Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An improved procedure for the isolation of interferons produced by mouse Ehrlich ascites tumor cells infected with Newcastle disease virus provides interferons of three size classes (33,000, 26,000, and 20,000 daltons) with specific activities between 2 and 3 x 10(9) units/mg of protein and a yield of 11 to 20%. The tryptic peptide maps of the two larger species are very similar; that of the smallest species is different, at least in part. The amino acid compositions of the three species are very close. Their NH2-terminal amino acids are identical and so are the amino acids released by carboxypeptidase A treatment. These data are consistent with the possibility that the differences in size between the three species may be due, at least in part, to unequal glycosylation.
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PMID:Structural characteristics of interferons from mouse Ehrlich ascites tumor cells. 43 51

The amino-terminal and the carboxy-terminal amino acids of the hemagglutinin-neuraminidase glycoprotein of the Ulster strain of Newcastle disease virus have been analyzed before and after proteolytic activation of the precursor HNo (Mr approximately 82K). The amino termini of HNo and of the large cleavage fragment HN (approximately 74K) obtained by in vivo and in vitro proteolysis could not be sequenced by Edman degradation. This indicates that in both instances the amino termini are blocked. The carboxy termini of HNo and HN are different as demonstrated by end-point digestion with carboxypeptidase A. Furthermore, a small cleavage fragment (approximately 9K) of HNo that was removed from the virion after trypsin treatment could be purified by HPLC. In contrast to HN, this fragment displays a free amino terminus susceptible to Edman degradation. These data indicate that conversion of HNo involves removal of a 9K glycopeptide from the carboxy-terminal end. Thus, it has to be concluded that, unlike most other viral glycoproteins, the hemagglutinin-neuraminidase is inserted in the envelope with its carboxy terminus exposed at the surface of the virus particle.
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PMID:The carboxyterminus of the hemagglutinin-neuraminidase of Newcastle disease virus is exposed at the surface of the viral envelope. 653 31

In addition to their well-characterized role in allergic inflammation, recent data confirm that mast cells play a more extensive role in a variety of viral infections. The contribution of mast cells to Newcastle disease pathogenesis has not been investigated. We evaluated mast cell activity after Newcastle disease virus (NDV) infection in specific pathogen free chickens using cytochemical and immunocytochemical analyses. The results were as follows. Severe tissue damage was observed in the proventriculus, duodenum, jejunum and caecal tonsil, and NDV antigens were detected and presented extensively in these tissues. Second, in the NDV-infected group, the mast cell population was increased markedly in the proventriculus, duodenum, jejunum and caecal tonsil at 24, 48, 72 and 96 h after infection (P<0.01). However, very few mast cells were observed in those same tissues in the control. More intriguingly, the greatest number of mast cells was found in the proventriculus, which also showed the greatest level of NDV antigens. Third, the content of tryptase was significantly higher (P<0.01) in the NDV-infected group compared with the control from 24 to 96 h post infection). Furthermore, as an important protease released by mast cells, tryptase had a positive correlation with mast cell distribution. These data indicated that mast cells were involved in the response to NDV. Our results also suggested that the broad range of mast cell mediators might have a role in the pathology of Newcastle disease.
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PMID:Increased mast cell density during the infection with velogenic Newcastle disease virus in chickens. 1902 56

We have previously demonstrated that mast cells were significantly increased during Newcastle disease virus (NDV) infection, but their precise role in the process is unknown. In this study, we investigated the role of mast cells in this process by using ketotifen, a mast cell membrane stabilizer. A total of 60 specific-pathogen-free chickens were randomly divided into 3 groups of 20 birds each (NDV-infected group, ketotifen-pretreated group, and the control group). The ketotifen-pretreated group was administered orally with ketotifen before NDV infection. On 12, 24, and 48 h postinfection, 5 chickens from each treatment were killed. Tissues of proventriculus were collected to quantify mast cells, the content of tryptase and histamine by cytochemistry, immunohistochemistry, and fluorescence analysis, respectively. The results showed that the population of mast cells and the content of tryptase and histamine were increased significantly in the proventriculus (P < 0.01) of infected birds compared with the control group. An acute mucosal injury was observed in the infected chickens. In contrast, among chickens pretreated with ketotifen, followed by NDV infection, the mast cells number and the content of tryptase and histamine were decreased significantly (P < 0.01). Likely as a result, the mucosal injury was remitted remarkably. The overall results of this experiment suggest that mast cells are implicated in NDV-induced mucosal injury. Inhibition of mast cell mediator release may represent a novel strategy to modulate this process.
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PMID:Evidence for a role of mast cells in the mucosal injury induced by Newcastle disease virus. 1921 24