Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.10 (IKK)
 4,900 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

At the instance of the chronic liver diseases (Nr. 571 and 573 IKK) is shown in form of a model which high value of information the process of the stored data of the headline of a medical record suited for documentation. Thus informations concerning the clinical morbidity/mortality, analyses according to age and sex, residence and admitting institution, comparison of admission, treatment and post-mortem diagnoses, ascertainment of the diagnosis and finally economic data may be got. From this result the epidemiological conclusions and the statements for analyses of factors.
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PMID:[Experience and results in the evaluation of documentation-oriented medical records in the German Democratic Republic]. 30 80

Stomatological examination was carried out on 173 patients with schizophrenia (IKK-Nr. 295). It was observed that this group of patients showed a diminished dental and oral care in comparison to the average population of the same region. The close cooperation of dentists with the institutions for chronic patients will be as prophylactic measure in favour of the patients encouraged.
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PMID:[Stomatologic studies in schizophrenic patients--contributions to the problem of medical and social integration of psychiatric patients]. 373 76

The actual debate on temporal or regional clustering of childhood leukaemias includes an intensive discussion, whether or not the observed patterns of frequency distribution are governed merely or mainly by random processes. With the "Information System on Cancer Mortality and District Characteristics (IKK)" the Cumulative Mortality Rates of childhood leukaemias (up to age 15) are determined for the single district authority units (Kreis) in the Federal Republic of Germany (old Laender) between 1975 and 1990. The frequency distributions of the mortality rates as well as the dependencies on population density are analysed. No statistical significance for a deviation from the corresponding mere random distributions could be revealed.
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PMID:[Regional distribution of leukemia incidence in children in West Germany 1975-1990]. 771 45

On account of the lack of a comprehensive cancer registry with national coverage for the Federal Republic of Germany, the long-term and interregional evaluation of cancer mortality data is of particular relevance. Therefore, the TUV Rheinland instructed by the Federal Ministry for the Environment, Nature Protection, and Reactor Safety maintains an "Information System on Cancer Mortality and District Characteristics (IKK)" using official cause of death and resident population statistics. Mortality data for a variety of different cancer sites are documented with local and temporal separation for the area of the Federal Republic of Germany (before the German unification) and for a period of 20 years. The IKK data can be employed as a meaningful tool for epidemiological investigations relating to the correlation of cancer mortality and environmental agents. In the present paper the principles of the IKK are described and some examples of results are presented.
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PMID:[Information system on cancer mortality and district characteristics of the Rhineland TUV]. 846 93

Nuclear transcription factors of the NF-kappaB/Rel family are inhibited by IkappaB proteins, which inactivate NF-kappaB by trapping it in the cell cytoplasm. Phosphorylation of IkappaBs marks them out for destruction, thereby relieving their inhibitory effect on NF-kappaB. A cytokine-activated protein kinase complex, IKK (for IkappaB kinase), has now been purified that phosphorylates IkappaBs on the sites that trigger their degradation. A component of IKK was molecularly cloned and identified as a serine kinase. IKK turns out to be the long-sought-after protein kinase that mediates the critical regulatory step in NF-kappaB activation.
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PMID:A cytokine-responsive IkappaB kinase that activates the transcription factor NF-kappaB. 925 83

The results of treatment of 394 patients with gastric cancer were analysed to compare the effectiveness of surgical and two variants of combined treatment (preoperative irradiation with intensive-concentrated IKK method and dynamic DFD dose-fractioning). The advantages of combined treatment over surgical treatment are demonstrated. The 3-year survival in the combined treatment is 70.2%, in surgical treatment 34.5 +/- 6.2%. The advantages of SDF preoperative irradiation over IKK irradiation are revealed, that is proved by the increase of the 3-year survival rate (76 vs. 56.7%), and decrease in the rate of recurrence from 50 to 27.3%. The addition of metronidazol leads to increase of anticancer effectiveness, that is proved with the examination of tumor pathomorphosis and the rates of survival.
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PMID:[Combined treatment of stomach neoplasms]. 934 Mar 84

Activation of the transcription factor nuclear factor kappa B (NF-kappaB) is controlled by sequential phosphorylation, ubiquitination, and degradation of its inhibitory subunit IkappaB. A large multiprotein complex, the IkappaB kinase (IKK) signalsome, was purified from HeLa cells and found to contain a cytokine-inducible IkappaB kinase activity that phosphorylates IkappaB-alpha and IkappaB-beta. Two components of the IKK signalsome, IKK-1 and IKK-2, were identified as closely related protein serine kinases containing leucine zipper and helix-loop-helix protein interaction motifs. Mutant versions of IKK-2 had pronounced effects on RelA nuclear translocation and NF-kappaB-dependent reporter activity, consistent with a critical role for the IKK kinases in the NF-kappaB signaling pathway.
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PMID:IKK-1 and IKK-2: cytokine-activated IkappaB kinases essential for NF-kappaB activation. 938 Nov 93

