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B W Wren - One of the best experts on this subject based on the ideXlab platform.
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a family of clostridial and streptococcal ligand binding proteins with conserved c Terminal Repeat Sequences
Molecular Microbiology, 1991Co-Authors: B W WrenAbstract:Summary Analysis of the derived amino acid Sequences of toxins A and B from Clostridium difficile has identified an extraordinarily large number of Repeat amino acid units in the C-Terminal regions of the proteins. Nearly one third of each of the proteins consist of Repeating units which appear, at least in the case of toxin A, to be responsible for carbohydrate binding. Similar Repeat units are also found in the C-Terminal region of four glucosyltransferases from Streptococcus mutans and Streptococcus downel, and in four lytic enzymes from Streptococcus pneumoniae and its bacteriophages (HB-3, Cp-1 and Cp-9). In each case the Repeats constitute the ligand-binding portion of the respective enzymes. A glucan-binding protein from S. mutans, which lacks enzymatic activity, has similar Repeats spanning almost the entire molecule. This family of ligand-binding proteins appears to be of modular design, with one module consisting of a repetitive ligand-binding domain located in the C-Terminal region and the other module(s) providing enzymatic functions.
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A family of clostridial and streptococcal ligand‐binding proteins with conserved C‐Terminal Repeat Sequences
Molecular Microbiology, 1991Co-Authors: B W WrenAbstract:Summary Analysis of the derived amino acid Sequences of toxins A and B from Clostridium difficile has identified an extraordinarily large number of Repeat amino acid units in the C-Terminal regions of the proteins. Nearly one third of each of the proteins consist of Repeating units which appear, at least in the case of toxin A, to be responsible for carbohydrate binding. Similar Repeat units are also found in the C-Terminal region of four glucosyltransferases from Streptococcus mutans and Streptococcus downel, and in four lytic enzymes from Streptococcus pneumoniae and its bacteriophages (HB-3, Cp-1 and Cp-9). In each case the Repeats constitute the ligand-binding portion of the respective enzymes. A glucan-binding protein from S. mutans, which lacks enzymatic activity, has similar Repeats spanning almost the entire molecule. This family of ligand-binding proteins appears to be of modular design, with one module consisting of a repetitive ligand-binding domain located in the C-Terminal region and the other module(s) providing enzymatic functions.
Paul R Gorry - One of the best experts on this subject based on the ideXlab platform.
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transcriptional activity of blood and cerebrospinal fluid derived nef long Terminal Repeat Sequences isolated from a slow progressor infected with nef deleted human immunodeficiency virus type 1 hiv 1 who developed hiv associated dementia
Journal of NeuroVirology, 2006Co-Authors: Melissa J Churchill, Damian F. J. Purcell, John S Sullivan, Steven Lodewyk Wesselingh, Anna Figueiredo, Daniel Cowley, Dale A. Mcphee, Bruce J. Brew, Lachlan Robert Gray, Paul R GorryAbstract:The authors studied the transcriptional activity of blood- and cerebrospinal fluid (CSF)-derived nef/long-Terminal Repeat (LTR) Sequences isolated from a slow progressor infected with nef-deleted human immunodeficiency virus type 1 (HIV-1) who developed HIV-associated dementia (HIVD). The transcriptional activity of CSF-derived nef/LTR clones isolated during HIVD was up to 4.5-fold higher than blood-derived clones isolated before and during HIVD when tested under basal, phorbol 12-myristate 13-acetate-(PMA−), and Tat-activated conditions, and was associated with the presence of duplicated nuclear factor (NF)-κB and specificity factor-1 (Sp-1) binding sites coupled with a truncated nef sequence, increased replication capacity, and high CSF viral load. Thus, nef and LTR mutations that augment transcription may contribute to neuropathogenesis of nef-deleted HIV-1.
