Biomedical subjects

L Yu

Publications and source records attributed to L Yu.

At least 487 records · Page 27Linked to original sources

PubMed1996

Number of autoantibodies (against insulin, GAD or ICA512/IA2) rather than particular autoantibody specificities determines risk of type I diabetes.

We previously evaluated radioassays for insulin autoantibodies (IAA), glutamate decarboxylase autoantibodies (GAA) and ICA512bdc autoantibodies (ICA512bdcAA) in the prediction of type I diabetes. Among first degree relatives, the five year risk of diabetes was 0% if no autoantibody was positive, 15% if only one was positive, 44% if two were positive and 100% if all three were positive. We measured IAA, GAA and ICA512bdcAA in 45 patients with new onset type I diabetes (sampled within 7 days of insulin therapy), 882 first degree relatives of patients with type I diabetes, and 217 control subjects. ICA512bdc is a construct of the ICA512/IA2 molecule (amino acid residues 256-979), including the intracellular domain. Based on receiver-operating characteristic plots, there was no significant difference between the three assays in their ability to discriminate between disease and control subjects. The upper limits of normal for the assays were determined as the 99th percentile of levels in the control subjects or higher. Using these cut-offs, 76% of new onset patients were positive for two or more autoantibodies, and 98% were positive for one or more. In comparison, none of 198 control subjects tested for all three assays were positive for more than one autoantibody. In relatives with a single autoantibody, or exactly two autoantibodies, there was no difference in diabetes-free survival according to which one of the autoantibodies was present (P = 0.70, logrank test), or which particular combination of autoantibodies was present (P = 0.56, logrank test) respectively. Our conclusions were as follows: the number of autoantibodies (counting IAA, GAA and ICA512bdcAA) is important in prediction, rather than the particular autoantibody specificities present. Among patients with new onset insulin-dependent diabetes, the absence of any of these autoantibodies justifies the consideration of non-autoimmune forms of diabetes in the differential diagnosis.

Adolescent↗

PubMed1996

Beta-cell autoantibodies in infants and toddlers without IDDM relatives: diabetes autoimmunity study in the young (DAISY).

Little is known concerning the natural history of beta-cell autoimmunity in infants and toddlers, especially in those without a first degree IDDM relative. A population-based cohort of Colorado infants at increased IDDM risk due to their HLA genotype has been identified through a PCR-based HLA screening of cord blood and is being prospectively studied. We report the distribution of insulin (IAA), GAD65 (GAA), and ICA512 autoantibody levels in 312 children aged 9 months and in 131 children aged 15 months from this cohort, without family history of IDDM. The levels of IAA, GAA and ICA512 did not differ by the HLA genotype (DR3/4,DQB1*0302 vs. DR3/3, vs. DR2/DR4,DQB1*0302 vs. DRx/4,DQB1*0302, where x is not DR3 or DR2), by ethnicity (non-Hispanic whites vs. other ethnic groups), or by age (9 vs. 15 months). The 95th and 99th percentiles of the IAA distribution were respectively 40 and 61 nU/ml at the age of 9 months and 38 and 59 nU/ml at the age of 15 months. The 95th and 99th percentiles of the GAA distribution were respectively 0.020 and 0.046 at the age of 9 months and 0.022 and 0.098 at the age of 15 months. We propose to use IAA levels greater than 60 nU/ml and GAA index greater than 0.05 to define the presence of beta-cell autoimmunity in children younger than 2 years.

Alleles↗

PubMed1996

Limited loss of tolerance to islet autoantigens in ICA+ first degree relatives of patients with type I diabetes expressing the HLA dqb1*0602 allele.