Interleukin-1 (IL-1) is a central regulator of the immune and inflammatory responses. Recently, significant advances have been made in the area of IL-1 receptors and IL-1 signal transduction. A family of proteins has been described that share significant homology in their signaling domains with the Type I IL-1 receptor (IL-1RI). These include the IL-1 receptor accessory protein (IL-1AcP), which does not bind IL-1 but is essential for IL-1 signaling; a Drosophila protein Toll; a number of human Toll-like receptors (hTLRs); the putative IL-18/IL-1-gamma receptor IL-1Rrp (IL-1 receptor-related protein); and a number of plant proteins. All appear to be involved in host responses to injury and infection. These homologies also extend to novel signaling proteins implicated in IL-1 action. Two IL-1 receptor-associated kinases, IRAK-1 and IRAK-2, which have homologs in Drosophila (Pelle) and plants (Pto), have been implicated in the activation of the transcription factor, nuclear factor kappaB (NF-kappaB). IRAK-1 has also been implicated in AP1 induction, Jun amino-terminal kinase (JNK) activation, and IL-2 induction. It recruits the adapter protein TRAF6 to the IL-1 receptor complex via an interaction with IL-1AcP. TRAF6 then relays the signal via NF-kappaB-inducing kinase (NIK) to two I-kappaB kinases (IKK-1 and -2), leading to NF-kappaB activation. Progress has also been made on other IL-1-responsive kinases, including JNK and p38 MAP kinase, with the latter having a role in multiple responses to IL-1. The remarkable conservation between diverse species indicates that the IL-1 system represents an ancient signaling machine critical for responses to environmental stresses and attack by pathogens.
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PMID:Signal transduction pathways activated by the IL-1 receptor family: ancient signaling machinery in mammals, insects, and plants. 962 Jun 55

We have characterized a flat cellular variant of HTLV-1 Tax-transformed rat fibroblasts, 5R, which is unresponsive to all tested NF-kappaB activating stimuli, and we report here its genetic complementation. The recovered full-length cDNA encodes a 48 kDa protein, NEMO (NF-kappaB Essential MOdulator), which contains a putative leucine zipper motif. This protein is absent from 5R cells, is part of the high molecular weight IkappaB kinase complex, and is required for its formation. In vitro, NEMO can homodimerize and directly interacts with IKK-2. The NEMO cDNA was also able to complement another NF-kappaB-unresponsive cell line, 1.3E2, in which the protein is also absent, allowing us to demonstrate that this factor is required not only for Tax but also for LPS, PMA, and IL-1 stimulation of NF-kappaB activity.
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PMID:Complementation cloning of NEMO, a component of the IkappaB kinase complex essential for NF-kappaB activation. 965 55

A critical step in the signal-induced activation of the transcription factor NF-kappaB is the site-specific phosphorylation of its inhibitor, IkappaB, that targets the latter for degradation by the ubiquitin-proteasome pathway. We have previously shown that mitogen-activated protein kinase/ERK kinase kinase 1 (MEKK1) can induce both this site-specific phosphorylation of IkappaB alpha at Ser-32 and Ser-36 in vivo and the activity of a high molecular weight IkappaB kinase complex in vitro. Subsequently, others have identified two proteins, IkappaB kinase alpha (IKK-alpha) and IkappaB kinase beta (IKK-beta), that are present in a tumor necrosis factor alpha-inducible, high molecular weight IkappaB kinase complex. These kinases are believed to directly phosphorylate IkappaB based on the examination of the kinase activities of IKK immunoprecipitates, but more rigorous proof of this has yet to be demonstrated. We show herein that recombinant IKK-alpha and IKK-beta can, in fact, directly phosphorylate IkappaB alpha at Ser-32 and Ser-36, as well as homologous residues in IkappaB beta in vitro, and thus are bona fide IkappaB kinases. We also show that MEKK1 can induce the activation of both IKK-alpha and IKK-beta in vivo. Finally, we show that IKK-alpha is present in the MEKK1-inducible, high molecular weight IkappaB kinase complex and treatment of this complex with MEKK1 induces phosphorylation of IKK-alpha in vitro. We conclude that IKK-alpha and IKK-beta can mediate the NF-kappaB-inducing activity of MEKK1.
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PMID:MEKK1 activates both IkappaB kinase alpha and IkappaB kinase beta. 968 78


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