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Transcriptional activity of blood- and cerebrospinal fluid-derived nef/long-Terminal Repeat Sequences isolated from a slow progressor infected with nef-deleted human immunodeficiency virus type 1 (HIV-1) who developed HIV-associated dementia
Journal of NeuroVirology, 2006Co-Authors: Melissa J Churchill, Damian F. J. Purcell, John S Sullivan, Anna Figueiredo, Daniel Cowley, Lachlan Gray, Dale A. Mcphee, Steven L. Wesselingh, Bruce J. Brew, Paul R GorryAbstract:The authors studied the transcriptional activity of blood- and cerebrospinal fluid (CSF)-derived nef /long-Terminal Repeat (LTR) Sequences isolated from a slow progressor infected with nef -deleted human immunodeficiency virus type 1 (HIV-1) who developed HIV-associated dementia (HIVD). The transcriptional activity of CSF-derived nef /LTR clones isolated during HIVD was up to 4.5-fold higher than blood-derived clones isolated before and during HIVD when tested under basal, phorbol 12-myristate 13-acetate-(PMA−), and Tat-activated conditions, and was associated with the presence of duplicated nuclear factor (NF)-κB and specificity factor-1 (Sp-1) binding sites coupled with a truncated nef sequence, increased replication capacity, and high CSF viral load. Thus, nef and LTR mutations that augment transcription may contribute to neuropathogenesis of nef -deleted HIV-1.
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longitudinal analysis of human immunodeficiency virus type 1 nef long Terminal Repeat Sequences in a cohort of long term survivors infected from a single source
Journal of Virology, 2006Co-Authors: Melissa J Churchill, David I Rhodes, Jennifer Learmont, John S Sullivan, Steven Lodewyk Wesselingh, Ian Cooke, Nicholas J Deacon, Paul R GorryAbstract:We studied the evolution of human immunodeficiency virus type 1 (HIV-1) in a cohort of long-term survivors infected with an attenuated strain of HIV-1 acquired from a single source. Although the cohort members experienced differing clinical courses, we demonstrate similar evolution of HIV-1 nef/long-Terminal Repeat (LTR) Sequences, characterized by progressive sequence deletions tending toward a minimal nef/LTR structure that retains only sequence elements required for viral replication. The in vivo pathogenicity of attenuated HIV-1 is therefore dictated by viral and/or host factors other than those that impose a unidirectional selection pressure on the nef/LTR region of the HIV-1 genome.
Demetrios A. Spandidos - One of the best experts on this subject based on the ideXlab platform.
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Transcriptional activation of the human immunodeficiency virus long Terminal Repeat Sequences by retinoic acid in human epithelial and fibroblast tumor cell lines.
The International Journal of Biological Markers, 1996Co-Authors: Vassilis Zoumpourlis, M. Ergazaki, Demetrios A. SpandidosAbstract:We employed a recombinant plasmid, pBHIV1, carrying the long Terminal Repeat (LTR) Sequences of HIV-1, linked to the reporter chloramphenicol acetyl transferase (CAT) gene and to the aminoglycoside phosphotransferase (aph) gene as a selectable marker. We introduced pBHIV1 into human epithelial and fibroblast tumor cell lines (HeLa and MRCSV40TGR), and obtained stable geneticin-resistant HLHIVI-A and SVTGHIVI-A cells, respectively. The response to the retinoic acid was studied on the LTR regulated CAT activity in both cell lines. It was found that retinoic acid at a concentration of 1x10 -5 effects a 3.2 - fold increase in CAT expression compared to HIV LTR in HLHIV1-A, but requires a concentration of 5x10 -5 M to enhance this expression 4.6-fold in SVTGHIV1-A cells. These data show that retinoic acid may play a critical role in HIV-1 expression in human epithelial and fibroblast cell lines.
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Mitomycin C stimulates the expression of human immunodeficiency virus long Terminal Repeat Sequences in rat and human fibroblasts.
Biochemical Pharmacology, 1993Co-Authors: Vassilis Zoumpourlis, Demetrios A. SpandidosAbstract:Abstract We have employed a recombinant plasmid, pBHIVl, carrying the long Terminal Repeat (LTR) Sequences of the human immunodeficiency virus-1 (HIV-1) linked to the reporter chloramphenicol acetyl transferase (CAT) gene and to the aminoglycoside phospnotransferase ( aph ) gene as a selectable marker. We have introduced pBHIV1 into rat 208F and human MRCSV40TGR fibroblasts and obtained stable geneticin resistant RFBHIV1-1 and SVTGHIV1-1 cells, respectively. Both transfectant cells express CAT activity from the HIV LTR promoter. The response to the antineoplastic drug mitomycin C was studied on the LTR regulated CAT activity in both cell lines. It was found that mitomycin C at 10 μg/mL concentration stimulates the expression of CAT from the HIV LTR 77-fold in rat RFBHIV1-1 and 3.1-fold in human SVTGHIV1-1 cells.
