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E Oda

Publications and source records attributed to E Oda.

At least 19 recordsLinked to original sources
PubMed1995

Determination of the active site of CD59 with synthetic peptides.

CD59 inhibits the formation of membrane attack complex (MAC) of human complement by binding to C8 and C9 in the nascent membrane attack complex and inhibiting C9 binding to C8 in C5b-8 and C9 polymerization. Considering five disulfide bridges of CD59, we divided the molecule into two portions and synthesized the two peptides. One represented an amino-terminal half, P1-41, consisting of residues 1-41, while another represented a carboxyl-terminal half, P42-77, consisting of residues 42-77. P1-41 inhibited the MAC formation much more strongly than P42-77, indicating that the amino-terminal half contained the active site. We further synthesized P4-18 that consisted of residues 4-18 and P19-41 that consisted of residues 19-41. The activity of P4-18 was less than that of P19-41. Surprisingly, P19-41 showed higher activity than P1-41 and was comparable to urine CD59. Residues 19-41 were further divided into two portions: P20-25 which consisted of residues 20-25 and P27-38 which consisted of residues 27-38. Although their activities were significantly less than the activity of P19-41, P27-38 showed higher activity than P20-25. Residues 27-38 were further divided into three portions: P27-32 which consisted of residues 27-32, P30-34 which consisted of residues 30-34 and P33-38 which consisted of residues 33-38. When these peptides were assayed for the activities, all of them showed significant activities, even though they needed 10-fold more concentrations than P19-41. These data suggest that the portion made up of residues 27-38 is the active site constituting the binding site to C8 and C9.

Amino Acid Sequence↗
PubMed1995

Purification and characterization of a novel glycoprotein which has significant homology to heavy chains of inter-alpha-trypsin inhibitor family from human plasma.

Plasmapheresis with a dextran sulfate column is a treatment for patients with hypercholesteremia. When proteins bound to the column during the treatment were fractionated to prepare some known proteins, we found a 57 kDa glycoprotein designated GP57 which showed a new N-terminal amino acid sequence. Western-blot analysis of human plasma revealed that only a 120 kDa protein, GP120, reacted with anti-GP57 antibody. Since GP120 and GP57 had an identical N-terminal amino acid sequence, GP120 is probably the intact form of GP57. The isoelectric point of GP120 was 6.8. N-Glycanase treatment decreased the molecular weight of GP120 by 15 kDa. Neuraminidase and O-glycanase, however, did not affect the molecular weight. Amino acid sequence analyses of the lysylendopeptidase digest of GP120 revealed significant homology to the heavy chains of inter-alpha-trypsin inhibitor (ITI) family. Since GP120 showed no bikunin sequence, and chondroitinase treatment and alkaline treatment of GP120 did not affect its molecular weight, we concluded that GP120 was not a complex with bikunin. We designated GP120 as IHRP (ITI heavy chain-related protein).

Alpha-Globulins↗
PubMed1995

G10BP, an E1A-inducible negative regulator of Sp1, represses transcription of the rat fibronectin gene.

Downregulation of the fibronectin (FN) gene in a rat 3Y1 derivative cell line, XhoC, transformed by the adenovirus E1A and E1B genes seems to be caused by the induction of a negative regulator, G10BP, which binds to three G-rich sequences in the promoter (T. Nakamura, T. Nakajima, S. Tsunoda, S. Nakada, K. Oda, H. Tsurui, and A. Wada, J. Virol. 66:6436-6450, 1992). These are the G10 stretch and two GC boxes consisting of the G10 stretch with one internal C residue insertion. The recognition sequences of G10BP and Sp1 (GGGCGG) overlap in these GC boxes. To analyze the mechanism of the downregulation, G10BP was purified by DNA affinity chromatography, and its molecular mass was estimated to be about 30 kDa. The promoter was modified by substituting the sequence GGGG with ATCC or CTTA in these G-rich sequences, leaving the Sp1 motif intact, and by replacing the Sp1 motif by the T stretch. Transcription of FN promoter-chloramphenicol acetyltransferase fusion genes carrying the base substitution in one or more of these G-rich sequences both in vivo and in vitro revealed that the base substitution in any G-rich sequence results in reduction of promoter activity, although the downstream GC box (GCd) plays a primary role. The addition of G10BP severely inhibited the activities of the FN promoters carrying the wild-type GCd in vitro, while the promoters carrying the mutant GCd were unaffected. The binding affinity of G10BP and Sp1 to each of the G-rich sequences, analyzed by gel shift assays, indicated that G10BP binds strongly to the GCd, moderately to the G10 stretch, and weakly to GCu, while Sp1 binds strongly to GCu, moderately to GCd, and weakly to the G10 stretch. Sp1 binding to GCd and the G10 stretch was inhibited by G10BP, while binding to GCu was unaffected. These results indicate that FN gene transcription is inhibited in XhoC cells primarily by exclusion of Sp1 binding to GCd by G10BP and that G10BP is a new class of Sp1 negative regulator.

