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

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Query: EC:2.7.11.1 (protein kinase)
81,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The N-terminal sequences of mouse Ehrlich ascites tumor cell IFN beta (35,000-40,000 daltons) and IFN alpha (20,000 daltons) differ in 18 out of 20 positions. Furthermore, these two IFN species show little immunological cross reactivity. We treated mouse L929 cells and human HeLa S3 cells with essentially pure mouse IFN alpha or IFN beta or both at various concentrations and for various lengths of time. From the treated cells we prepared extracts and compared in these the activities of (2'-5')(A)n synthetase, an enzyme that was earlier shown to be induced by partially purified IFN preparations. The effects of treatment of mouse L929 cells with pure IFN alpha or IFN beta on (2'-5') (A)n accumulation in the cell extracts were very similar both in respect to the dependence on the length of exposure of the cells to the IFNs and on IFN concentration. Treatment with both IFN alpha and IFN beta at concentrations resulting in only partial induction of the enzyme led to an additive rather than to a synergistic effect. The maximal level of enzyme induced was the same in cells treated with high concentrations of IFN alpha or IFN beta or both. Mouse IFN alpha was as active as IFN beta in inducing a double-stranded RNA-dependent protein kinase in mouse L cells. The treatment of HeLa S3 cells with IFN beta did not affect the accumulation of (2'-5') (A)n in their extracts whereas treatment with IFN alpha boosted the accumulation though to a lesser extent than in the case of mouse L cells. These results are in line with the finding that mouse IFN alpha can, but mouse IFN beta cannot convert HeLa S3 cells into the antiviral state and also with the more pronounced homology in N-terminal sequence between mouse IFN alpha and a human (lymphoblastoid) IFN chi than between mouse IFN beta and a human IFN beta.
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PMID:Studies with pure mouse Ehrlich ascites tumor interferons alpha and beta: patterns of induction of (2'-5') (A)n synthetase and of a double-stranded RNA-dependent protein kinase in mouse cells and human cells. 618 51

Treatment of mouse L cells with mouse IFN gamma induced a cytoplasmic Ca-dependent protein kinase, which highly phosphorylated cellular enzymes such as phosphodiesterase and RNase in vitro. The kinase partially purified from IFN gamma-treated cells (100 units/ml, 12 h at 37 degrees C) was different from IFN-induced dsRNA-dependent protein kinase since it was dsRNA independent. The kinase may have played an important role in mediating IFN-induced biological effects, since cellular enzymes were found to alter enzyme activity after phosphorylation by the kinase in vitro.
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PMID:Interferon gamma-induced Ca-dependent protein kinase in mouse L cells. 618 56

Virus induced IFN (IFN alpha or beta) suppresses the antibody response in both mouse and human. The suppression may be related to IFN effect on intermediary metabolism (inhibition of hexose monophosphate shunt) which could result in activation of protein kinase activities. Immune IFN (IFN gamma) also suppresses the antibody response with purified IFN gamma more effective than crude, suggesting that crude IFN gamma preparations contain an antagonist. The cellular interactions that regulate IFN gamma production are similar to those for antibody production with helper and suppressor cell activities. T-cell growth factor or interleukin 2 will mediate helper cell requirements and appears to be an absolute requirement for IFN gamma production.
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PMID:Effect of interferon on antibody formation. 618 7

The effect of double-stranded RNA on the dephosphorylation of purified, 32P-labeled eIF-2 was examined in cell-free extracts prepared from interferon-treated mouse L929 cells. Dephosphorylation of the alpha subunit of eIF-2 occurred at comparable rates in the presence and in the absence of reovirus dsRNA. By contrast, the beta subunit of eIF-2 was not dephosphorylated to any significant extent in either the presence or the absence of dsRNA. These results indicate that the enhanced phosphorylation of eIF-2 alpha observed in IFN-treated systems in the presence of double-stranded RNA (dsRNA) is indeed caused by an activation of a protein kinase rather than to an inhibition of a phosphoprotein phosphatase by the dsRNA.
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PMID:Mechanism of interferon action: eIF-2 alpha phosphatase in interferon-treated mouse fibroblasts is double-stranded RNA independent. 629 May 78

Two cell lines derived from human choriocarcinomas (HCCM-5 and BeWo) are resistant to several biological effects of human interferon such as inhibition of VSV multiplication and inhibition of cell growth, but they develop a normal antiviral activity against EMCV. Nevertheless, in both cell lines, 2-5A synthetase and protein kinase are induced by IFN. 2-5A-dependent endonuclease can be measured by two independent methods and 2-5A itself is detected at least in poly(rI):poly(rC)- and IFN-treated BeWo cells. This is another example of two cell lines that are partially, with respect to the antiviral effect toward VSV, and totally, with respect to the anticellular effect, refractory to IFN treatment, although all the known elements of the 2-5A system are present.
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PMID:Effect of interferon on two human choriocarcinoma-derived cell lines. 631 Aug 68

When mouse L cells are infected by vaccinia virus, a specific kinase inhibitory factor is produced which inhibits the interferon-induced, double-stranded RNA-dependent protein kinase (P. Whitaker-Dowling and J. S. Youngner (1983) Virology 131, 128-136). This inhibitory factor appears early in vaccinia infection (90 min) and its production requires protein synthesis. It inhibits the phosphorylation of the alpha subunit of protein synthesis initiation factor eIF-2 and it is active in mixed extracts of IFN-treated cells and vaccinia-infected cells. The vaccinia-mediated inhibition of the IFN-induced protein kinase is not due to a specific phosphatase or a specific protease and can be reversed by the addition of excess double-stranded RNA. Evidence is presented which suggests that the specific kinase inhibitory factor interacts in a stoichiometric manner with the double-stranded RNA which is required for the activation of the interferon-induced protein kinase.
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PMID:Characterization of a specific kinase inhibitory factor produced by vaccinia virus which inhibits the interferon-induced protein kinase. 647 31

