catalyze the conversion of 5'-UMP to 5'-UTP and provide enzymes involved in UDP-GlcNAc synthesis using 5'-UTP and glucosamine as substrates. However, this conventional method is not suitable for practical production of UDP-GlcNAc because of the low yield of the product. We found that the yqgR gene product of Bacillus subtilis, which has been identified as a glucokinase, can catalyze the phosphorylation of N-acetylglucosamine (GlcNAc) to give GlcNAc-6-phosphate, an intermediate of UDP-GlcNAc biosynthesis. The addition of the yqgR gene product to the yeast-based reaction system enabled us to synthesize UDP-GlcNAc using GlcNAc in place of glucosamine. The addition of two enzymes, GlcNAc-phosphate mutase and UDP-GlcNAc pyrophosphorylase, increased the yield of UDP-GlcNAc. Using this novel method, UDP-GlcNAc was produced at an amount of 78 mM from 100 mM 5'-UMP and 100 mM GlcNAc.

Amino Acid Sequence↗

PubMedDate not supplied

Establishment and characterization of a continuous cell line from pupal ovaries of Japanese oak silkworm Antheraea yamamai Guerin-Meneville.

Pupal ovaries of the wild oak silkworm Antheraea yamamai Guerin-Meneville were cultured in MGM-448 (Modified Grace Medium-448) medium containing 10% fetal bovine serum. After the primary culture was set up in 1988, a continuous cell line was obtained in 1991, designated as NISES-Anya-0611 (Anya-0611). The population doubling time was 54 hrs. and 19 min. at 96 passages and 88 hrs. and 29 min. at 387 passages. Spindle-shaped and spherical cells coexisted in the cell group. The cell line karyotype line was typical of lepidopteran cell lines, consisting of numerous small chromosomes. The cell line was distinguished from other lepidopteran cell lines by comparing malic enzyme, phosphoglucose isomerase, phosphoglucose mutase, and isocitric dehydrogenase isozyme patterns. The cell line was highly infected to the Antheraea yamamai nuclear polyhedrosis virus (Anya NPV). The luciferase gene of recombinant Bm NPV (BmNPVP6ETL) was able to express in the cell line, too, so that luciferase recombinant products were able to be detected in the cell body and in supernatant. The Anya NPV clone group was isolated on the cell seat using plaque purification.

Animals↗