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)

Homogenates of a human brain from a case of Creutzfeldt-Jakob disease and a homogenate of mouse brains from mouse passage 1 of the disease in mice contained no detectable conventional viruses. Both human material and mouse-passaged material were inoculated into nude mice, and the mouse-passaged material was also inoculated into eight different tissue culture lines. The tissue cultures showed no cytopathic changes or hemadsorption and failed to produce an increased amount of reverse transcriptase. The nude mice inoculated with human brain suspensions developed a disease identical to that in immunocompetent mice, with a nearly identical incubation period of 9 to 13 months. The incubation period of the disease in mice was under host genetic control and was, additionally, directly related to the inoculum size. The agent was resistant to 10% Formalin, 5% deoxycholate, 1% Triton X-100, and 5% glutaraldehyde; however, glutaraldehyde treatment resulted in a significant loss of infectivity. Approximately 1 log of infectivity was lost by heating brain suspensions to 80 degrees C for 15 min, with no additional loss upon further incubation up to 45 min. Heating at 100 degrees C for 15 min led to a 3-log loss of infectivity.
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PMID:Evidence for an unconventional virus in mouse-adapted Creutzfeldt-Jakob disease. 675 18

Cyclooxygenases (COXs) mediate inflammation, immunomodulation, blood flow, apoptosis, and fever in various diseases of the brain. Whereas COX-2 is cytokine inducible, COX-1 is expressed by macrophages/microglial cells that accumulate in pathological foci. We analyzed the localization of COX-1 and COX-2 in postmortem cortex slices of eight patients who died with sporadic Creutzfeldt-Jakob disease (CJD) and four neuropathologically unaltered controls by immunohistochemical double-labeling, reverse transcriptase polymerase chain reaction (RT-PCR), and Western blotting experiments. In healthy brains, COX-1 was expressed by single macrophages/microglial cells and COX-2 by disseminated neurons. In patients with CJD, significantly (p = 0.0195) more COX-1-expressing macrophages/microglial cells were detected adjacent to neurons. COX-2 expression was predominantly observed in neurons, and their number was significantly higher (p < 0.0001) compared to controls. RT-PCR and Western blotting revealed more COX-1 and COX-2 mRNA and protein in one CJD patient than in one control patient. These data show that accumulation of COX-1-expressing macrophages/microglial cells and COX-2-expressing neurons might represent important regulatory mechanisms in the complex process of neuronal degeneration in CJD patients.
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PMID:Cyclooxygenase-1 and -2 in brains of patients who died with sporadic Creutzfeldt-Jakob disease. 1266 31

The allograft inflammatory factor-1 (AIF-1) is a 17-kDa IFN-gamma inducible Ca(2+)-binding EF-hand protein that is encoded within the HLA class III genomic region and is involved in immune dysfunction and smooth muscle cell activation. We used immunohistochemistry double labelling experiments to analyse the spatial distribution and cell-type-specific localization of AIF-1 in the brains of patients who died as a result of sporadic Creutzfeldt-Jakob disease (CJD) and neuropathologically unaltered controls. Significantly more AIF-1 immunoreactive macrophages/microglial cells and, interestingly, neurones were observed in CJD patients compared to controls. Western blotting confirmed more prominent AIF-1 immunoreactive bands of approximately 50 kDa in four CJD patients compared to three controls. Chaotropic SDS-PAGE of the recombinant AIF-1 resulted in almost complete reduction of the 50 kDa band and mass spectrometry revealed only AIF-1-specific tryptic protein fragments suggesting that trimerized AIF-1 is the predominant form in vivo. Finally, we analysed mechanisms of neuronal AIF-1 induction. Following H2O2 challenge, a model of general cell stress, we observed the gradual induction of AIF-1 and, more interestingly, release to the supernatant of SKNSH neurones. Parallel reverse transcriptase polymerase chain reaction and sequencing was used to confirm AIF-1 mRNA expression.
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PMID:The allograft inflammatory factor-1 in Creutzfeldt-Jakob disease brains. 1288 99