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K Saigo

Publications and source records attributed to K Saigo.

At least 73 records · Page 4Linked to original sources
PubMed1998

[Acute transformation of chronic myelomonocytic leukemia with t(1;3) (p36;q21) abnormality].

A 66-year-old man was given a peripheral blood test because of low grade fever. Leukocytosis was detected, and the blood and bone marrow findings were consistent with those of chronic myelomonocytic leukemia. Three months later the hematological findings were: WBC 58,800/microliter (19% blastoid cells, 22% monocytes), Hb 9.0 g/dl, and a platelet count of 116 x 10(4)/microliters. A bone marrow examination revealed the presence of 52.6% blastoid cells and dysmegakaryocytopoiesis, including micromegakaryocytes. Serum and urinary lysozyme levels were elevated. Karyotypic analysis detected t(1; 3) (p36;q21), but not major bcr/abl mRNA. The patient was given a diagnosis of acute transformation of chronic myelomonocytic leukemia. Despite treatment, he died about 3 months later. t(1;3) is occasionally observed in cases of myelodysplastic syndrome (MDS) and leukemia. Patients with t(1;3) often exhibit dysmegakaryocytopoiesis; furthermore, acute leukemia develops more readily in those who also have MDS. Cases of long-term survival are rare.

Aged↗
PubMed1997

Still life, a protein in synaptic terminals of Drosophila homologous to GDP-GTP exchangers.

The morphology of axon terminals changes with differentiation into mature synapses. A molecule that might regulate this process was identified by a screen of Drosophila mutants for abnormal motor activities. The still life (sif) gene encodes a protein homologous to guanine nucleotide exchange factors, which convert Rho-like guanosine triphosphatases (GTPases) from a guanosine diphosphate-bound inactive state to a guanosine triphosphate-bound active state. The SIF proteins are found adjacent to the plasma membrane of synaptic terminals. Expression of a truncated SIF protein resulted in defects in neuronal morphology and induced membrane ruffling with altered actin localization in human KB cells. Thus, SIF proteins may regulate synaptic differentiation through the organization of the actin cytoskeleton by activating Rho-like GTPases.

Actins↗
PubMed1997

Identification of hepatitis B virus integration in hepatitis C virus-infected hepatocellular carcinoma tissues.

BACKGROUND/AIMS: The integration of HBV DNA is thought to be involved in the initial stage of hepatocarcinogenesis, and it has been reported that transactivating factors encoded by the X and preS2/S genes stimulate transcription of multiple viral and cellular genes. We assessed the possible contributions of hepatitis B virus integration to the occurrence of hepatocellular carcinoma in hepatitis C virus-infected as well as in hepatitis B virus-infected patients by identifying the integrated HBV DNA sequence, and the X and preS2/S regions were further investigated in HBV DNA-integrated cases. METHODS: Southern blot hybridization for detecting HBV DNA in tumor tissues from 28 hepatocellular carcinoma patients was carried out with full-length HBV DNA, and then with X and preS2/S regions as probes. We also carried out reverse transcription-polymerase chain reaction for detecting HCV RNA to confirm hepatitis C virus-infection in liver tissues. RESULTS: Clonally integrated HBV DNA sequences were demonstrated in 16 of 28 patients (57.1%), including five HBsAg seropositive and 11 HBsAg seronegative patients. Of these 11 HBsAg seronegative patients, 10 were also positive for anti-HCV in their sera, and all nine examined cases had HCV RNA in liver. Furthermore, the X region was identified in 14 of 16 HBV DNA integrated cases (87.5%), and the preS2/S region in 6/16 (37.5%). CONCLUSIONS: The present Southern blot analysis demonstrates that clonally integrated HBV DNA sequences were identified even in hepatitis C virus-infected hepatocellular carcinoma patients at a high rate (10/18, 55.6%), and suggests that integrated hepatitis B virus, whose major component is the X gene, may play an important role in hepatocarcinogenesis in hepatitis B virus-integrated cases with and without hepatitis C virus infection.

Adult↗
PubMed1997

Requirements of DFR1/Heartless, a mesoderm-specific Drosophila FGF-receptor, for the formation of heart, visceral and somatic muscles, and ensheathing of longitudinal axon tracts in CNS.

DFR1 encodes a mesoderm-specific fibroblast growth factor receptor in Drosophila. Here, we identified and characterized a protein-null mutant of DFR1 and examined DFR1 expression in embryos using anti-DFR1 antibody. Mutant phenotypes were completely rescued by a genomic fragment from the DFR1 locus. After invagination, mesodermal cells expressing DFR1 undergo proliferation and spread out dorsally to form a monolayer beneath the ectoderm. In mutant embryos, however, the mesoderm is not capable of extending to the normal dorsal limit and consequently mesodermal cells fail to receive ectodermal signals and thus rendered incapable of differentiating into primordia for the heart, visceral and somatic muscles. DFR1 is also required for normal development of the central nervous system. The absence of DFR1 resulted in the failure of longitudinal glia to enwrap longitudinal axon tracts. DFR1 mutant phenotypes were partially mimicked by the targeted expression of activated Yan, thus demonstrating the MAP kinase pathway to be involved in differentiation of mesoderm.

