Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It was recently reported that some strains of senescence-accelerated mouse (SAM) including SAMR1 had a spontaneous retroviral insertional mutation in the ATP-binding cassette, sub-family B, member 1A (Abcb1a) gene, while other strains including SAMP8 had not. The Abcb1 gene product, P-glycoprotein, is a representative efflux transporter of cerebral vessels. In this study, using brain samples of SAMR1, Abcb1a gene-mutant mice, and of SAMP8 without that mutation, we examined the gene expression of some representative ATP-binding cassettes, such as Abcb1a, Abcb1b, Abcc, and Abcg2, and the protein expression of P-glycoprotein by real-time quantitative reverse transcriptase-polymerase chain reaction (RT-PCR), Western blotting, and immunohistochemical techniques. The gene expression of Abcb1a was decreased in the brain samples of SAMR1 compared with those of SAMP8, while that of Abcb1b was increased in the samples of SAMR1 compared with those of SAMP8. There were no differences in the gene expression of Abcc and Abcg2 between the samples of SAMR1 and SAMP8. The protein expression of P-glycoprotein was decreased in the brain samples of SAMR1 compared with those of SAMP8. Immunosignals of P-glycoprotein were seen in vessels walls, mainly CD34-positive endothelial cells and partially astrocytic cells, in both mice. These findings indicate that SAMR1, Abcb1a-mutant mice, showed decreased expression of Abcb1a gene and P-glycoprotein and increased gene expression of Abcb1b, compared with those of SAMP8 without that mutation, suggesting no clear effect of increased gene expression of Abcb1b on decreased expression of P-glycoprotein. The combination of SAMR1 and SAMP8 may be a good tool to investigate which transporter, Abcb1a or Abcb1b, can be used in drug delivery into the brain.
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PMID:Abcb1a and Abcb1b expression in senescence-accelerated mouse (SAM). 1942 29

SAMP8, senescence-accelerated mice with age-related deficits in memory and learning, are known to show age-related increases of amyloid precursor protein (APP) expression and to be under elevated oxidative stress. The receptor for advanced glycation end product (RAGE) is a representative influx transporter of APP or amyloid-beta (A beta) protein in cerebral vessels, while low-density lipoprotein receptor (LDLR) and LDL-related protein 1 (LRP1) are efflux transporters. These receptors play roles not only in clearance of A beta protein but also in control of oxidative stress. In this study, we examined the gene and protein expressions of these receptors, by real-time quantitative reverse transcriptase-polymerase chain reaction (RT-PCR), Western blotting, and immunohistochemical techniques. SAMR1 mice with lower expression of APP were as controls. The gene and protein expressions of RAGE were lower in SAMP8 brains than in SAMR1. Those of LDLR were higher in SAMP8 brains than those of SAMR1. There were no differences in the expressions of LRP1 between SAMP8 and SAMR1. Immunosignals of RAGE and LDLR were seen in the cytoplasm of CD34-positive endothelial cells and also in astrocytes, in both strains of mice. These findings suggest that the lower expression of RAGE and the higher expression of LDLR may contribute to clearance of toxic substances and, in addition, be related to elevated oxidative stress in SAMP8 brains.
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PMID:RAGE, LDL receptor, and LRP1 expression in the brains of SAMP8. 1953 95

