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PubMed1996

Involvement of different ion channels in osteoblasts' and osteocytes' early responses to mechanical strain.

The involvement of functional ion channels in previously documented early responses of osteocytes and osteoblasts to mechanical strain in bone tissue was investigated in explants of rat ulnae by the use of ion channel blockers. Gadolinium chloride (a blocker of stretch/shear-sensitive cation channels) elevated basal prostaglandin (PG) E2 and prostacyclin (PGI2) release and osteocyte glucose-6-phosphate dehydrogenase (G6PD) activity, but was associated with a reduction in basal nitric oxide (NO) production. Gadolinium abolished loading-related increases in the release of PGI2 and NO and osteocyte G6PD activity. Gadolinium also reduced the loading-related release of PGE2 assumed to originate from osteoblasts and the magnitude of loading-related increases in G6PD activity in these cells. Nifedipine (a blocker of L-type voltage-dependent calcium channels) had no effect on basal levels of prostanoid or NO release, or G6PD activity in osteocytes or osteoblasts, and did not affect loading-related release of PGI2 or increase in osteocyte G6PD. However, nifedipine prevented loading-related increases in PGE2 and NO release and osteoblast G6PD activity. These results are consistent with osteocytes' response to bone loading requiring activatable ion channels sensitive to gadolinium, but not those sensitive to nifedipine. In osteoblasts, the early responses to bone loading appear to be associated with ion channels sensitive to gadolinium and nifedipine; however, the nifedipine-sensitive channels seem to have the dominant effect.

Animals↗
PubMed1996

Resistance of glucose-6-phosphate dehydrogenase deficiency to malaria: effects of fava bean hydroxypyrimidine glucosides on Plasmodium falciparum growth in culture and on the phagocytosis of infected cells.

The balanced polymorphism of glucose-6-phosphate dehydrogenase deficiency (G6PD-) is believed to have evolved through the selective pressure of malarial combined with consumption of fava beans. The implicated fava bean constituents are the hydroxypyrimidine glucosides vicine and convicine, which upon hydrolysis of their beta-O-glucosidic bond, became protein pro-oxidants. In this work we show that the glucosides inhibit the growth of Plasmodium falciparum, increase the hexose-monophosphate shunt activity and the phagocytosis of malaria-infected erythrocytes. These activities are exacerbated in the presence of beta-glucosidase, implicating their pro-oxidant aglycones in the toxic effect, and are more pronounced in infected G6PD- erythrocytes. These results suggest that G6PD- infected erythrocytes are more susceptible to phagocytic cells, and that fava bean pro-oxidants are more efficiently suppressing parasite propagation in G6PD- erythrocytes, either by directly affecting parasite growth, or by means of enhanced phagocytic elimination of infected cells. The present findings could account for the relative resistance of G6PD- bearers to falciparum malaria, and establish a link between dietary habits and malaria in the selection of the G6PD- genotype.

Animals↗
PubMed2001

Neonatal jaundice--traditional Chinese medicine approach.

Herbal treatment of neonatal jaundice (NNJ) has been practiced in China for a long time. Even to-date, a variety of herbal items, including "Yin-chin" (Artemisia), "Huang-qin" (Scutellaria), "Da-huang" (Rheum officinale), "Gan-cao" (Glycyrrhiza), and "Huang-lin" (Coptis chinesis), are still being prescribed to jaundiced infants, often in combination with modern treatment such as phototherapy and exchange transfusion. Their efficacy has, however, not been tested by properly conducted randomised controlled trial. On the other hand, exposure to herbs either before or after birth has been suspected to be a cause of hemolysis and jaundice in the newborns. It is also widely believed in the Chinese community that a number of herbal items are hemolytic agents in infants deficient in the enzyme glucose-6-phosphate dehydrogenase (G6PD). The belief is so deep rooted that each infant detected to have G6PD deficiency by neonatal cord blood screening is given a G6PD deficiency alert card, which states that the child must avoid these herb items for life. In a cohort of 1008 mother-infant pairs, however, we have previously shown that there was no association between maternal herb consumption during pregnancy and the incidence or severity of neonatal hyperbilirubinemia in their offsprings, including those who were deficient in G6PD. A thorough search of medical literature also fails to detect any evidence that any of the herbs stated in the G6PD deficiency alert card causes hemolysis in G6PD-deficient subjects. Thus, there are many misunderstandings and unsubstantiated beliefs about the relationship between herbal medicine and NNJ. Given the potential usefulness of Chinese traditional medicine, which has been practiced for almost 3000 years and is still gaining momentum in the modern days, extensive scientific studies to determine the therapeutic efficacy and potential harmful effects of the various herbal items are warranted.