The DQB1*0602 allele confers dominant protection from Type I diabetes even among islet cell antibody positive (ICA+) first degree relatives of affected individuals. Lack of progression to diabetes in these subjects, despite ICA positivity, could be explained by a loss of tolerance limited to fewer islet autoantigens than in ICA+ relatives progressing to the disease. To test this hypothesis we have determined autoantibodies by radioassay to three islet autoantigens, glutamic acid decarboxylase (GAD), insulin and the novel neuroendocrine antigen ICA512/IA-2 in 84 HLA-typed ICA+ first degree relatives of patients with Type I diabetes. Among the eleven relatives expressing the 0602 allele (0602+) only two were positive for more than one antibody as determined by radioassay. In contrast, 55/73 ICA+ relatives lacking this allele (non-0602) expressed more than one autoantibody (P < 0.01). The prevalence of antibodies to GAD (GAA) was not significantly different in ICA+ relatives with and without the 0602 allele (7/11 in 0602+ versus 60/73 in non-0602). In contrast, anti-insulin antibodies (IAA) were present in only 2/11 0602+ ICA+ relatives versus 47/70 in non-0602 ICA+ relatives (P < 0.01). Similarly, only one individual carrying the 0602 allele was positive for ICA512 autoantibodies versus 33/70 in the non-0602 group (P < 0.01). These data indicate that even among ICA+ relatives the 0602 allele is associated with a limited immune response to islet antigens and amongst 0602+ relatives this response is mostly directed against GAD.

Adolescent↗

PubMed1996

Evaluation of Bacillus thuringiensis and Bacillus sphaericus Strains from Chinese Soils Toxic to Mosquito Larvae

During our research to isolate and screen microbial agents, eight Bacillus thuringiensis isolates and five Bacillus sphaericus isolates were shown to have high toxicity to mosquito larvae. Comparing the LC50 values, four B. sphaericus isolates with LC50 values ranging from 0.50 to 1.47 ng/ml were about two to six times more toxic than strain 1593 (LC50 3.00 ng/ml) against larvae of Culex quinquefasciatus. Four B. thuringiensis isolates (LC50 values ranging from 3.80 to 7.54 ng/ml) and four B. sphaericus isolates with LC50 of 17.0 to 43.7 ng/ml were more toxic to Aedes aegypti than strain 1897 (LC50 8.46 ng/ml) and strain 1593 (LC50 67.3 ng/ml). As to Anopheles hyrcanus, the LC50 values of three B. sphaericus isolates ranging from 3.63 to 5.73 ng/ml were three to five times smaller than that of strain 1593 (LC50 16.1 ng/ml). Two B. sphaericus isolates showed high toxicity against mosquito larvae in the three genera Culex, Aedes, and Anopheles.

Journal Article↗

PubMed1996

Abnormal regulation of the LDL-R and HMG CoA reductase genes in subjects with familial hypercholesterolemia with the "French Canadian mutation".

Familial hypercholesterolemia (FH) is seen with high frequency in the province of Québec, Canada. A large deletion (> 10 kb) of the 5'-end of the low density lipoprotein receptor (LDL-R) gene is the major mutation of the LDL-R in FH subjects in Québec (approximately 60% of FH subjects). No mRNA is produced from the allele bearing the mutation, and cellular cholesterol obtained by receptor-mediated endocytosis is under the control of the non-deletion allele. We have previously reported that some patients with the 10-kb deletion (approximately 9%) fail to respond to the hydroxymethylglutaryl coenzyme A reductase (HMG CoA reductase) inhibitor class of medications. We studied mRNA levels of the LDL-R and HMG CoA reductase genes in response to the HMG CoA reductase inhibitor lovastatin in a time- and dose-dependent fashion in cultured human skin fibroblasts and we devised an in vitro model to study the response to drug therapy in subjects with FH. We determined mRNA levels by RNase protection assay in skin fibroblasts obtained from controls (n = 3) and FH subjects with the > 10-kb deletion (responders, n = 3; non responders, n = 3; to drug therapy). We measured 125I-LDL binding on skin fibroblasts grown in the presence of lipoprotein-deficient serum with or without 1 microM lovastatin, using 10 micrograms/mL of 125I-LDL protein. Control subjects exhibited coordinate regulation of the LDL-R and HMG CoA reductase genes in response to lovastatin, 0.1-25 microM, for 0-24 h. Correlation coefficients between mRNA levels of both genes were > 0.9 in controls and FH subjects. However, by linear regression analysis, the corresponding slopes for the correlation between both genes were 0.98 (controls), 3.36 and 3.63 (FH responders and non-responders), indicating a pattern of dissociated but still coordinate regulation in FH subjects. The magnitude of increase of mRNA levels of the LDL-R gene was approximately five-fold over LPDS in controls, two-fold in FH responders and two-fold in non-responders. Binding studies using 125I-LDL reveal that a control subject and all responders had a 2-2.5-fold increase in binding to cell surface receptors but two out of three FH non-responders showed no increase in binding in response to 1 microM lovastatin. The LDL-R and HMG CoA reductase genes are expressed in coordinate regulation in fibroblasts from subjects with FH due to the > 10-kb deletion, but with a proportionately greater up-regulation of the HMG CoA reductase gene. Some subjects, with FH caused by the > 10-kb deletion of the LDL-R gene, who fail to respond to HMG CoA reductase inhibitors have abnormal LDL receptor binding activity at the cell surface in response to lovastatin in vitro.