Mesenchymal stem cells (MSCs) have the capacity to differentiate into several cell lineages, some of which can generate bone, cartilage, or adipose tissue. The presence of MSCs in the synovial membrane was recently reported. Data from comparative studies of MSCs derived from various mesenchymal tissues suggest that MSCs from synovial membranes have a superior chondrogenesis capacity. Previous chondrogenic differentiation studies have used the total population of MSCs, including cells with several MSC markers, such as CD44, CD90, CD105, or CD73. However the chondrogenic capacity of an individual population of MSCs has not been examined. Our aim was to study the chondrogenic capacity of the cellular MSC subset, CD105(+), derived from synovial membrane tissues of patients with osteoarthritis (OA) and normal donors. The tissues were digested with a cocktail of collagenase/dispase and the isolated MSCs were seeded into plates. The subpopulation of CD105(+)-MSCs was separated using a magnetic separator. The MSCs were then differentiated towards chondrocyte-like cells using a specific medium to promote spheroid formation. Spheroids were collected after 14, 28, and 46 days in chondrogenic medium and stained with hematoxylin, eosin, Safranin O or Alcian blue to evaluate the extracellular matrix. Immunohistochemistry was performed to study collagen types I (COLI) and II (COLII) and aggrecan expression. Phenotypic characterization of the isolated CD105(+)-MSCs shows that these cells are also positive for CD90 and CD44, but negatives for CD34 and CD45. In addition, this cellular subset expressed Sox-9. Spheroids appeared after 7 days in culture in the presence of chondrogenic medium. Our studies show no differences between MSCs obtained from OA and normal synovial membranes during chondrogenesis. The morphological analysis of spheroids revealed characteristics typical of chondrocyte cells. The intensity of Safranin O, Alcian blue and aggrecan staining was positive and constant throughout the culture period. However, the intensity of COL2 staining was higher at 28 days (84.29 +/- 0.1 U) than at 46 days (61.28 +/- 01 U), while COL1 staining was not detected in any samples analyzed. These results were confirmed by reverse transcriptase-polymerase chain reaction assays. We conclude that the cellular subset of CD105(+)-MSCs has chondrogenic capacity. The study also show the similar chondrogenic capacity of CD105(+)-MSCs cultured from normal and OA synovial membranes.
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PMID:Differentiation of synovial CD-105(+) human mesenchymal stem cells into chondrocyte-like cells through spheroid formation. 1954 99

Aurora kinase A, also known as aurora A, is a serine/threonine kinase that plays critical roles in mitosis entry, chromosome alignment, segregation, and cytokinesis. Overexpression of aurora A has been observed in many solid tumors and some hematopoietic neoplasms, but little is known about its expression in myeloid diseases. Because cytogenetic abnormalities play an essential role in the pathogenesis of myeloid malignancies, we hypothesized that aurora A deregulation may be involved in myelodysplastic syndromes and acute myeloid leukemia and contribute to the chromosomal instability observed in these diseases. We assessed aurora A mRNA levels in CD34(+) bone marrow blasts from nine patients with acute myeloid leukemia, 20 patients with myelodysplastic syndromes, and five normal patients serving as controls. CD34(+) blasts were isolated from bone marrow aspirate specimens using magnetic activated cell separation technology. RNA was extracted from purified CD34(+) cells, and quantitative real-time reverse transcriptase polymerase chain reaction for aurora A was performed. Immunocytochemical analyses for total aurora A, phosphorylated aurora A, Ki-67, and activated caspase 3 were performed on cytospin slides made from purified CD34(+) cells in myelodysplastic syndrome patients using standard methods. Aurora A mRNA and protein levels were correlated, as was aurora A mRNA level, with blast counts, cytogenetic abnormalities, and International Prognostic Scoring System score. We found that CD34(+) cells in myelodysplastic syndromes and acute myeloid leukemia expressed aurora A at significantly higher levels (P = 0.01 and P = 0.01, respectively) than normal CD34(+) cells. Aurora A mRNA levels correlated with total and phosphorylated protein levels (P = 0.0002 and P = 0.02, respectively). No significant correlation was found between aurora A mRNA level and blast count, blast viability, cytogenetic abnormalities, or the International Prognostic Scoring System score in patients with myelodysplastic syndromes. We conclude that aurora A is up-regulated in CD34(+) blasts from myeloid neoplasms.
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PMID:Analysis of Aurora kinase A expression in CD34(+) blast cells isolated from patients with myelodysplastic syndromes and acute myeloid leukemia. 1966 17

Dental pulp stem cells were primarily derived from the pulp tissues of exfoliated deciduous teeth, primary incisors and permanent third molar teeth. The aim of this study was to isolate and extensively characterise SCs derived from human natal dental pulp (hNDP). For characterisation, proliferation capacity, phenotypic properties, ultrastructural and differentiation characteristics and gene expression profiles were utilised. A comparison was done between the properties of NDP-SCs and the properties of mesenchymal stem cells (MSCs) from bone marrow (BM) of the human. Stem cells isolated from hNDP and hBM were analysed by flow cytometry, reverse transcriptase-PCR, Real Time-PCR, and immunocytochemistry. Both cell lines were directionally differentiated towards adipogenic, osteogenic chondrogenic, myogenic and neurogenic lineages. hNDP-SCs and hBM-MSCs expressed CD13, CD44, CD90, CD146 and CD166, but not CD3, CD8, CD11b, CD14, CD15, CD19, CD33, CD34, CD45, CD117, and HLA-DR. Ultrastructural characteristics of hNDP-SCs showed more developed and metabolically active cells. hNDP-SCs and hBM-MSCs expressed some adipogenic (leptin, adipophilin and PPARgamma), myogenic (desmin, myogenin, myosinIIa, and alpha-SMA), neurogenic (gamma-enolase, MAP2a,b, c-fos, nestin, NF-H, NF-L, GFAP and betaIII tubulin), osteogenic (osteonectin, osteocalcin, osteopontin, Runx-2, and type I collagen) and chondrogenic (type II collagen, SOX9) markers without any stimulation towards differentiation under basal conditions. Embryonic stem cell markers Oct4, Rex-1, FoxD-3, Sox2, and Nanog were also identified. The differentiation potential of hNDP-SCs and hBM-MSCs to adipogenic, osteogenic, chondrogenic, myogenic and neurogenic was shown. This report described the first successful isolation and characterisation of hNDP-SCs.
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PMID:Isolation and in vitro characterisation of dental pulp stem cells from natal teeth. 1981 4