Drugs, Chinese Herbal↗
PubMed1981

An increase in a circulating inhibitor of Na+,K+-dependent ATPase: a possible link between salt intake and the development of essential hypertension.

1. The plasma's ability to stimulate guinea-pig renal glucose 6-phosphate dehydrogenase (G6PD) in vitro was measured by a cytochemical technique in 23 normotensive subjects and 19 patients with hypertension, all of whom were studied on their normal sodium intake. The ability of plasma to stimulate renal G6PD was significantly (P less than 0.001) increased in the hypertensive patients (mean 195 +/- 52 units/ml) compared with the normotensive subjects (mean 22.2 +/- 5.8 units/ml). In all 42 individuals, there was a significant correlation between diastolic pressure and the ability of plasma to stimulate G6PD (r = 0.69 P less than 0.001). 2. The ability of plasma to stimulate G6PD was greatest in the hypertensive patients with values of plasma renin activity below the normal range. In the normotensive subjects the ability of plasma to stimulate G6PD was significantly greater in the older subjects. 3. As the ability of plasma to stimulate G6PD reflects its ability to inhibit Na+,K+-dependent ATPase, these results suggest that patients with essential hypertension have an increase in a circulating inhibitor of Na+,K+-ATPase. The results support the hypothesis that a rise in a circulating sodium transport inhibitor may, in part, be responsible for the rise in blood pressure in essential hypertension, and may form the link between salt intake, abnormalities of sodium transport and a rise in blood pressure.

Adult↗
PubMed2002

Protein methylation as a marker of aspartate damage in glucose-6-phosphate dehydrogenase-deficient erythrocytes: role of oxidative stress.

The 'Mediterranean' variant of glucose-6-phosphate dehydrogenase (G6PD) deficiency is due to the C563CT point mutation, leading to replacement of Ser with Phe at position 188, resulting in acute haemolysis triggered by oxidants. Previous work has shown increased formation of altered aspartate residues in membrane proteins during cell ageing and in response to oxidative stress in normal erythrocytes. These abnormal residues are specifically recognized by the repair enzyme L-isoaspartate (d-aspartate) protein O-methyltransferase (PCMT; EC 2.1.1.77). The aim of this work was to study the possible involvement of protein aspartate damage in the mechanism linking the G6PD defect and erythrocyte injury, through oxidative stress. Patients affected by G6PD deficiency (Mediterranean variant) were selected. In situ methylation assays were performed by incubating intact erythrocytes in the presence of methyl-labelled methionine. Altered aspartate residues were detected in membrane proteins by methyl ester quantification. We present here evidence that, in G6PD-deficient erythrocytes, damaged residues are significantly increased in membrane proteins, in parallel with the decay of pyruvate kinase activity, used as a cell age marker. Erythrocytes from patients were subjected to oxidative stress in vitro, by treatment with t-butylhydroperoxide, monitored by a rise in concentration of both methaemoglobin and thiobarbituric acid-reactive substances. L-Isoaspartate residues increased dramatically in G6PD-deficient erythrocytes in response to such treatment, compared with baseline conditions. The increased susceptibility of G6PD-deficient erythrocytes to membrane protein aspartate damage in response to oxidative stress suggests the involvement of protein deamidation/isomerization in the mechanisms of cell injury and haemolysis.

Aspartic Acid↗
PubMed2003

Screening for glucose-6-phosphate dehydrogenase deficiency using a modified formazan method: a pilot study on Filipino male newborns.

BACKGROUND: Glucose-6-phosphate dehydrogenase (G6PD) deficiency has increased prevalence rates in tropical Africa, tropical and subtropical Asia and some parts of the Mediterranean. Earlier studies on G6PD deficiency in the Philippines have shown prevalence rates of 4.5% to 25.7%. METHODS: In the present study, 3278 male newborns were screened for G6PD deficiency using the modified formazan method, a simple screening procedure affordable in the setting of a developing country. Subjects with positive screening results were recalled for confirmatory testing using a commercial assay kit for quantitative enzyme determination. RESULTS: Of the 3278 boys studied, 186 revealed positive screening results. Of the 186, 65 boys had confirmatory testing. Of these 65 boys, 45 were confirmed to have G6PD deficiency and 20 had normal results. This study reveals an incidence of G6PD deficiency of 3.9% among male Filipinos. CONCLUSIONS: This study recommends the inclusion of G6PD deficiency in the panel of disorders for newborn screening among Filipino newborns.

