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
Query: UMLS:C0038362 (
stomatitis
)
8,852
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
In addition to the five previously described vesicular
stomatitis
virus (VSV) proteins (L, G, N, NS, and M), a protein (Mr 17,500) accumulated late in infection of Chinese hamster ovary cells. The protein, designated M', was a cleavage product of the viral M protein (Mr 26,000) both in vivo and in vitro. (a) M' was precipitated by anti VSV serum, indicating that it is of viral origin. (b) M' peptides generated using Staphylococcus V8 protease or chymotrypsin were shared by M, but not by the other VSV proteins. (c) The conversion of M to M' was enzymatic. The enzyme denoted M protease was heat labile, was inhibited by the
serine protease inhibitor
phenylmethylsulfonyl fluoride, and its accumulation, which commenced between 2 and 3 hr after infection, required protein synthesis. (d) The amounts of L, G, N, and NS increased in CHO-infected cells while the amount of M increased for only 3-4 hr and decreased thereafter. Since M has been implicated in the inhibition of VSV transcription, it is possible that regulation of the amount of M by degradation is important in the regulation of VSV transcription.
...
PMID:Identification of a new protein present in vesicular stomatitis virus-infected Chinese hamster ovary cells as a degradation product of viral M protein. 631 34
Cytotoxic cells provide a crucial defense against DNA and RNA viral infections. Here we describe an in vitro model to study the fate of vesicular
stomatitis
virus (VSV) RNA in cells undergoing apoptosis. Using the [3H]uridine release assay, we show that human LAK cells induce the degradation of RNA in infected U937 cells in addition to inhibiting the production of infectious virions. LAK cell-mediated RNA degradation was blocked by the
serine protease inhibitor
, 3,4-dichloroisocoumarin. Purified human granzyme B but not inactivated granzyme B, granzyme A, or perforin rapidly induced degradation of RNA in VSV-infected U937 cells in a dose- and time-dependent manner without lysing the cells and suppressed viral production. Northern analysis of RNA extracted from infected cells with a VSV full-length cDNA probe confirmed that levels of viral transcripts were reduced by treatment with granzyme B. Nevertheless, the amount of host beta-actin mRNA was also reduced in infected cells, suggesting that treatment with granzyme B induced apoptosis. Consistent with this notion, infected cells exposed to granzyme B rapidly developed DNA strand breakage. Taken together, the data suggest that granzyme B in the absence of perforin reduced VSV production by activating a mechanism that degraded viral transcripts in infected U937 cells.
...
PMID:Granzyme B independently of perforin mediates noncytolytic intracellular inactivation of vesicular stomatitis virus. 931 33