Anticholesteremic Agents↗

PubMed1996

Recording of brainstem evoked potentials and their association with gentamicin in neonates.

Brainstem auditory evoked potential (BAEP) recording was used to screen presymptomatically the hearing of 200 neonates treated with ampicillin (100 mg/kg daily) and gentamicin sulfate (5 mg/kg daily). The study included 130 male and 70 female neonates; post-conceptional age ranged from 34 to 57 weeks (mean 42.36 weeks). We divided neonates into 2 groups according to duration of antibiotic treatment; group 1 consisted of 179 patients who were treated with antibiotic agents for < or = 7 days. Although 15 (8.4%) in this group initially manifested abnormal BAEP recordings, only 8 of these brain-damaged neonates (4.5%) (6 with peripheral and 2 with central dysfunction) later manifested abnormal recordings. Group 2 consisted of 21 neonates who were treated for 10 to 30 days; BAEP recordings were abnormal in 7 patients (33.3%) (4 with peripheral and 3 with central dysfunction). We conclude that BAEP is indicated only for neonates treated with gentamicin sulfate for > 10 days. In this group, infants so treated usually have underlying disease or severe infection, including birth asphyxia, hypoxia, sepsis, and meningoencephalitis, all of which are clinically significant indicators of high risk for auditory pathway dysfunction.

Anti-Bacterial Agents↗

PubMed1996

Protein kinase modulation of mu opioid receptor signalling.

The mu opioid receptor mediates the pain-relieving effects of opioid narcotics. Cellular signalling of the mu receptor involves G-proteins, and the effectors include adenylyl cyclase and ion channels. Studies in which the cloned mu opioid receptor is used for cellular expression show that the receptor function is modulated by multiple protein kinases.

Animals↗

PubMed1996

Effects of castration and androgen replacement on tumour growth of human hepatocellular carcinoma in nude mice.

BACKGROUND/AIMS: Previous clinical investigations suggest that androgen and its receptor (AR) may play an important role in the growth of hepatocellular carcinoma. Few studies are available concerning the effect of androgen manipulation on the growth of AR-positive hepatocellular carcinoma in vivo. METHODS: AR-positive (SM10) and AR-negative (SM2) sublines derived from a human hepatocellular carcinoma line KYN-1 were implanted subcutaneously in the lower abdomen of nude mice. The tumour size and expression of proliferating cell nuclear antigen and Lewis Y antigen were examined in intact males, castrated males, intact females, and castrated males with androgen replacement. AR of the tumour was measured with binding assay, ultracentrifugation, and Western blotting. RESULTS: The growth of SM10 was significantly better in intact males and castrated males with 5a-dihydrotestosterone injection than in intact females and castrated males. Castration did not suppress the growth of SM2. The tumour AR level was reduced by castration but maintained by the hormone substitution. Although proliferating cell nuclear antigen expression was closely associated with tumour growth, Lewis Y antigen expression did not differ among the groups. CONCLUSIONS: These data may indicate that this hepatocellular carcinoma subline (SM10) is androgen-responsive and that androgen ablation can cause the inhibition of the tumour growth, which might be due to decreased proliferative and not increased apoptotic activities. In addition, such androgen-stimulated tumour growth seems to be mediated through AR.

Androgens↗

PubMed1996

Inhibition of growth and induction of TGF-beta 1 in human hepatocellular carcinoma with androgen receptor by cyproterone acetate in male nude mice.

