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)

Adherent cells display an important accessory role on normal T-cell colony formation. Since the in-vitro proliferation of T colony-forming cells (T-CFC) from AIDS patients is extremely impaired we studied the effect of patients' adherent cells on T-CFC growth. Patients' peripheral blood mononuclear cells (PBMC) were fractionated on the basis of rosette formation with sheep red blood cells and complement-mediated cytotoxicity with OKT3 monoclonal antibody (E-T3-). Both mature (E+) T cells and E-OKT3- cell fractions failed to generate T-cell colonies although colony growth could be obtained from unfractionated PBMC. In five out of 12 AIDS patients, adherent cell-depletion of PBMC enhanced the plating efficiency. Moreover, patients' but not normal adherent cells could inhibit normal T-cell colony growth in a dose-dependent manner. Media conditioned by patients' unstimulated adherent cells (LCM-A+p) also inhibit normal T-cell colony formation. In addition, LCM-A+p were capable of inhibiting interleukin 2-receptor (IL2-R) expression and interleukin 2 (IL2) production by normal mitogen-stimulated T cells. These LCM-A+p did not contain detectable reverse transcriptase activity nor could they infect the CEM T-cell line which is permissive to human immunodeficiency virus (HIV). Conversely, this adherent cell-derived inhibitory activity could be abrogated by heating or treatment with proteolytic enzymes. These findings indicate that the low T-cell colony formation in some AIDS patients could be due to adherent cell-derived inhibitory activity(ies).
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PMID:Peripheral blood adherent cells from AIDS patients inhibit normal T-colony growth through decreased expression of interleukin 2-receptors and production of interleukin 2. 311 67

Cell-specific gene expression profiling from heterogeneous human tissues is confounded by cell purification limitations. Here, we describe a technique to generate gene expression profiles of pure populations of prostate cancer cells obtained from fresh-frozen prostatectomy specimens and small initial quantities of RNA by combining laser capture microdissection and microserial analysis of gene expression (LCM-microSAGE). Two microSAGE libraries were obtained from approximately 100,000 laser pulses, estimated to contain fewer than 3 x 10(5) cells and 20-30 ng mRNA. Two libraries were sequenced to a depth of 10,111 and 10,463 unique tags from normal and cancer cells, representing 6453 and 6923 genes, respectively. Most transcripts were expressed at similar levels, but cancer cells compared with normal cells had increased expression of 385 tags and decreased expression of 389 tags. A total of 20 genes were differentially expressed (P<0.05); five of these genes were upregulated and 15 were downregulated in cancer cells. Quantitative reverse transcriptase-polymerase chain reaction results from three selected genes corroborated the existence of cell-specific gene expression in LCM-microSAGE-derived libraries. In conclusion, the LCM-microSAGE approach demonstrates that large-scale expression profiles of known and unknown transcripts can be generated from pure populations of target cells obtained from human tissue samples comprised of heterogeneous mixtures of cell types.
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PMID:Combined laser capture microdissection and serial analysis of gene expression from human tissue samples. 1552 82