Abdomen↗
PubMed1997

Transcriptional regulation of breathless FGF receptor gene by binding of TRACHEALESS/dARNT heterodimers to three central midline elements in Drosophila developing trachea.

The development of Drosophila trachea is under the control of spatially and/or quantitatively regulated activity of BREATHLESS FGF receptor, which is also essential for midline glial migration. Here, we identified the minimum enhancer region of breathless, cloned the Drosophila ARNT gene (dARNT), and showed biochemical and genetic evidence that breathless expression in developing trachea is regulated by direct interactions between TRACHEALESS/dARNT heterodimers and three central midline elements (TACGTGs) situated in the minimum enhancer region. Our results also showed that SINGLE-MINDED/dARNT heterodimers, which are essential for breathless expression in midline precursor cells, share DNA targets in common with TRACHEALESS/dARNT, indicating that two different basic helix-loop-helix-PAS protein complexes act through the same target sites in vivo.

Amino Acid Sequence↗
PubMed1997

[Analysis of mechanism of increased platelet counts during preoperative autologous blood donation].

Autologous blood transfusion is advantageous in that it eliminates the risk of transfusion-transmitted infection or complications caused by the immune reaction. Increased platelet counts after repeated phlebotomy are commonly observed. This study was carried out to clarify the mechanism of increased platelets during preoperative autologous blood donation. Eleven patients of elective surgery in which is in good preoperative condition and there is no emergency were selected for this study. Blood cell counts, platelet size distribution(PDW, MPV, P-LCR) and serum concentration of erythropoietin(EPO), interleukin-3(IL-3) and interleukin-6(IL-6)were measured. A transient increase in platelet was seen in almost patients during preoperative autologous blood donation. No marked changes in platelet size distribution and serum concentration of EPO, IL-3 and IL-6. These results suggest that increased platelet counts during preoperative autologous blood donation might be caused by some specific cytokines related to megakaryocyte differentiation such as c-MPL ligand.

Adult↗
PubMed1996

Regulation of cell-cell contacts in developing Drosophila eyes by Dsrc41, a new, close relative of vertebrate c-src.

In Drosophila, Dsrc64 is considered a unique ortholog of the vertebrate c-src; however, we show evidence to the contrary. The closest relative of vertebrate c-src so far found in Drosophila is not Dsrc64, but Dsrc41, a gene identified for the first time here. In contrast to Dsrc64, overexpression of wild-type Dsrc41 caused little or no appreciable phenotypic change in Drosophila. Both gain-of-function and dominant-negative mutations of Dsrc41 caused the formation of supernumerary R7-type neurons, suppressible by one-dose reduction of boss, sev, Ras1, or other genes involved in the Sev pathway. Dominant-negative mutant phenotypes were suppressed and enhanced, respectively, by increasing and decreasing the copy number of wild-type Dsrc41. Colocalization of Dsrc41 protein, actin fibers and DE-cadherin, and Dsrc41-dependent disorganization of actin fibers and putative adherens junctions in precluster cells suggested that Dsrc41 may be involved in the regulation of cytoskeleton organization and cell-cell contacts in developing ommatidia.

Actins↗
PubMed1996

Gene cloning, purification, and characterization of NfsB, a minor oxygen-insensitive nitroreductase from Escherichia coli, similar in biochemical properties to FRase I, the major flavin reductase in Vibrio fischeri.

nfsB, encoding a minor oxygen-insensitive nitroreductase, was isolated by PCR using primers corresponding to two amino acid sequences conserved among the major flavin reductase from Vibrio fischeri and classical nitroreductases from Salmonella typhimurium and Enterobacter cloacae. The gene product, NfsB, was purified to homogeneity from extracts of Escherichia coli cells overexpressing it. NfsB was found to be situated at 13 min on the E. coli map. Biochemical analysis indicated NfsB to be a polypeptide having a calculated molecular weight of 23,904, capable of forming a homodimer and associated tightly with FMN as a prosthetic group. Although it exhibited a lower affinity to the NfsB apoenzyme than FMN, FAD could serve as an effective substitute for FMN. It was also shown that NfsB has a broad electron acceptor specificity and is associated with a low level of the NAD(P)H-flavin oxidoreductase. The NfsB catalysis obeys the ping pong Bi-Bi mechanism. The Km value for NADH varied depending on the second substrate used.

