anemia/phosphatase

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Chicken anemia virus VP2 is a novel dual specificity protein phosphatase.

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The function of viral protein 2 (VP2) of the immunosuppressive circovirus chicken anemia virus (CAV) has not yet been established. We show that the CAV VP2 amino acid sequence has some similarity to a number of eukaryotic, receptor, protein-tyrosine phosphatase (PTPase) alpha proteins as well as to

Health status of Indochinese refugees in Japan: statistical analyses on anemia, eosinophilia and serum alkaline phosphatase.

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Detailed statistical analyses were attempted on anemia, eosinophilia and elevation in serum alkaline phosphatase in the Indochinese refugees in Japan. A high statistical correlation was found between hemoglobin concentration and hematocrit for most of the refugees except the Cambodian females.

Reduced leucocyte alkaline phosphatase activity and decreased NBT reduction test in induced iron deficiency anaemia in rabbits.

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Iron deficiency anaemia was induced in rabbits by repeated bleeding. The leucocyte alkaline phosphatase (LAP) of 26 +/- 28 units was significantly reduced compared with control values of 233 +/- 35 units (P less than 0.001). Leucocyte NBT reduction was also diminished, both in Hanks solution (P less

The PTEN phosphatase functions cooperatively with the Fanconi anemia proteins in DNA crosslink repair.

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Fanconi anemia (FA) is a genetic disease characterized by bone marrow failure and increased cancer risk. The FA proteins function primarily in DNA interstrand crosslink (ICL) repair. Here, we have examined the role of the PTEN phosphatase in this process. We have established that PTEN-deficient

Abnormal red cell membrane phosphatase activity in an unidentified congenital hemolytic anemia.

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The erythrocyte membrane contains a neutral phosphatase, which was studied with p-nitrophenyl-phosphate as the substrate. The enzyme was investigated in four members of the same family, suffering from a congenital spherocytic hemolytic anemia. Although the condition was transmitted as a dominant

Oxidative stress-associated protein tyrosine kinases and phosphatases in Fanconi anemia.

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CONCLUSIONS Fanconi anemia (FA) is a genetic disorder featuring chromosomal instability, developmental defects, progressive bone marrow failure, and predisposition to cancer. Besides the predominant role in DNA damage response and/or repair, many studies have linked FA proteins to oxidative stress.

Serum alkaline phosphatase isoenzymes in sickle cell anemia.

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Alkaline phosphatase isoenzymes in sera from patients with sickle cell anemia were separated by electrophoresis on starch gel. Physical and biochemical criteria identified bone alkaline phosphatase as the principal, although not necessarily the sole, enzyme fraction that increases during symptomatic

Mutation of chicken anemia virus VP2 differentially affects serine/threonine and tyrosine protein phosphatase activities.

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Novel dual-specificity protein phosphatases (DSPs), which catalyse the removal of phosphate from both phosphotyrosine and phosphoserine/phosphothreonine substrates, have recently been identified in two viruses within the family Circoviridae. Viral protein 2 (VP2) of chicken anemia virus (CAV) and

The critical role of SRC homology domain 2-containing tyrosine phosphatase-1 in recombinant human erythropoietin hyporesponsive anemia in chronic hemodialysis patients.

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The molecular mechanism of anemia that is hyporesponsive to recombinant human erythropoietin (rHuEPO) in hemodialysis patients without underlying causative factors has not been investigated fully in hematopoietic stem cell system. Circulating CD34+ cells (1 x 10(4)) were isolated from rHuEPO

Identification of a novel c-DNA overexpressed in Fanconi's anemia fibroblasts partially homologous to a putative L-3-phosphoserine-phosphatase.

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We applied the cDNA differential display technique (DDT) in a DNA-repair deficient cell model to isolate genes involved in dysregulation of cell proliferation and development of cancer. The comparative analysis of mRNA expression patterns of human diploid fibroblasts from Fanconi's amemia (FA) and

Deregulation of vital mitotic kinase-phosphatase signaling in hematopoietic stem/progenitor compartment leads to cellular catastrophe in experimental aplastic anemia.

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Aplastic anemia, the paradigm of bone marrow failure, is characterized by pancytopenic peripheral blood and hypoplastic bone marrow. Among various etiologies, inappropriate use of DNA alkylating drugs like cyclophosphamide and busulfan often causes the manifestation of the dreadful disease. Cell

Pituitary-adrenal axis function in sickle cell anemia and its relationship to leukocyte alkaline phosphatase.

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The function of the pituitary-adrenal axis and leukocyte alkaline phosphatase activity were evaluated in eight patients with sickle cell disease during a painful crisis and when crisis-free. The leukocyte alkaline phosphatase (LAP) score did not increase during crisis; the scores were in the

Sustained trilineage response in a patient with ALG-resistant severe aplastic anaemia after treatment with G-CSF, erythropoietin and cyclosporin A: association of recovery with marked elevation of serum alkaline phosphatase.

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Aplastic anaemia is characterized by multilineage bone marrow failure resulting in pancytopenia. We have successfully treated a young woman with severe aplastic anaemia (SAA) who was resistant to antilymphocyte globulin (ALG) and corticosteroids, with a combination therapy consisting of

Mechanisms of anemia in SHP-1 protein tyrosine phosphatase-deficient "viable motheaten" mice.

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OBJECTIVE Viable motheaten mice (abbreviated gene symbol me(v)) are deficient in SHP-1, a critical negative regulator of signal transduction in hematopoietic cells. These mice exhibit severe immune dysfunction accompanied by hyperproliferation of myeloid cells, widespread inflammatory lesions, and

Variations in the phosphatase activity in two patients with cancer of the prostate and pernicious anaemia.

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