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Transcriptional activation of the human immunodeficiency virus long Terminal Repeat Sequences by tumor necrosis factor.
Anticancer research, 1992Co-Authors: Vassilis Zoumpourlis, A. G. Eliopoulos, Demetrios A. SpandidosAbstract:The recombinant plasmid pBHIV-1 carrying the long Terminal Repeat (LTR) of the human immunodeficiency virus 1 (HIV-I), linked to the reporter chloramphenicol acetyl transferase (CAT) gene, was introduced into human and rat fibroblasts. Stable transfectants were obtained which were resistant to geneticin and expressed CAT-activity from the HIV-1 LTR. The response to TNFα was studied. It was found that, at the optimum concentration of 100 IU/ml in human and 1000 IU/ml in rat fibroblasts, the expression of CAT was stimulated by 2.1 and 2.5-fold respectively
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Hexamethylene bisacetamide stimulates the expression of human immunodeficiency virus long Terminal Repeat Sequences in rat and human fibroblasts.
Anti-Cancer Drugs, 1992Co-Authors: Zoumpourlis, Demetrios A. SpandidosAbstract:We have employed a recombinant plasmid, pBHIV1, carrying the long Terminal Repeat (LTR) sequence of the human immunodeficiency virus-1 (HIV-1) linked to the reporter chloramphenicol acetyl transferase (CAT) gene and to the aminoglycoside phosphotransferase (aph) gene as a selectable marker. We have introduced pBHIV1 in rat 208F and human MRCSV40TGR fibroblasts and obtained stable geneticin resistant RFBHIV1-1 and SVTGHIV1-1 cells, respectively. Both transfectant cells express CAT activity from the HIV LTR promoter. The response to anti-neoplastic drug hexamethylene bisacetamide (HMBA) was studied on the LTR regulated CAT activity in both cell lines. It was found that HMBA at 5mM concentration stimulates the expression of CAT from the HIV LTR in rat and human cells by 28- and 1.9-fold, respectively.
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Carboplatin as opposed to cisplatin does not stimulate the expression of the human immunodeficiency virus long Terminal Repeat Sequences.
Biochemical Pharmacology, 1992Co-Authors: Vassilis Zoumpourlis, David J. Kerr, Demetrios A. SpandidosAbstract:The recombinant plasmid pBHIV1 carrying the long Terminal Repeat (LTR) of the human immunodeficiency virus 1 (HIV-1), linked to the chloramphenicol acetyl transferase (CAT) gene, was introduced into human and rat fibroblasts. Stable transfectants resistant to geneticin expressed CAT activity from the HIV-1 LTR. It was found that the cytotoxic drug cis-diammine(1,1-cyclobutanedicarboxylato)platinum(II) (carboplatin) at concentrations from 1 x 10(-6) to 1 x 10(-4) M does not stimulate the expression of CAT from the HIV-1 LTR. These results differ from previous studies with the related drug cis-diamminedichloroplatinum(II) which showed stimulation of gene expression from the HIV-1 LTR and suggest that carboplatin could be used in the treatment of cancer patients with Acquired Immune Deficiency Syndrome.
Ana Carolina Paulo Vicente - One of the best experts on this subject based on the ideXlab platform.
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htlv 1a tax gene and long Terminal Repeat Sequences from argentinean strains reveal disagreement with tax restriction fragment length polymorphism subtyping
AIDS Research and Human Retroviruses, 2007Co-Authors: Alena Mayo Iniguez, Koko Otsuki, Rene Gastaldello, Sandra Gallego, Ana Carolina Paulo VicenteAbstract:Sequence and cluster analysis have shown two HTLV-1a tax gene subgroups, tax A and tax B, which are related to long Terminal Repeat (LTR) molecular subtypes. On the basis of subgroup-specific nucleotide substitutions, restriction fragment length polymorphism (RFLP) analysis of the tax gene for subtyping HTLV-1a isolates was proposed. In this study we genetically characterized the tax gene from 63 HTLV-1-positive Argentinean individuals, including 14 patients with HTLV-1-associated myelopathy/tropical spastic paraparesis and 49 healthy HTLV-1 carriers. RFLP analysis showed that 48 samples yielded the tax A profile (76.19%) and that 15 samples contained the uncut tax B profile (23.81%). However, the LTR and tax sequence analysis revealed that in fact only 2 from the 15 samples belonged to the HTLV-1aB subgroup, presenting four tax B subgroup-specific nucleotide substitutions. The tax gene cluster analysis also confirmed that the majority of Argentinean strains belonged to the Transcontinental HTLV-1aA subgr...