Amino Acid Sequence↗
PubMed1996

Biochemical characterization of NfsA, the Escherichia coli major nitroreductase exhibiting a high amino acid sequence homology to Frp, a Vibrio harveyi flavin oxidoreductase.

We identified the nfsA gene, encoding the major oxygen-insensitive nitroreductase in Escherichia coli, and determined its position on the E. coli map to be 19 min. We also purified its gene product, NfsA, to homogeneity. It was suggested that NfsA is a nonglobular protein with a molecular weight of 26,799 and is associated tightly with a flavin mononucleotide. Its amino acid sequence is highly similar to that of Frp, a flavin oxidoreductase from Vibrio harveyi (B. Lei, M. Liu, S. Huang, and S.-C. Tu, J. Bacteriol. 176:3552-3558, 1994), an observation supporting the notion that E. coli nitroreductase and luminescent-bacterium flavin reductase families are intimately related in evolution. Although no appreciable sequence similarity was detected between two E. coli nitroreductases, NfsA and NfsB, NfsA exhibited a low level of the flavin reductase activity and a broad electron acceptor specificity similar to those of NfsB. NfsA reduced nitrofurazone by a ping-pong Bi-Bi mechanism possibly to generate a two-electron transfer product.

Amino Acid Sequence↗
PubMed1996

Conversion of NfsB, a minor Escherichia coli nitroreductase, to a flavin reductase similar in biochemical properties to FRase I, the major flavin reductase in Vibrio fischeri, by a single amino acid substitution.

NfsB is an oxygen-insensitive nitroreductase of Escherichia coli with significant amino acid sequence homology to the major flavin reductase (FRase I) of Vibrio fischeri. Here, we show that NfsB is convertible to an FRase I-like flavin reductase three times as active as the authentic FRase I by a single amino acid substitution in the least-conserved region.

Amino Acid Sequence↗
PubMed1996

hedgehog signaling independent of engrailed and wingless required for post-S1 neuroblast formation in Drosophila CNS.

The hedgehog gene product, secreted from engrailed-expressing neuroectoderm, is required for the formation of post-S1 neuroblasts in rows 2, 5 and 6. The hedgehog protein functions not only as a paracrine but also as an autocrine factor and its transient action on the neuroectoderm 1-2 hours (at 18 degrees C) prior to neuroblast delamination is necessary and sufficient to form normal neuroblasts. In contrast to epidermal development, hedgehog expression required for neuroblast formation is regulated by neither engrailed nor wingless. hedgehog and wingless bestow composite positional cues on the neuroectodermal regions for S2-S4 neuroblasts at virtually the same time and, consequently, post-S1 neuroblasts in different rows can acquire different positional values along the anterior-posterior axis. The average number of proneural cells for each of three eagle-positive S4-S5 neuroblasts was found to be 5-9, the same for S1 NBs. As with wingless (Chu-LaGraff et al., Neuron 15, 1041-1051, 1995), huckebein expression in putative proneural regions for certain post-S1 neuroblasts is under the control of hedgehog. hedgehog and wingless are involved in separate, parallel pathways and loss of either is compensated for by the other in NB 7-3 formation. NBs 6-4 and 7-3, arising from the engrailed domain, were also found to be specified by the differential expression of two homeobox genes, gooseberry-distal and engrailed.

Animals↗
PubMed1996

eagle, a member of the steroid receptor gene superfamily, is expressed in a subset of neuroblasts and regulates the fate of their putative progeny in the Drosophila CNS.

We isolated and characterized the eagle gene, encoding a member of the steroid receptor superfamily in Drosophila. In the central nervous system eagle RNA was expressed in a limited number of cells. During stages 10 and 11, eagle RNA expression was observed in four neuroblasts, NB2-4, NB3-3, NB6-4 and NB7-3. Except for NB6-4, eagle RNA expression reached a maximum at the very beginning of expression or in the period of neuroblast delamination. Weak eagle RNA expression was also observed in a few putative progeny of NB7-3 during stages, late 11 and 12. All eagle RNA in abdominal segments disappeared at stage 13. Using an eagle-kinesin-lacZ fusion gene as a reporter, the division, migration, and axonogenesis in eagle-positive cells and their derivatives were examined. At stage 14, several types of neural or glial cells were detected which include EG and EW interneurons joining to the anterior and posterior commissures, respectively. Lack of eagle expression caused altered axonogenesis in an appreciable fraction of eagle-Kinesin-LacZ-positive neurons. Some EG cells failed to acquire the neural fate or underwent an extremely delayed differentiation, while EW neurons produced neurites in abnormal directions, suggesting that eagle may play a critical role in development of the progeny of eagle-positive neuroblasts.

Amino Acid Sequence↗
PubMed1995

Molecular cloning of a fish gene encoding a novel seven-transmembrane receptor related distantly to catecholamine, histamine, and serotonin receptors.

