Nf Kappab
Mostrando 1-12 de 34 artigos, teses e dissertações.
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1. Evaluation of nuclear NF-κB, transglutaminase2, and ERCC1 as predictors of platinum resistance in testicular tumors
ABSTRACT Purpose: Testicular germ cells tumor (TGCT) are associated with a high cure rate and are treated with platinum-based chemotherapy. However, a group of testicular cancer patients may have a very unfavorable evolution and insensitivity to the main therapeutic agent chemotherapy (CT) cisplatin. The aim of this study was to evaluate the risk of recurre
Int. braz j urol.. Publicado em: 2020-06
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2. Biochemical and Molecular Mechanisms of Glucose Uptake Stimulated by Physical Exercise in Insulin Resistance State: Role of Inflammation
Resumo A obesidade associada à inflamação sistêmica induz resistência à insulina (RI), com consequente hiperglicemia crônica. Este processo envolve o aumento na liberação de citocinas pró-inflamatórias, ativação da enzima c-Jun N-terminal cinase (JNK), do fator nuclear kappa-B (NF-κB) e dos receptores do tipo Toll 4 (TLR4). Dentre as ferramenta
Arq. Bras. Cardiol.. Publicado em: 21/10/2019
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3. Ação protetora da eritropoietina na injúria renal aguda em modelo experimental de sepse / Erithropoietin protects from acute kidney injury in a experimental model of sepsis
A sepse envolve mecanismos complexos de respostas imunológicas e inflamatórias, e o papel do NF- B é essencial. A diminuição da NO sintase endotelial (eNOS) durante a sepse contribui com a disfunção endotelial. A eritropoietina (EPO) é uma citocina protetora de diversos tecidos durante o estresse. Investigamos o papel da EPO na injúria renal aguda (
Publicado em: 2010
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4. Regulation of the the rat pineal gland hormonal production by modulators of the inflammatory process / Regulação da produção hormonal da glândula pineal de ratos por moduladores do processo inflamatório
The melatonin, synthetized by the pineal gland, exihibits a number of regulatory activities on the internal dynamic homeostasis of mammals. These functions are related to the regulation of endogenous circadian and seasonal rhythms during healthy and physiopathological processes. This study evaluates the effects of the inflammatory modulators, corticosterone,
Publicado em: 2009
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5. Regulation of stem cell factor expression in inflammation and asthma
Stem cell factor (SCF) is a major mast cell growth factor, which could be involved in the local increase of mast cell number in the asthmatic airways. In vivo, SCF expression increases in asthmatic patients and this is reversed after treatment with glucocorticoids. In vitro in human lung fibroblasts in culture, IL-1beta, a pro-inflammatory cytokine, confirms
Memórias do Instituto Oswaldo Cruz. Publicado em: 2005-03
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6. A new member of the I kappaB protein family, I kappaB epsilon, inhibits RelA (p65)-mediated NF-kappaB transcription.
A novel member of the I kappaB family has been identified as a protein that associated with the p50 subunit of NF-kappaB in a yeast two-hybrid screen. Similar to previously known I kappaB proteins, this member, I kappaB epsilon, has six consecutive ankyrin repeats. I kappaB epsilon mRNA is widely expressed in different human tissues, with highest levels in s
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7. Characterization of a mutant cell line that does not activate NF-kappaB in response to multiple stimuli.
Numerous genes required during the immune or inflammation response as well as the adhesion process are regulated by nuclear factor kappaB (NF-kappaB). Associated with its inhibitor, I kappaB, NF-kappaB resides as an inactive form in the cytoplasm. Upon stimulation by various agents, I kappaB is proteolyzed and NF-kappaB translocates to the nucleus, where it
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8. The kappaB sites in the human immunodeficiency virus type 1 long terminal repeat enhance virus replication yet are not absolutely required for viral growth.
The dependence of human immunodeficiency virus type 1 (HIV-1) on its NF-kappaB binding sites (kappaB sites) for replication in transformed and primary T-cell targets was examined by infecting cells with HIV-1 reporter viruses containing kappaB site enhancer mutations. Viral transcription was measured either with luciferase-expressing HIV-1 that infects for a
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9. Identification of a novel NF-kappaB p50-related protein in B lymphocytes.
In most cell types other than mature B lymphocytes and macrophages, the transcription factor NF-kappaB remains in an inactive form in the cytosol by being bound to the inhibitory proteins IkappaBalpha and IkappaBbeta. To investigate the regulation of constitutively active NF-kappaB in B lymphocytes, we have examined the composition of Rel protein complexes i
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10. I kappaB alpha physically interacts with a cytoskeleton-associated protein through its signal response domain.
The I kappaB alpha protein is a key molecular target involved in the control of NF-kappaB/Rel transcription factors during viral infection or inflammatory reactions. This NF-kappaB-inhibitory factor is regulated by posttranslational phosphorylation and ubiquitination of its amino-terminal signal response domain that targets I kappaB alpha for rapid proteolys
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11. Synergistic activation of NF-kappaB by tumor necrosis factor alpha and gamma interferon via enhanced I kappaB alpha degradation and de novo I kappaBbeta degradation.
Tumor necrosis factor alpha (TNF-alpha) and gamma interferon (IFN-gamma) are required for an effective immune response to bacterial infection and these cytokines synergize in a variety of biological responses, including the induction of cytokine, cell adhesion, and inducible nitrous oxide synthase gene expression. Typically, the synergistic effect on gene ex
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12. Induction of nuclear factor kappaB by the CD30 receptor is mediated by TRAF1 and TRAF2.
CD30 is a lymphoid cell-specific surface receptor which was originally identified as an antigen expressed on Hodgkin's lymphoma cells. Activation of CD30 induces the nuclear factor kappaB (NF-kappaB) transcription factor. In this study, we define the domains in CD30 which are required for NF-kappaB activation. Two separate elements of the cytoplasmic domain