BACKGROUND/AIMS: Hepatocellular carcinoma possesses androgen receptor but its true role is not known. This study aimed to investigate the effect of an anti-androgen cyproterone acetate on the growth of androgen receptor-positive hepatocellular carcinoma. METHODS: Androgen receptor-positive human hepatocellular carcinoma cells (KYN-1/SM-10) were subcutaneously transplanted into male nude mice. When the tumor size was about 10 mm, animals were subcutaneously administered cyproterone acetate (0.1 mg/day and 0.8 mg/day) or solvent alone for 21 days. Animals were serially sacrificed for measurements of testicular weight, tumor size, and cytosolic and nuclear androgen receptor levels in tumor. Proliferating cell nuclear antigen, transforming growth factor-alpha, and transforming growth factor-beta 1 in tumor were investigated immunohistochemically, using monoclonal antibodies. Apoptotic activity was also studied by the in situ DNA nick end labeling method. RESULTS: Cyproterone acetate depressed testicular weight, suppressed tumor growth, and decreased both cytosolic-androgen receptor and nuclear-androgen receptor levels dose-dependently. Numbers of proliferating cell nuclear antigen-positive cells were decreased transiently with the low dose but continuously with the high dose of cyproterone acetate. Transforming growth factor-alpha expression was not influenced by cyproterone acetate, but the high dose of cyproterone acetate induced higher expression of transforming growth factor-beta 1, associated with increased numbers of apoptotic tumor cells, peaking on day 3. CONCLUSIONS: The inhibition of growth of androgen receptor-positive hepatocellular carcinoma with cyproterone acetate in male nude mice could be due to G1-phase cell cycle arrest, and to some extent apoptosis induced by increased synthesis of transforming growth factor-beta 1 in tumor, caused by the direct action of cyproterone acetate through androgen receptors, as well as decreased testosterone levels in blood due to cyproterone acetate-induced testicular atrophy.

Androgen Antagonists↗

PubMed1996

Use of synthetic peptides to confirm that the Pseudomonas aeruginosa PAK pilus adhesin and the Candida albicans fimbrial adhesin possess a homologous receptor-binding domain.

Pseudomonas aeruginosa PAK pili and Candida albicans fimbriae are adhesins present on the microbial cell surfaces which mediate binding to epithelial cell-surface receptors. The receptor-binding domain (adhesintope) of the PAK pilus adhesin has been shown previously to reside in the carboxy-terminal disulphide-bonded region of P. aeruginosa pilin (PAK128-144). The delineation of the C. albicans fimbrial adhesintope was investigated in these studies using synthetic peptides which correspond to the whole (PAK128-144) or part of (PAK134-140) adhesintope of the PAK pilus and their respective anti-peptide antisera and biotinylated PAK pili (Bt-PAK pili), fimbriae (Bt-fimbriae), P. aeruginosa whole cells (Bt-P. aeruginosa) and C. albicans whole cells (Bt-C. albicans). The results from these studies confirmed that a structurally conserved motif akin to the PAK(128-144) peptide sequence is present in C. albicans fimbrial adhesin and that the seven-amino-acid residue PAK(134-140) sequence plays an important role in forming the adhesintope for both P. aeruginosa PAK pilus and C. albicans fimbrial adhesins.

Adhesins, Bacterial↗

PubMed1996

Induction of morphological and functional differentiation of human promyelocytic leukemia cells (HL-60) by Tubeimoside 1.

Two functional parameters evaluated by nitroblue tetrazolium (NBT) dye reduction and zymosan particle phagocytosis and a morphological change assessed by the Wright-Giemsa stain of human promyelocytic leukemia cells (HL-60 cells) were used to determine the extent of HL-60 cell differentiation induced by tubeimoside 1. The results revealed that under the action of tubeimoside 1, HL-60 cells could be induced to differentiate to more mature cells with the functional characteristics of granulocytes. Therefore, tubeimoside 1 could be considered as a promising antileukemic agent for further animal trials.

Antineoplastic Agents, Phytogenic↗

PubMed1996

The mu opioid receptor: from molecular cloning to functional studies.

Opioids have been used and abused by humans for centuries. The mu opioid receptor represents the high affinity binding site for opioid narcotics with high abuse liability such as morphine, codeine and fentanyl. Heroin (diacetylmorphine), a semi-synthetic derivative of morphine, crosses the blood-brain barrier more readily than morphine due to its increased hydrophobicity. Once in the brain heroin is hydrolyzed to morphine, which acts at the mu opioid receptor and results in euphoria, thus conferring the reinforcing properties of heroin. Using molecular biology techniques, the mu opioid receptors from several species have been cloned. This article reviews recent progress in this area, with respect to the two major cellular functions of the mu opioid receptor: reduction of intracellular cAMP concentration by inhibiting adenylyl cyclase activity, and inhibition of neuronal firing by modulating membrane ion channels.