Indeterminate fibrohistiocytic lesions of the skin share histological and immunohistochemical features of both benign fibrous histiocytoma/dermatofibroma and dermatofibrosarcoma protuberans (DFSP). Unlike dermatofibroma, DFSP harbors recurrent genetic aberrations resulting in the fusion of COL1A1 on chromosome 17 and PDGFB on chromosome 22. Because indeterminate fibrohistiocytic lesions share some features with DFSP, they were evaluated for the possible presence of COL1A1-PDGFB chimeric transcripts. Twelve formalin-fixed paraffin-embedded cases were examined for COL1A1-PDGFB chimeric transcripts using a previously validated sensitive multiplex reverse transcriptase-polymerase chain reaction assay. The median patient age was 52.5 years (33-70 years) with 9 females and 3 males. The most common site was the extremities (n = 8) followed by the trunk (n = 2) and the head and neck region (n = 2). All demonstrated the expected reactivity for both CD34 and factor XIIIa, and the majority focally infiltrated into subcutaneous fat. Of the 6 patients with follow-up, 2 had residual tumor excised, but no patient developed a recurrence. None of the tumors harbored COL1A1-PDGFB fusion transcripts identified by reverse transcriptase-polymerase chain reaction. Although indeterminate fibrohistiocytic lesions share some features with DFSP, the lack of COL1A1-PDGFB chimeric transcripts suggests that they are distinct entities.
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PMID:COL1A1:PDGFB chimeric transcripts are not present in indeterminate fibrohistiocytic lesions of the skin. 1994 Jul 48

BMMNCs (bone marrow mononuclear cells) were isolated by density gradient centrifugation from unstimulated diagnostic marrow tap to propagate and characterize hBMSCs (human bone marrow stromal cells) and to explore their plasticity towards neuronal and other lineages. hBMSCs were characterized by flow cytometry for established markers, serially passaged and differentiated into adipo, osteo, chondro and neuronal lineages. Neural differentiation was analysed by RT-PCR (reverse transcriptase-PCR), ICC (immunocytochemistry) and Western blotting. The hBMSCs (n = 39) were spindle-shaped and immunoreactive for mesenchymal markers such as CD71, CD106, CD105, CD90 and Vimentin and negative for haematopoietic markers such as CD11c, CD34 and CD45. These cells showed differentiation into adipocytes, osteocytes and chondrocytes. Upon neuronal differentiation, hBMSCs expressed neuronal markers, i.e. beta-III tubulin, GAP43 (growth-associated proteins), neurofilament by ICC, RT-PCR and Western blotting. Our study demonstrates that minimal volumes of unstimulated diagnostic marrow tap forms a minimally invasive and reliable source for isolation of BMMNCs to establish cultures of mesenchymal stem cells and expand them. The plasticity observed in these cells towards mesenchymal (adipogenic, osteogenic and chondrocytic) and non-mesenchymal lineage (neural) substantiates the nature of mesenchymal stem cells and warrants further studies to evaluate their functional role.
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PMID:Unstimulated diagnostic marrow tap--a minimally invasive and reliable source for mesenchymal stem cells. 1994 16