The imidazoquinolineamine derivative 1-(2-methyl propyl)-1H-imidazole [4,5-c]quinoline-4-amine (imiquimod) has been shown to induce alpha interferon (IFN-alpha) synthesis both in vivo and in peripheral blood mononuclear cells in vitro. In this study, we show that, in these cells, imiquimod induces expression of several IFNA genes (IFNA1, IFNA2, IFNA5, IFNA6, and IFNA8) as well as the IFNB gene. Imiquimod also induced the expression of interleukin (IL)-6, IL-8, and tumor necrosis factor alpha genes. Expression of all these genes was transient, independent of cellular protein synthesis, and inhibited in the presence of tyrosine kinase and protein kinase C inhibitors. Infection with Sendai virus led to expression of a similar set of cytokine genes and several of the IFNA genes. Imiquimod stimulates binding of several induction-specific nuclear complexes: (i) the NF-kappa B-specific complexes binding to the kappa B enhancer present in the promoters of all cytokine genes, but not in IFNA genes, and (ii) the complex(es) binding to the A4F1 site, 5'-GTAAAGAAAGT-3', conserved in the inducible element of IFNA genes. These results indicate that imiquimod, similar to viral infection, stimulates expression of a large number of cytokine genes, including IFN-alpha/beta, and that the signal transduction pathway induced by both of these stimuli requires tyrosine kinase and protein kinase activity.
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PMID:Stimulation of interferon and cytokine gene expression by imiquimod and stimulation by Sendai virus utilize similar signal transduction pathways. 753 79

Local administration of high-dose r-TNF alpha with IFN gamma in the limbs of melanoma patients has proved to be a very promising treatment. To understand the role played by the effect of TNF on melanoma cells in tumor destruction, we have investigated the expression of TNF-receptors in melanoma cells using monoclonal antibodies specific for the type-A (75-kDa) and the type-B (55-kDa) TNF receptors. Flow cytometric analysis of cultured melanoma cells indicated the presence of both types of receptor. Quantificative differences in the relative levels of receptors were observed for different cells lines, although the type-B receptor was generally more strongly expressed. Similar results were obtained by immunohistochemistry on cryosections from tumor samples. Positive staining of variable intensity was observed for the type-B TNF-receptor in a high percentage of tumor cells. The type-A TNF-receptor was also detected, but with a weaker staining. The total TNF-binding activity of cultured melanoma cells, as measured by binding of 125I-labeled TNF alpha, was up-regulated between 2- and 4-fold by incubation of cells with activators of protein kinase A or IFN gamma. Treatment of cultured melanoma cells with dbc-AMP resulted in a selective induction of type-A TNF-receptors, without affecting the type-B receptor level. In contrast, IFN gamma was able to induce either type of receptor in a cell-line-dependent fashion. Addition of TNF alpha to melanoma cells induced the activation of the nuclear transcription factor kappa B, as measured in an electrophoretic mobility shift assay, thus indicating the biological significance of the TNF-receptors on these cells.
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PMID:Expression of type A and B tumor necrosis factor (TNF) receptors on melanoma cells can be regulated by dbc-AMP and IFN gamma. 760 71

It was shown that human recombinant gamma IFN given to volunteers intramuscularly (90 x 10(3) IU) and by inhalation (120 x 10(3) IU) induced 5-10-fold increase circulating IFN (up to 40-60 IU/ml); the activities of 2,5-oligoadenylate synthetase increased 1.5-2 fold and protein kinase of lymphocytes--3-5-fold. The repeated doses of gamma IFN at 12-15-hour intervals maintained a relatively stable IFN status, the inhalatory route of application being more effective. Convalescents after influenza different from healthy donors by a higher level of serum interferon and activity of 2.5-oligoadenylate synthetase but the activity of protein kinase was lowered in lymphocytes and plasma. The side effects induced by IFN administration were more marked only after intramuscular injections of 90 10 IU and were absent after inhalation of IFN (120,000 IU).
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PMID:[Clinical trials of recombinant gamma-interferon. Circulating interferon and the 2,5-oligoadenylate synthetase activity after intramuscular and inhalation administrations]. 769 Jun 16

Addition of IFN-beta resulted in a dose-dependent reduction of growth, a drop in [3H]thymidine incorporation into DNA, and a concurrent 69% and 15% increase in the S and G2/M phases, of the human prostatic JCA-1 cells. No correlation existed between the antimitogenicity of IFN and increases in the double-stranded RNA-dependent protein kinase activity. Although IFN elicited a large increase in 2-5A synthetase activity, activation of the 2-5A-dependent RNase L could not be demonstrated in JCA-1 cells rendered permeable to 2-5A, implying that the 2-5A pathway is not involved in the anti-proliferative effects of IFN. Analysis of endogenous proteins phosphorylated in vitro show that some IFN-inducible phosphoproteins were dependent upon the presence of double-stranded DNA.
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PMID:Effects of IFN-beta on growth of human prostatic JCA-1 cells. 790 34


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