Journal Article↗

PubMed1996

Functional coupling of a mu opioid receptor to G proteins and adenylyl cyclase: modulation by chronic morphine treatment.

A cloned mu opioid receptor was used to study its coupling to signal transduction pathways and its involvement in morphine-induced opioid dependence in stably transfected Chinese hamster ovary (CHO) cells. Membrane binding assays with a mu-selective agonist [(3)H]DAMGO showed that one cell line expresses a high level of mu opioid receptors with a B(max) of approximately 630 fmol/mg membrane protein and a K(d) of 0.47 nM for DAMGO. Stimulation of the transfected cells with DAMGO led to an increase in the low K(m) GTPase activity, indicative of activation of guanine nucleotide regulatory proteins (G proteins), and this effect was blocked by the opioid antagonist naloxone. In addition, binding of the mu opioid receptor to DAMGO was affected by GTP and nonhydrolizable GTP analogs, Gp(NH)pp and GTP-gamma-S. These results suggest a functional coupling between the mu opioid receptor and G proteins. Furthermore, DAMGO treatment of the cells produced a dose-dependent inhibition of the intracellular cyclic adenosine monophosphate (cAMP) level, with an EC(50) value of approximately 30 nM. Chronic treatment of the cells with morphine not only elevated the basal and forskolin-stimulated cAMP levels after morphine withdrawal, but also increased the extent of the DAMGO-induced reduction of intracellular cAMP levels. The whole cell binding assay with [(3)H]DAMGO, on the other hand, did not detect receptor down-regulation after chronic morphine treatment. These results suggest that chronic morphine treatment may trigger a compensatory mechanism in cellular signaling pathways to offset the inhibitory input from the mu receptor without down-regulation of the surface receptor number, and that withdrawal of chronic inhibition leads to elevated activities of adenylyl cyclase to provide a basis for system sensitization.

Journal Article↗

PubMed1996

Serum transferrin receptor concentrations in women with mild malnutrition.

We determined the influence of undernutrition on blood soluble transferrin receptor (sTfR) concentrations, an indicator of iron deficiency, in 99 Zairean women (aged 16-45 y) without inflammation. They were recruited during a survey on iron deficiency in rural Bas-Zaire. sTfR was measured by enzyme immunoassay, and indicators of nutritional status [albumin, transthyretin (or prealbumin), and retinol binding protein] were measured by radial immunodiffusion. Undernutrition was diagnosed if the concentration of any one of the indicators was below normal: albumin < 35 g/L, transthyretin < 160 mg/L, and retinol binding protein < 30 mg/L. The sTfR concentration ranged from 1.89 to 19.1 mg/L (mean: 8.7 mg/L). Mean values for indicators of nutritional status, serum ferritin, and transferrin saturation were within the normal range for health subjects. Regardless of the iron status (iron sufficiency, anemia, or iron deficiency with or without anemia) and whether women were pregnant or nonpregnant, undernutrition did not significantly reduce sTfR concentrations. A higher percentage (80%) of iron-deficient women with two or three protein values below normal had sTfR concentrations > 8 mg/L (which are suggestive of iron-deficiency erythropoiesis) compared with iron-deficient women with no (72.7%) or one (66.7%) protein value below normal, anemic women (46-60%) and iron-sufficient women (18.2-36.8%). Results suggest that sTfR can be used as an indicator of iron deficiency in field studies without in-depth assessment of nutritional status. However, the effect of severe malnutrition on this index requires further investigation.

Adolescent↗

PubMed1996

Engineering a de novo-designed coiled-coil heterodimerization domain off the rapid detection, purification and characterization of recombinantly expressed peptides and proteins.

Using the techniques of genetic engineering and the principles of protein de novo design, we have developed a unique affinity matrix protein tag system as a rapid, convenient and sensitive method to detect, purify and characterize newly expressed recombinant peptides or proteins from cell extracts. The method utilizes two de novo-designed linear peptide sequences that can selectively dimerize to form the stable protein motif, the two-stranded alpha-helical coiled-coil. In this method, a recombinant bacterial expression vector pRLDE has been engineered so that one of the dimerization strands (E-coil) is expressed as a C-terminal fusion tag on newly expressed peptides or proteins, while the other (K-coil) is either biotin-labeled for detection in a Western blot-type format or immobilized on an insoluble silica support for selective dimerization affinity chromatography. Recombinantly expressed peptides from Escherichia coli containing the dimerization tag have been produced, detected and purified using this method. The recombinant peptides were easily and clearly identified using the biotin-labeled coil, while the single-step affinity purification results indicated the purity of the affinity purified expressed peptides to be > 95%, as assessed by reversed-phase chromatography. The stability of the dimerization domain also allows for the purified peptide to be left attached to the matrix, thus creating a new peptide-bound column that can be used to study peptide-protein or peptide-ligand interactions. Therefore this system offers a new alternative to existing peptide or protein fusion tags and demonstrates the utility of a de novo-designed system.