Melissa J Churchill - One of the best experts on this subject based on the ideXlab platform.
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transcriptional activity of blood and cerebrospinal fluid derived nef long Terminal Repeat Sequences isolated from a slow progressor infected with nef deleted human immunodeficiency virus type 1 hiv 1 who developed hiv associated dementia
Journal of NeuroVirology, 2006Co-Authors: Melissa J Churchill, Damian F. J. Purcell, John S Sullivan, Steven Lodewyk Wesselingh, Anna Figueiredo, Daniel Cowley, Dale A. Mcphee, Bruce J. Brew, Lachlan Robert Gray, Paul R GorryAbstract:The authors studied the transcriptional activity of blood- and cerebrospinal fluid (CSF)-derived nef/long-Terminal Repeat (LTR) Sequences isolated from a slow progressor infected with nef-deleted human immunodeficiency virus type 1 (HIV-1) who developed HIV-associated dementia (HIVD). The transcriptional activity of CSF-derived nef/LTR clones isolated during HIVD was up to 4.5-fold higher than blood-derived clones isolated before and during HIVD when tested under basal, phorbol 12-myristate 13-acetate-(PMA−), and Tat-activated conditions, and was associated with the presence of duplicated nuclear factor (NF)-κB and specificity factor-1 (Sp-1) binding sites coupled with a truncated nef sequence, increased replication capacity, and high CSF viral load. Thus, nef and LTR mutations that augment transcription may contribute to neuropathogenesis of nef-deleted HIV-1.
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Transcriptional activity of blood- and cerebrospinal fluid-derived nef/long-Terminal Repeat Sequences isolated from a slow progressor infected with nef-deleted human immunodeficiency virus type 1 (HIV-1) who developed HIV-associated dementia
Journal of NeuroVirology, 2006Co-Authors: Melissa J Churchill, Damian F. J. Purcell, John S Sullivan, Anna Figueiredo, Daniel Cowley, Lachlan Gray, Dale A. Mcphee, Steven L. Wesselingh, Bruce J. Brew, Paul R GorryAbstract:The authors studied the transcriptional activity of blood- and cerebrospinal fluid (CSF)-derived nef /long-Terminal Repeat (LTR) Sequences isolated from a slow progressor infected with nef -deleted human immunodeficiency virus type 1 (HIV-1) who developed HIV-associated dementia (HIVD). The transcriptional activity of CSF-derived nef /LTR clones isolated during HIVD was up to 4.5-fold higher than blood-derived clones isolated before and during HIVD when tested under basal, phorbol 12-myristate 13-acetate-(PMA−), and Tat-activated conditions, and was associated with the presence of duplicated nuclear factor (NF)-κB and specificity factor-1 (Sp-1) binding sites coupled with a truncated nef sequence, increased replication capacity, and high CSF viral load. Thus, nef and LTR mutations that augment transcription may contribute to neuropathogenesis of nef -deleted HIV-1.
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longitudinal analysis of human immunodeficiency virus type 1 nef long Terminal Repeat Sequences in a cohort of long term survivors infected from a single source
Journal of Virology, 2006Co-Authors: Melissa J Churchill, David I Rhodes, Jennifer Learmont, John S Sullivan, Steven Lodewyk Wesselingh, Ian Cooke, Nicholas J Deacon, Paul R GorryAbstract:We studied the evolution of human immunodeficiency virus type 1 (HIV-1) in a cohort of long-term survivors infected with an attenuated strain of HIV-1 acquired from a single source. Although the cohort members experienced differing clinical courses, we demonstrate similar evolution of HIV-1 nef/long-Terminal Repeat (LTR) Sequences, characterized by progressive sequence deletions tending toward a minimal nef/LTR structure that retains only sequence elements required for viral replication. The in vivo pathogenicity of attenuated HIV-1 is therefore dictated by viral and/or host factors other than those that impose a unidirectional selection pressure on the nef/LTR region of the HIV-1 genome.