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primary immunodeficiency diseases/phosphatase
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Protein tyrosyl phosphatases in T cell activation: implication for human immunodeficiency virus transcriptional activity.
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The protein tyrosine phosphatases (PTPs) superfamily is a large group of enzymes showing a wide diversity of structure and biological functions. Their implication in the regulation of signal transduction processes is critical for homeostasis and efficient cellular activation. Disturbance of the
Use of a novel human immunodeficiency virus type 1 reporter virus expressing human placental alkaline phosphatase to detect an alternative viral receptor.
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We report here on the construction and use of a novel human immunodeficiency virus (HIV) type 1 reporter vector, HIV-AP, that encodes human placental alkaline phosphatase. Upon staining with chromogenic alkaline phosphatase substrates 24 to 36 h postinfection, cells infected with HIV-AP develop an
Human immunodeficiency virus-1-tat induces matrix metalloproteinase-9 in monocytes through protein tyrosine phosphatase-mediated activation of nuclear transcription factor NF-kappaB.
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We have previously shown that human immunodeficiency virus (HIV)-1-tat induces the production of matrix metalloproteinase-9 (MMP-9) in human monocytes by a mechanism that is not understood. In the present report, we demonstrate that HIV-tat-induced expression of MMP-9 is blocked by inhibitors of
Alkaline phosphatase band-10 fraction as a possible surrogate marker for human immunodeficiency virus type 1 infection in children.
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We report the utility of a possible lymphocyte fraction of alkaline phosphatase (ALP band-10) activity in serum to predict human immunodeficiency virus type 1 (HIV-1) infection in children born to HIV-1-seropositive mothers. The presence of ALP band 10 in serum consistently correlated with HIV-1
Human immunodeficiency virus type 1 Vpr-mediated G(2) cell cycle arrest: Vpr interferes with cell cycle signaling cascades by interacting with the B subunit of serine/threonine protein phosphatase 2A.
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The Vpr protein of primate lentiviruses arrests cell cycling at the G(2)/M phase through an inactivation of cyclin B-p34(cdc2) and its upstream regulator cdc25. We provide here biochemical and functional evidence demonstrating that human immunodeficiency virus type 1 (HIV-1) Vpr mediates G(2) arrest
Value of liver biopsy for the rapid diagnosis of infection in human immunodeficiency virus-infected patients who have unexplained fever and elevated serum levels of alkaline phosphatase or gamma-glutamyl transferase.
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We prospectively determined the value of liver biopsy for microbiological diagnosis of infection in patients infected with the human immunodeficiency virus (HIV) who had unexplained fever and whose serum levels of alkaline phosphatase or gamma-glutamyl transferase were at least 1.5 times the upper
Induction of nuclear factor-kappa B and the human immunodeficiency virus long terminal repeat by okadaic acid, a specific inhibitor of phosphatases 1 and 2A.
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We have used a specific phosphatase inhibitor, okadaic acid, to examine the role of two phosphatases, PP1 and PP2A, in the induction of NF-kappa B and the long terminal repeat of the human immunodeficiency virus type 1 (HIV-LTR). Treatment of Jurkat cells with okadaic acid induced NF-kappa B in
Autoimmunity in primary antibody deficiency is associated with protein tyrosine phosphatase nonreceptor type 22 (PTPN22).
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BACKGROUND
The 1858T allele of protein tyrosine phosphatase nonreceptor type 22 (PTPN22; R620W) exhibits one of the strongest and most consistent associations with sporadic autoimmune disease. Although autoimmunity is common in patients with primary antibody deficiency (PAD), it remains unknown
Protein phosphatase 2A enhances activation of human immunodeficiency virus type 1 by phorbol myristate acetate.
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The viral replication rate in patients infected with human immunodeficiency virus type 1 (HIV-1) is controlled in part by regulation of the transcription of viral genes. The rate of transcription is determined by a complex interplay between cellular and viral proteins and the promoter elements found
Mutations in the tyrosine phosphatase CD45 gene in a child with severe combined immunodeficiency disease.
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The hematopoietic-specific transmembrane protein tyrosine phosphatase CD45 functions to regulate Src kinases required for T- and B-cell antigen receptor signal transduction. So far, there have been no reports to our knowledge of a human deficiency in a tyrosine-specific phosphatase. Here, we
Phosphatase and tensin homolog (PTEN) mutation can cause activated phosphatidylinositol 3-kinase δ syndrome-like immunodeficiency.
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Activated phosphatidylinositol 3-kinase δ syndrome (APDS) is a recently discovered primary immunodeficiency disease (PID). Excess phosphatidylinositol 3-kinase (PI3K) activity linked to mutations in 2 PI3K genes, PIK3CD and PIK3R1, causes APDS through hyperphosphorylation of AKT, mammalian target of
A protein phosphatase from human T cells augments tat transactivation of the human immunodeficiency virus type 1 long-terminal repeat.
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HIV-1 Tat protein regulates viral gene expression by modulating the activity and association of cellular transcription factors with RNA polymerase II (RNAPII). Possible mechanisms include Tat-associated protein kinase(s) and phosphatase(s) that regulate phosphorylation of the C-terminal domain (CTD)
Alkaline phosphatase in the developing bursa of Fabricius. A comparative study of the cyclophosphamide- and testosterone-induced immunodeficiencies in the chick embryo.
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The ontogeny of alkaline phosphatase in the bursa of Fabricius was studied by histochemical and biochemical methods. According to the quantitative determinations, the activity of alkaline phosphatase increased from the 11th to 17th day of incubation--that is, during the time of the lymphoid follicle
A deletion mutation of the protein tyrosine phosphatase kappa (Ptprk) gene is responsible for T-helper immunodeficiency (thid) in the LEC rat.
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Bone marrow (BM)-derived T-cell progenitors differentiate into CD4 or CD8 single-positive (SP) cells in the thymus. We have previously reported that a single autosomal mutation, thid, causes a defect in the maturation of CD4 SP thymocytes and an abnormality of peripheral helper T cells in the LEC
Human immunodeficiency virus type 1 Vpr-mediated G(2) cell cycle arrest: Vpr interferes with cell cycle signaling cascades by interacting with the B subunit of serine/threonine protein phosphatase 2A.
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