A genomic DNA fragment encoding a G protein-coupled seven-transmembrane receptor was isolated from Medaka fish, Oryzias latipes. The encoded protein is similar in sequence to other receptors including catecholamine, histamine and serotonin receptors. However, the similarity is much lower than those among members of these receptor subfamilies, thus suggesting this seven-transmembrane receptor to be an orphan receptor whose ligand has not yet been identified. Genomic Southern blot analysis suggested that the fish genome contains additional receptor genes related to the isolated gene, indicating that this novel receptor, possibly with its related receptors, might constitute a novel subfamily of the seven-transmembrane receptor superfamily.

Amino Acid Sequence↗
PubMed1995

An intragenic tandem duplication of genomic DNA is responsible for the f3N mutation of Drosophila melanogaster.

Among the numerous X chromosome-linked forked bristle (f) mutations described in Drosophila melanogaster, one designated f3N exhibits the unusual property of reverting spontaneously to wild type at an inordinate frequency, a frequency that can be increased with x-ray irradiation. In contrast to the f mutants described thus far, all of which are associated with the insertion of mobile DNA elements, f3N is associated with an intragenic duplication of 2.8 kb of genomic DNA that resolves to the normal sequence when reversions occur. Consideration is given to intrachromosomal recombination as the mechanism of reversion and truncation of the forked protein as a cause for the mutant phenotype.

Amino Acid Sequence↗
PubMed1995

Cloning of cDNA and genomic DNA encoding fibroblast growth factor receptor-4 of Xenopus laevis.

We have isolated and characterized the cDNA and genomic DNA encoding fibroblast growth factor receptor-4 of Xenopus laevis (XFGFR-4). The gene encompassing the total coding sequence spans about 10 kb, consists of 17 exons, and has an organization very similar to those of mammalian genes encoding FGFR-1 and -2, except that the XFGFR-4 gene does not contain an alternative exon for the third immunoglobulin-like domain nor an internal poly(A)-addition site. Thus, XFGFR-4 appears not to generate multiple forms of mRNA, as are identified for the mammalian FGFR-1, -2 and -3 genes. The amino-acid sequence of XFGFR-4 shows high homology to other vertebrate FGFR-4 species, but the similarity was significantly lower than in the cases of FGFR-1 and -2. Northern blot analysis showed the XFGFR-4 mRNA to occur throughout X. laevis early embryogenesis in a profile different from those of X. laevis FGFR-1 and -2.

Amino Acid Sequence↗
PubMed1995

[Hematologic improvement by alpha-interferon in a case of the 5q- syndrome with basophilia and eosinophilia].

An 82-year-old female was diagnosed as having 5q- syndrome accompanied by basophilia, eosinophilia and thrombocytosis. Since cytogenetic abnormalities other than 5q- were also detected, she was considered to be type B of 5q- syndrome. According to the FAB classification a diagnosis of refractory anemia with excess of blasts (RAEB) was made. She was treated with recombinant interferon alpha 2b, because peripheral blood findings resembled those of chronic myelogenous leukemia. Interferon was effective, and resulted in disappearance of peripheral blasts, normalization of platelet numbers, and improvement of basophilia. These changes were interferon-dependent. After 1 year, cytogenetic studies revealed that about 2/3 of metaphases showed normal karyotype. Twenty months after diagnosis, myeloid blastic crisis occurred and eventually the patient died. However, treatment with interferon in this case might support the usefulness of the drugs for this kind of disease.

Aged↗
PubMed1995

[Philadelphia chromosome-negative chronic myelogenous leukemia with trisomy 13].

Trisomy 13, as a sole karyotypic abnormality in acute leukemia, has been reported in several cases. However, in chronic myelogenous leukemia (CML), only two cases with this abnormality were reported so far. We describe herein a 68-year-old case with Philadelphia chromosome-negative CML and trisomy 13. Leukocytosis was pointed out during the treatment for other diseases. After 7 months, abrupt increase in leukocyte count (108,000/microliters) and splenomegaly developed. Decreased neutrophil alkaline phosphatase activity and morphological features fulfilled the diagnostic terms for CML. However, the karyotypic analysis revealed trisomy 13 instead of Philadelphia chromosome, and the BCR gene rearrangement was not detected. In cases with acute leukemia accompanied by trisomy 13, malignant transformation of an immature hematopoietic precursor cell has been suggested by the expression of antigens characteristic of both the myeloid and lymphoid lineage. In a few cases with myelodysplastic syndrome, a multipotent stem cell disorder, trisomy 13 has also been reported. From these standpoints, there might be a possibility that trisomy 13 as a sole abnormality in hematologic disorders would be related to tumorigenesis in the levels of multipotent stem cells.

Aged↗