Amino Acid Sequence↗

PubMed1996

Radiation therapy of metastatic pheochromocytoma: case report and review of the literature.

Malignant pheochromocytomas are rare tumors, which are considered radioresistant on the basis of little information. We report a patient, with cranial nerve deficits from a pheochromocytoma metastatic to the parasellar region, who promptly responded to radiation therapy (2,500 cGy) with reversal of neurologic deficit. The disease recurred 2 years later and again promptly responded upon treatment to 2,000 cGy. Hepatic metastases were controlled for over 1 year with 3,240 cGy. The radiotherapy of pheochromocytoma and chemodectoma is reviewed, and the similarities between the two kinds of tumor are discussed. We speculate that a higher initial radiation dose might have resulted in a more sustained remission in our patient and recommend doses of 4,000-5,000 cGy if they can be safely administered, in 4-5 weeks for pheochromocytomas.

Adrenal Gland Neoplasms↗

PubMed1996

Helper virus-free transfer of herpes simplex virus type 1 plasmid vectors into neural cells.

Herpes simplex virus type 1 (HSV-1) plasmid vectors have promise for genetic intervention in the brain, but several problems caused by the helper virus have compromised their utility. To develop a helper virus-free packaging system for these vectors, the DNA cleavage/packaging signals were deleted from a set of cosmids that represents the HSV-1 genome. Following cotransfection into cells, this modified cosmid set supported replication and packaging of vector DNA. However, in the absence of the DNA cleavage/packaging signals, the HSV-1 genome was not packaged, and consequently vector stocks were free of detectable helper virus. In the absence of helper virus, the vectors efficiently infected rat neural cells in culture or in the brain with minimal cytopathic effects. beta-galactosidase-positive cells were observed for at least 1 month in vivo, and vector DNA persisted for this period. This system may facilitate studies on neuronal physiology and potential therapeutic applications.

Animals↗

PubMed1996

Mutational analysis of the RNA triphosphatase component of vaccinia virus mRNA capping enzyme.

Vaccinia virus mRNA capping enzyme is a multifunctional protein with RNA triphosphatase, RNA guanylyltransferase, and RNA (guanine-7-) methyltransferase activities. The enzyme is a heterodimer of 95- and 33-kDa subunits encoded by the vaccinia virus D1 and D12 genes, respectively. The N-terminal 60-kDa of the D1 subunit (from residues 1 to 545) is an autonomous domain which catalyzes the triphosphatase and guanylyltransferase reactions. Mutations in the D1 subunit that specifically inactivate the guanylyltransferase without affecting the triphosphatase component have been described (P. Cong and S. Shuman, Mol. Cell. Biol. 15:6222-6231, 1995). In the present study, we identified two alanine-cluster mutations of D1(1-545), R77A-K79A and E192A-E194A, that selectively inactivated the triphosphatase, but not the guanylyltransferase. Concordant mutational inactivation of RNA triphosphatase and nucleoside triphosphatase functions (to approximately 1% of wild-type specific activity) suggests that both gamma-phosphate cleavage reactions occur at a single active site. The R77A-K79A and E192A-E194A mutant enzymes were less active than wild-type D1(1-545) in the capping of triphosphate-terminated poly(A) but could be complemented in vitro by D1(1-545)-K260A, which is inert in nucleotidyl transfer but active in gamma-phosphate cleavage. Whereas wild-type D1(1-545) formed only the standard GpppA cap, the R77A-K79A and E192A-E194A enzymes synthesized an additional dinucleotide, GppppA. This finding illuminates a novel property of the vaccinia virus capping enzyme, the use of triphosphate RNA ends as an acceptor for nucleotidyl transfer when gamma-phosphate cleavage is rate limiting.

Acid Anhydride Hydrolases↗