Adenovirus E1A Proteins↗
PubMed1993

Determination of carboxyl-terminal residue and disulfide bonds of MACIF (CD59), a glycosyl-phosphatidylinositol-anchored membrane protein.

MACIF (CD59) is a glycosyl-phosphatidylinositol (GPI)-anchored membrane glycoprotein which inhibits the formation of membrane attack complex of human complement. MACIF prepared from human erythrocyte membranes was digested with pronase. When the digest was subjected to two-phase partition with butanol and 0.1 N HCl, the carboxyl-terminal peptide was recovered in the butanol phase because of the attachment of the highly hydrophobic GPI. The amino acid sequence of the peptide was determined to be Asn72 at its amino-terminus and up to Glu76, while the presence of Asn77 was ambiguous. To allow unequivocal determination of the carboxyl-terminus, a soluble form of MACIF was prepared from human urine on a large scale. The carboxyl-terminal peptide from the soluble form was prepared by tryptic digestion followed by reversed-phase HPLC. The sequence and composition of the peptide unequivocally revealed Asn77 as the carboxyl-terminus. The pattern of disulfide bonds of MACIF was also determined with the membrane form as well as the soluble form. Cystine-containing peptides were prepared by chymotryptic and tryptic digestion, purified by HPLC, and their amino acid sequences were determined. The results indicated that disulfide bonds were formed at Cys3-Cys26, Cys6-Cys13, Cys19-Cys39, Cys45-Cys63 (or 64), and Cys63 (or 64)-Cys69.

Amino Acid Sequence↗
PubMed1991

Tetrasomy 8 in acute myelomonocytic leukemia developing after a gastric cancer operation.

A 70 year-old-Japanese man underwent gastrectomy for early gastric cancer with preoperative hypocellular marrow. Three weeks later, acute myelomonocytic leukemia developed with tetrasomy for chromosome 8 (48,XY,+8,+8). The patient died of leukemia on the 33rd postoperative day. Whether or not the operation triggered the leukemia remains unknown.

Adenocarcinoma↗
PubMed1989

Molecular cloning and characterization of MACIF, an inhibitor of membrane channel formation of complement.

Human erythrocytes contain a membrane protein, MACIF, which inhibits the formation of a membrane attack complex (MAC) of complement. We have cloned and sequenced the complementary DNA of MACIF messenger RNA. The amino acid sequence predicted from its nucleotide sequence consists of 128 amino acids. The amino-terminal 25 residues may correspond to a signal peptide. The carboxy-terminal sequence confirmed that MACIF is a glycosylphosphatidylinositol (GPI)-anchored protein. The amino acid sequence of MACIF was partially determined by established techniques for protein chemistry and the resultant sequence was consistent with that predicted from the nucleotide sequence. The results of sequence analyses also suggested that asparagine at the 18th position was N-glycosylated. When mRNA obtained from the MACIF cDNA clone with SP6 RNA polymerase was microinjected into Xenopus oocytes, the oocytes synthesized a product which exhibited MACIF activity and reacted with anti-MACIF antibody. Comparison of the predicted sequence revealed significant homology with mouse Ly-6 antigens.

Amino Acid Sequence↗
PubMed1986

Changes in QT interval during exercise testing in patients with VVI pacemakers.

The changes in QT intervals were studied in nine patients with normal sinus node function who had VVI pacemakers. Though PP intervals uniformly shortened during exercise, the change in QaT* intervals during exercise was variable. The correlation between PP and QaT intervals varied from case to case. A good correlation was found in only two cases (r = +0.816 or +0.897); a fair correlation was found in four cases (r = +0.672, +0.615, +0.615, or -0.669) and in the remaining three, the correlation was poor (r = +0.494, +0.467 or -0.424). In patients who are candidates for VTI pacemaker implantation, changes in QaT intervals should be assessed during exercise stress testing to determine if the intervals shorten during exercise or not.