Formazans↗
PubMed1971

Expression of two X-linked genes in human hair follicles of double heterozygotes.

Expression of the two X-linked loci glucose-6-phosphate dehydrogenase (G6PD; EC 1.1.1.49) and hypoxanthine:guanine phosphoribosyltransferase (HGPRT; EC 2.4.2.8) was studied in single hair follicles of two females who were heterozygous for both of these genes (double heterozygotes). The coupling phase for these two loci was known to be g6pd A and hyprt(-) on the maternal X chromosome and g6pd B and hgprt(+) on the paternal X. Three phenotypic classes of hair follicles were observed in both double heterozygotes: G6pd A follicles with deficient HGPRT activity, G6pd B follicles with normal HGPRT activity, and G6pd AB follicles with intermediate HGPRT activity. These data directly demonstrate one of the predictions of the Lyon hypothesis that for two X-linked loci, those genes in cis position are turned on or off in a cell and its clone, while in trans only one gene or the other is expressed.

Adenine↗
PubMed1982

Preparation of a monoclonal antibody to rat liver glucose-6-phosphate dehydrogenase and the study of its immunoreactivity with native and inactivated enzyme.

A monoclonal antibody of the IgG class was prepared against rat liver glucose-6-phosphate dehydrogenase (G6PD; D-glucose-6-phosphate:NADP+ 1-oxidoreductase, EC 1.1.1.49) by the hybridoma technique. This antibody does not affect the catalytic activity of the enzyme and shows crossreactivity with the palmitoyl CoA-inactivated G6PD. By solid phase radioimmunoassay, the presence of crossreacting materials in comparable amounts was determined in liver homogenate supernatants from rats that had been starved and refed a high-sucrose diet (containing a high level of G6PD activity) and from rats that had been starved and refed a high-fat diet (containing a low level of G6PD activity). These findings indicate that G6PD is present in an inactive form in rats fed a high-fat diet. The monoclonal antibody will facilitate isolation and characterization of the inactive variant G6PD.

Animals↗
PubMed1986

Complete reactivation of X chromosomes from human chorionic villi with a switch to early DNA replication.

Mammalian sex-dosage compensation is mediated by maintaining activity of only one X chromosome. The asynchronous DNA synthesis characterizing the silent human X chromosome is thought to be reversible only during ontogeny of oocytes. We have previously shown that the glucose-6-phosphate dehydrogenase (G6PD) locus (G6PD) on the allocyclic X chromosome in chorionic villi is partially expressed. We now show that in hybrids derived from a clone of chorionic villi cells (heterozygous for G6PD A) and mouse A9 cells, the loci for G6PD, hypoxanthine phosphoribosyltransferase (HPRT) and phosphoglycerate kinase are expressed on both human X chromosomes; the human X chromosomes carrying either G6PD A or B replicate synchronously with each other and with murine chromosomes. The X chromosome with G6PD A was identified as the original late-replicating X, because methylation in the body of the HPRT gene on this chromosome remained characteristic of the inactive X chromosome. These results indicate that X-chromosome inactivation is completely reversible in cells of trophoblast origin; induction of full transcriptional activity is accompanied by acquisition of isocyclic replication, showing an intimate relationship between these processes. The molecular events responsible for this reversal may be similar to those occurring during maturation of oocytes. Chorionic villi and derivative hybrids provide in vitro models for exploring early events that program the single active X chromosome.

Animals↗
PubMed2001

Modulation of glucose-6-phosphate dehydrogenase activity and expression is associated with aryl hydrocarbon resistance in vitro.

