Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of the present study was to isolate a lectin from fresh fruiting bodies of the mushroom Pleurotus citrinopileatus and examine it for various biological activities. The isolation procedure comprised ion exchange chromatography on DEAE-cellulose, CM-celluloses, and Q-Sepharose, and gel filtration on Superdex 75. A homodimeric 32.4 kDa lectin displaying high hemagglutinating activity was isolated with over 110 fold of purification. Its N-terminal amino acid sequence, QYSQMAQVME, has not been reported for other lectins. The lectin was unadsorbed on DEAE-cellulose in 0.001 M NH4HCO3 buffer (pH 9.4), but adsorbed on CM-cellulose in 0.001 M NH4OAc buffer (pH 4.8) and eluted by approximately 0.05 M NaCl in the same buffer. The lectin was subsequently adsorbed on Q-Sepharose and eluted by a linear gradient of 0-0.2 M NaCl in 10 mM NH4HCO3 buffer (pH 8.5). The lectin was obtained in a purified form after gel filtration by fast protein liquid chromatography on Superdex 75. The hemagglutinating activity of the lectin was inhibited by maltose, O-nitrophenyl-beta-d-galactopyranoside, O/P-nitrophenyl-beta-d-glucuronide and insulin. It was stable at temperatures up to 60 degrees C, and in NaOH and HCl solutions up to 0.1 M and 0.006 M concentration, respectively. It was sensitive to inhibition by HgCl2 and potentiation by AlCl3. The lectin exerted potent antitumor activity in mice bearing sarcoma 180, and caused approximately 80% inhibition of tumor growth when administered intraperitonealy at 5 mg/kg daily for 20 days. It elicited a mitogenic response from murine splenocytes in vitro with the maximal response at a lectin concentration of 2 microM. The lectin inhibited HIV-1 reverse transcriptase with an IC50 of 0.93 microM. It was devoid of antifungal activity.
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PMID:A novel lectin with potent antitumor, mitogenic and HIV-1 reverse transcriptase inhibitory activities from the edible mushroom Pleurotus citrinopileatus. 1796 26

Sonodynamic therapy employs a combination of ultrasound and a sonosensitizer to enhance the cytotoxic effect of ultrasound and promote apoptosis. However, the mechanism underlying the synergistic effect of ultrasound and hematoporphyrin is still unclear. In this study, we investigated mechanism of the induction of apoptosis by sonodynamic therapy in Sarcoma 180 cells. The cell suspension was treated by 1.75-MHz focused continuous ultrasound at an acoustic power (I(SATA)) of 1.4+/-0.07 W/cm(2) for 3 min in the absence or presence of 20 microg/ml hematoporphyrin. The proportion of apoptotic cells was determined by flow cytometry. We then analyzed the reactive oxygen species generation and localization by confocal microscopy. Western blotting and reverse transcriptase-polymerase chain reaction were used to analyze the expression of caspase-8, caspase-9, poly(ADP)-ribose polymerase, and nuclear factor-kappaB. The findings of our study indicate that ultrasound treatment induced the activation of nuclear factor-kappaB as an early stress response. When cells were pretreated with hematoporphyrin, the initial response to the therapy was the formation of (1)O(2) in the mitochondria. Our results primarily demonstrate that the mechanisms of induction of apoptosis by ultrasound and hematoporphyrin-sonodynamic therapies are very different. Our findings can provide a basis for explaining the synergistic effect of ultrasound and hematoporphyrin.
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PMID:Potential mechanism in sonodynamic therapy and focused ultrasound induced apoptosis in sarcoma 180 cells in vitro. 1964 May 55

Kefir is produced by adding kefir grains (a mass of proteins, polysaccharides, bacteria, and yeast) to pasteurized milk; it has been shown to control several cellular types of cancer, such as Sarcoma 180 in mice, Lewis lung carcinoma, and human mammary cancer. Human T-cell lymphotropic virus type 1 (HTLV-1) is the causative agent of adult T-cell leukemia, which is a fatal disease with no effective treatment. The current study aims at investigating the effect of a cell-free fraction of kefir on HuT-102 cells, which are HTLV-1-positive malignant T-lymphocytes. Cells were incubated with different kefir concentrations: the cytotoxicity of the compound was evaluated by determining the percentage viability of cells. The effect of all the noncytotoxic concentrations of kefir cell-free fraction on the proliferation of HuT-102 cells was then assessed. The levels of transforming growth factor (TGF)-alpha mRNA upon kefir treatment were then analyzed using reverse transcriptase polymerase chain reaction. Finally, the growth inhibitory effects of kefir on cell cycle progression and/or apoptosis were assessed by flow cytometry. The maximum cytotoxicity recorded at 80 microg/microL for 48 hours was only 43%. The percent reduction in proliferation was very significant, dose and time dependent, and reached 98% upon 60-microg/microL treatment for 24 hours. Kefir cell-free fraction caused the downregulation of TGF-alpha, which is a cytokine that induces the proliferation and replication of cells. Finally, a marked increase in cell cycle distribution was noted in the pre-G1 phase. In conclusion, kefir is effective in inhibiting proliferation and inducing apoptosis of HTLV-1-positive malignant T-lymphocytes. Therefore, further in vivo investigation is highly recommended.
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PMID:The antiproliferative effect of kefir cell-free fraction on HuT-102 malignant T lymphocytes. 1977 41