Adult↗
PubMed1985

Ventricular arrhythmia with postural dependency.

Ventricular arrhythmias associated with recumbency were noted in a 17-year-old man with mild idiopathic myocarditis. These arrhythmias were refractory to several anti-arrhythmic drugs. Frequent ventricular arrhythmias were reproducibly recorded in the supine position and in a 15 degree tilt from the horizontal, while they were completely abolished in positions tilted more than 30 degrees from the horizontal, at which time sinus rate increased to more than 70 beats/min. The ventricular arrhythmias were suppressed during treadmill exercise and markedly aggravated when the underlying sinus rate was decreased during sleep or lying flat in bed. The arrhythmias were entirely abolished by atropine 1 mg. Furthermore, they were suppressed during atrial pacing at the rates of 80 and 90 bpm. Ventricular tachycardia could not be induced by programmed right ventricular stimulation. The appearance of postural arrhythmias in this patient correlated with relative bradycardia suggesting that they may be related to enhanced vagal nerve activity.

Adolescent↗
PubMed1985

Sudden nocturnal death in young males from ventricular flutter.

Two young males who had no organic heart disease died unexpectedly during the night. In one patient, the monitor ECG showed a sinoatrial block and the electrophysiologic study revealed a sinoatrial conduction time at the upper limit of normal and a prolonged PA interval. The surface ECG showed left axis deviation. Ventricular ectopic beats were confined to the night when he died from ventricular flutter. The ECG of the other patient was normal except for the change in QRS configuration found when the preceding RR interval was prolonged, suggesting a phase 4 block in intraventricular conduction. He was completely free from arrhythmia except for the ventricular ectopic beats which developed around 9:00 p.m. and the ventricular flutter following an R-on-T type ventricular ectopic beat which resulted in death during the night. The autopsy showed no organic heart disease. ST elevation suggestive of acute ischemia was not found and the QT intervals were normal in both cases. No electrolyte imbalances were found. These 2 cases can be diagnosed as pokkuri disease which is well known in Japan. The victims are exclusively young males who have no apparent diseases to which death can be attributed.

Adult↗
PubMed1985

Diurnal variation of QT interval in patients with VVI pacemaker.

In nine patients with chronically implanted ventricular pacemaker (VVI), diurnal variation of the QT interval was studied. The mean age of the patients was 74.2 years and underlying diseases were atrioventricular block (three patients), sick sinus syndrome (four patients) and chronic atrial fibrillation with bradycardia and heart failure (two patients). Eight of the nine patients showed longer QT intervals during sleep than during waking. Only one patient showed no change in QT interval during sleep and during wake time. The mean QT interval of the nine patients at each hour was slightly longer (9 msec) during sleep than that during each awake hour (p less than 0.001). The prolongation of QT interval during sleep may offer a possible mechanism of some nocturnal arrhythmias.

Aged↗
PubMed1984

Hemolytic anemia in hereditary pyrimidine 5'-nucleotidase deficiency. II. Effect of pyrimidine nucleotides and their derivatives on glycolytic and pentose phosphate shunt enzyme activity.

We evaluated the glycolytic intermediate concentrations from the erythrocytes of a patient with hereditary pyrimidine 5'-nucleotidase (P5'N) deficiency. Conclusive evidence for a metabolic block was not found. We evaluated the effects of the pyrimidine (cytidine and uridine) tri- and diphosphate nucleotides (CTP, CDP, UTP, UDP) and the choline and ethanolamine derivatives of CDP (CDP-choline, CDP-ethanolamine) on the activities of key enzymes of the Embden-Meyerhof pathway. CTP and UTP inhibited fructose-6-phosphate competitively for phosphofructokinase and phosphoenolpyruvate competitively for pyruvate kinase. In both cases, the Ki of the pyrimidine nucleotide and Km of the glycolytic substrate were above their intraerythrocytic concentrations. CTP was a competitive inhibitor of ADP for pyruvate kinase with a Ki near its intraerythrocytic concentration. CDP-choline and CDP-ethanolamine had no effect on the activities of Embden-Meyerhof or pentose phosphate shunt enzymes. Thus, the nature of the hemolytic anemia in hereditary P5'N deficiency remains enigmatic.

5'-Nucleotidase↗