The mutagenic effect of environmental carcinogens has been well documented in animal models and in human studies but the mechanisms involved in preventing carcinogen insult have not been fully elucidated. In this study we examined the molecular and biochemical changes associated with carcinogen resistance in a series of aryl hydrocarbon-resistant MCF-7 cell lines developed by exposure to benzo[a]pyrene (BP). The cell lines were designated as AH(R40), AH(R100), and AH(R200) to denote their increasing fold resistance to BP compared with wild type cells. These cell lines were also resistant to another aryl hydrocarbon (AH), dimethylbenz[a]anthracene, but not to pleiotropic drugs (doxorubicin, vinblastine, and taxol). The resistant cell lines showed an increase in the level of the primary intracellular antioxidant, reduced glutathione, corresponding to increasing AH resistance. However, there was no change in glutathione reductase activity. The generation of reduced glutathione requires NADPH, and we therefore examined the activity and expression of the rate-limiting enzyme in NADPH production, glucose-6-phosphate dehydrogenase (G6PD). An increase in G6PD specific activity was associated with increasing aryl hydrocarbon resistance. This was due to an increased expression of G6PD in resistant cells, which was demonstrated by increases in both protein and mRNA levels. However, there was no increase in the transcription rate of G6PD in the resistant cell lines, indicating that the increase G6PD expression is due to a post-transcriptional modulation, which was confirmed by actinomycin D chase experiments. These results demonstrate that modulation of G6PD expression and activity is an important mechanism in AH resistance.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2003

Glucose-6-phosphate dehydrogenase expression associated with NADPH-dependent reactions in cerebellar neurons.

This review describes the variation of glucose-6-phosphate dehydrogenase (G6PD) activity in the main neurons of the molecular and granular layers as well as in the deep nuclei of the cerebellum as observed so far by optical and electron microscopy studies. Light microscopy and semiquantitative microphotometry of histochemical staining showed that the highest G6PD activity was expressed by Purkinje cells and neurons of the deep cerebellar nuclei; the elements of the molecular layer showed a diffuse G6PD staining, while the granular layer displayed only scattered G6PD activity. Electron microscopy analysis showed that the basket and stellate cells, as well as the Golgi cells, have a remarkable G6PD activity, while in the granule cells the enzyme was barely detectable. The results show that cerebellar G6PD activity changes with different neuron types as a function of its role in sustaining NADPH dependent pathways in these cells.

Animals↗
PubMed1989

Glucose-6-phosphate dehydrogenase deficiency and cancer in a Sardinian male population: a case-control study.

A case-control study was conducted to test the hypothesis whether the genetic condition of glucose-6-phosphate dehydrogenase (G6PD) deficiency is associated with a reduced risk of cancer. One hundred and eighty seven male cancer patients admitted to hospitals in Cagliari (Sardinia, Italy), between November 1984 and March 1986, were compared with 186 male patients with other diseases, except hemolytic anemia, admitted to the same hospitals in the same period. In contrast to previous reports, our study found no reduction of cancer risk in G6PD-deficient subjects. The study had sufficient statistical power to detect a 0.5-fold decrease in the risk of cancer. The recent suggestion from other studies that tumoral cells of G6PD-deficient subjects can produce their own G6PD, seems to be consistent with this negative finding. Among those subjects presenting some level of erythrocyte G6PD activity, the average enzyme activity was significantly higher in cancer patients than in controls. This finding is consistent with previous experimental studies suggesting a positive correlation between cell proliferation and G6PD activity.

Adult↗
PubMed1975

Regulation of gene activity by dosage compensation at the chromosomal level in drosophila.

Two models of dosage compensation have been tested by the measurement of G6PD and 6PGD enzymatic specific activities in flies hyperploid for regions of the X chromosome. Females duplicated for the proximal half of the X chromosomes (2 1/2 X's) have an increased level of G6PD and a normal level of 6PGD. Females duplicated for the distal half of the X chromosome (2 1/2 X's) have a normal level of G6PD and an increased level of 6PGD. Males bearing duplications of various segments of the X chromosome show control levels of G6PD and 6PGD, except where the duplicated region includes the structural gene for G6PD or 6PGD. These results fail to provide evidence for either the presence of discrete X-linked compensator (regulator) genes reducing the activity of other X-linked genes, or for a factor in limiting supply necessary for the transcription of all the genes on the X chromosome. Superfemales (3 X chromosomes) have the same G6PD and 6PGD activity levels as their diploid sisters. It would appear that the regulation of gene activity by dosage compensation is a chromosomal phenomenon in that the level of activity per gene copy for loci on the X chromosome is modulated in a stepwise fashion according to the total number of X chromosomes present.

Aneuploidy↗
PubMed1981

Autosomal factors with correlated effects on the activities of the glucose 6-phosphate and 6-phosphogluconate dehydrogenases in Drosophila melanogaster.