The t(16;21)(q24;q22), a rare chromosomal translocation involving chromosome 21 in de novo and therapy-related acute myeloid leukemia (AML), produces a RUNX1-CBFA2T3 fusion gene (previously AML1-MTG16) fusion gene. The translocation has been reported in 20 patients with AML, with eosinophilia present in 3 cases. Here we report a pediatric case of t(16;21)(q24;q22) in de novo AML with eosinophilia and suggest that eosinophilia is a hematologic characteristic of at least a subpopulation of AML with t(16;21)(q24;q22). A 4-year-old Korean girl was admitted with complaints of pale appearance and dizziness, and was diagnosed with acute myelomonocytic leukemia. On admission, laboratory evaluation revealed hemoglobin at 3.3 g/dL, platelets at 9.0 x 10(9)/L, and white blood cells at 9.1 x 10(9)/L with 10% eosinophils and 1% blasts. The bone marrow aspirate contained 31% blasts and 11% eosinophils. Flow cytometric analysis revealed the expression of CD13, CD14, CD19, CD33, CD34, and HLA-DR by the leukemic blasts. The karyotype was 47,XX, + 8,t(16;21)(q24;q22)[18]/46,XX[2]. Interphase fluorescence in situ hybridization analysis with a dual-color, dual-fusion translocation LSI AML1/ETO probe set for RUNX1 and RUNX1T1 produced three signals for each probe in 90% of interphases, but no fusion signals. We confirmed the presence of RUNX1-CBFA2T3 fusion transcripts with reverse transcriptase-polymerase chain reaction, using primers AML1ex5f1 and MTG16r2.
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PMID:Acute myeloid leukemia with t(16;21)(q24;q22) and eosinophilia: case report and review of the literature. 1996 44

P-glycoprotein, the gene product of ATP-binding cassette, sub-family B (Abcb1), is a representative efflux transporter of cerebral vessels. It was recently reported that the expressions of P-glycoprotein and Abcb1 gene were increased in hippocampal vessels with blood-brain barrier (BBB) damage in stroke-prone hypertensive rats. SAMP8, senescence-accelerated mice with age-related deficits in memory and learning, are known to show age-related damage of BBB. Accordingly, in this study, we examined the P-glycoprotein expression and the gene expression (Abcb1a/b) by real-time quantitative reverse transcriptase-polymerase chain reaction (RT-PCR), Western blotting, and immunohistochemical techniques. SAMR1, which has a spontaneous retroviral insertional mutation in Abcb1a gene, was used to assess the effects of Abcb1a gene mutation. The brain samples of SAMR1 showed decreased expressions of P-glycoprotein and Abcb1a genes and increased expression of Abcb1b gene, compared with those of SAMP8 mice. The P-glycoprotein expression increased with aging in the brain samples of SAMP8, but not in those of SAMR1. The gene expressions of Abcb1a and Abcb1b increased with aging in the brain samples of SAMP8. Immunosignals of P-glycoprotein were seen in vessel walls, mainly in the cytoplasm of CD34-positive endothelial cells and partially in astrocytes, in all mice. These findings indicate that the expressions of Abcb1a and Abcb1b genes and their gene products, P-glycoprotein, were increased with aging in SAMP8, suggesting age-related response to prevent toxic substance from accumulating in the brains of SAMP8.
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PMID:Age-related changes in P-glycoprotein expression in senescence-accelerated mouse. 2002 12

Identifying the targets of immune response after allogeneic hematopoietic cell transplantation (HCT) promises to provide relevant immune therapy candidate proteins. We used protein microarrays to serologically identify nucleolar and spindle-associated protein 1 (NuSAP1) and chromatin assembly factor 1, subunit B (p60; CHAF1b) as targets of new antibody responses that developed after allogeneic HCT. Western blots and enzyme-linked immunosorbent assays (ELISA) validated their post-HCT recognition and enabled ELISA testing of 120 other patients with various malignancies who underwent allo-HCT. CHAF1b-specific antibodies were predominantly detected in patients with acute myeloid leukemia (AML), whereas NuSAP1-specific antibodies were exclusively detected in patients with AML 1 year after transplantation (P < .001). Complete genomic exon sequencing failed to identify a nonsynonymous single nucleotide polymorphism (SNP) for NuSAP1 and CHAF1b between the donor and recipient cells. Expression profiles and reverse transcriptase-polymerase chain reaction (RT-PCR) showed NuSAP1 was predominately expressed in the bone marrow CD34(+)CD90(+) hematopoietic stem cells, leukemic cell lines, and B lymphoblasts compared with other tissues or cells. Thus, NuSAP1 is recognized as an immunogenic antigen in 65% of patients with AML following allogeneic HCT and suggests a tumor antigen role.
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PMID:Antibodies specifically target AML antigen NuSAP1 after allogeneic bone marrow transplantation. 2005 54


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