Isogenic lines, in which chromosomes sampled from natural populations of C. melanogaster are substituted into a common genetic background, were used to detect and partially characterize autosomal factors that affect the activities of the two pentose phosphate pathway enzymes, glucose 6-phosphate dehydrogenase (G6PD) and 6-phosphogluconate dehydrogenase (6PGD). The chromosome 3 effects on G6PD and 6PGD are clearly correlated; the chromosome 2 effects, which are not so great, also appear to be correlated, but the evidence in this case is not so strong. Examination of activity variation of ten other enzymes revealed that G6PD and 6PGD are not the only pair of enzymes showing a high positive correlation, but it is among the highest in both sets of lines. In addition, there was some evidence that the factor(s) affecting G6PD and 6PGD may also affect two other metabolically related enzymes, transaldolase and phosphoglucose isomerase.--Rocket immunoelectrophoresis was used to estimate specific CRM levels for three of the enzymes studied: G6PD, 6PGD and ME. This experiment shows that a large part of the activity variation is accounted for by variation in CRM level (especially for chromosome 3 lines), but there remains a significant fraction of the genetic component of activity variation that is not explained by CRM level.--These results suggest that the autosomal factors are modifiers involved in regulation of the expression of the X-linked structural genes for G6PD and 6PGD, but a role in determining part of the enzymes' primary structure cannot be excluded with the present evidence.

Animals↗
PubMed1976

Dietary fatty acids on the control of glucose-6-phosphate dehydrogenase and malic enzyme in the starved-refed rat.

The role of dietary unsaturated fat in the control of hepatic glucose-6-phosphate dehydrogenase (G6PD) (EC 1.1.1.49) and malic enzyme (ME) (EC 1.1.1.40) was studied in rats subjected to one or two cycles of starvation-refeeding. Rats starved and refed a control (5% corn oil) diet showed a threefold increase in G6PD activity and a twofold increase in ME activity compared to ad libitum-fed rats. After a second cycle of starvation-refeeding G6PD and ME activities showed fourfold and threefold increases, respectively, as compared to ad libitum-fed rats. Feeding rats diets containing 8% linoleic acid (as triglycerides) prevented the increase in G6PD and ME activities upon starvation-refeeding, diets with oleic, palmitic, and stearic acis when fed did not prevent this increase. Feeding rats various combinations of linoleic, linolenic and oleic acids following starvation prevented the additional increase in G6PD and ME activities after a second starvation-refeeding cycle; however, linoleic acid fed alone during the first refeeding prevented the additional increase in ME activity but not in G6PD activity. It is suggested that the dietary control of these enzymes involves one or more specific polyunsaturated fatty acids.

Animals↗
PubMed1976

Effects in the rat of environmental temperature, diet dilution, and treadmill running on liver and adipose enzymes and metabolism of 14C-glucose: a multiple regression analysis.

The effects of two environmental temperatures (T; 16 degrees and 31 degrees), five diet dilutions (D; 0%, 12.5%, 25%, 37.5% and 50%), and five daily treadmill running periods (E; 10 minutes, 40 minutes, 70 minutes, 100 minutes, and 130 minutes) upon enzyme activities of liver and adipose tissue of male rats were observed. Liver enzymes studied were glucose-6-phosphatase (G6Pase), 6-P-gluconate dehydrogenase (6PGD), glucose-6-phosphate dehydrogenase (G6PD), fructose diphosphatase (FDPase), NADP-isocitrate dehydrogenase (ICDH), and malic enzyme (ME). Adipose tissue (epididymal fat) enzymes (6PGD, G6PD, and ME) were studied as well as the in vitro incorporation of the 14C of [U-14C] glucose into liberated 14CO2 and into the triglycerides, free fatty acids, and total lipids by adipose tissue slices. Equations describing regression surfaces for these responses (expressed as units/100 g body weight) could contain significant linear coefficients of the independent variables (T, D, and E), their first order interactions, and quadratic coefficients for D and E. Significnat regression coefficients for activities of liver enzymes associated with increased lipogenesis (6PGD, G6PD, and ME) produced response surfaces with conformations generally concave downward. All enzymes possessed positive and negative linear and quadratic coefficients for D which caused response surfaces to be concave downward with respect to that variable. Also, 6PGD and G6PD (positive linear and negative quadratic coefficients for E) exhibited response surfaces concave downward with respect to E. Additionally, 6PGD showed greater activity at 31 degrees than at 16 degrees while G6PD showed no effect of temperature on activity. Liver ICDH, probably important in supplying reducing equivalents for fatty acid synthesis, evidenced response surfaces almost identical to those for 6PGD. Significant regression coefficients for activity of liver enzymes associated with increased gluconeogenesis (FDPase and G6Pase) produced for FDPase a response surface concave downward with respect to both D and E with greater values at 31 degrees than at 16 degrees; but for G6Pase non-concave surfaces with lesser values at 31 degrees than at 16 degrees. Significant regression coefficients for activities of adipose enzymes associated with increased lipogenesis produced for 6PGD a response surface concave upward due to negative linear and positive quadratic coefficients for both D and E. For G6PD and ME regression surfaces were concave upward with respect to E, but these were modified by positive and negative linear coefficients, respectively, for D. Significant regression coefficients for incorporation of the 14C of glucose into triglycerides and free fatty acids of adipose tissue slices and their production of 14CO2 yielded response surfaces concave upward with respect to E (negative linear and positive quadratic coefficients). In addition, the surface for free fatty acids was concave upward with respect to D. The 14CO2 production was greater at 16 degrees than at 31 degrees...

Adipose Tissue↗
PubMed1979

Interrelationships in rats among dietary vitamin B6, glycine and hydroxyproline. Effects of oxalate, glyoxylate, glycolate, and glycine on liver enzymes.

Urinary endogenous oxalate was increased by feeding vitamin B6-deficient or control rats with 5.2% hydroxyproline, or 3% glycine plus 5.2% hydroxyproline. The activities of liver lactic dehydrogenase (LDH), glucose-6-phosphate dehydrogenase (G6PD) , malic enzyme (ME), and ATP citrate lyase were decreased in vitamin B6-DEFICIENT RATS, AND THEIR LIVEr G6PD was further decreased by the addition of glycine and hydroxyproline to their diets. Supplementing control diets with the two amino acids decreased the activities of rat liver LDH, G6PD, and ATP citrate lyase. The effects of glycine and hydroxyproline feeding on the enzymes studied did not appear related to alterations in insulin availability. Since in vitamin B6-deficient rats, there are increases in urinary levels of oxalic and glycolic acids, and glycine, and increases in tissue levels of glyoxylic acid and glycine, the effects of these metabolites on the activities of the above mentioned enzymes were measured. Oxalic acid inhibited the activities of LDH, G6PD, and ME. Glyoxylic acid inhibited LDH and ME, but not G6PD. Glycolic acid inhibited G6PD and ME, but not LDH. ATP citrate lyase was not affected by these substances. Glycine had no effect on the enzymes studied. Diets which increased oxalate excretion generally reduced or did not alter liver and kidney levels of oxalate, glycolate, and glyoxylate. However, the feeding of glycine and hydroxyproline increased kidney oxalate, and liver and kidney glyoxylate in vitamin B6-deficient rats.

ATP Citrate (pro-S)-Lyase↗
PubMed2004

Nutritional regulation of mRNA processing.

Understanding how a cell adapts to dietary energy in the form of carbohydrate versus energy in the form of triacylglycerol requires knowledge of how the activity of the enzymes involved in lipogenesis is regulated. Changes in the activity of these enzymes are largely caused by changes in the rate at which their proteins are synthesized. Nutrients within the diet can signal these changes either via altering hormone concentrations or via their own unique signal transduction pathways. Most of the lipogenic genes are regulated by changes in the rate of their transcription. Glucose-6-phosphate dehydrogenase (G6PD) is unique in this group of enzymes in that nutritional regulation of its synthesis involves steps exclusively at a posttranscriptional level. G6PD activity is enhanced by the consumption of diets high in carbohydrate and is inhibited by the consumption of polyunsaturated fat. In this review, evidence is presented that changes in the rate of synthesis of the mature G6PD mRNA involves regulation of the efficiency of splicing of the nascent G6PD transcript. Furthermore, this regulation involves the activity of a cis-acting sequence in the G6PD primary transcript. This sequence in exon 12 is essential for the inhibition of G6PD mRNA splicing by PUFA. Understanding the mechanisms by which nutrients alter nuclear posttranscriptional events will provide new information on the breadth of mechanisms involved in gene regulation.

Animals↗