Results 281 to 290 of about 360,317 (299)

The expression and significance of NF-κB, MMP1, and MMP2 in rats with abdominal aortic aneurysm

Cellular and Molecular Biology, 2020
This study aimed to investigate the expression and significance of NF-κB, matrix metal protein1 (MMP1), and matrix metal protein2 (MMP2) in rats with abdominal aortic aneurysm (AAA). 48 Wistar rats were collected, then they were divided into an experiment group and a control group (n=24).
Tao Fang, Zhilei Xie
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217 Altered Regulation of the Inhibitor IκBα Contributes to Changes in NF-κB Regulated Genes in the TILRR ko Mouse

Heart, 2015
Introduction Inflammatory responses are key drivers in the pathogenesis of atherosclerosis. We have identified a co-receptor, TILRR, a prominent activator of NF-IoB controlled responses, which we have demonstrated is highly expressed in atherosclerotic lesions.
Sheila E. Francis, Emer Murphy, Sarah Kate Smith, Andriy O. Samokhin, Eva E. Qwarnstrom   +4 more
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NF-κB is 25

Nature Immunology, 2011
NF-κB-mediated inflammatory biology can be formulated as the following five states: latency, induction, response, resolution and pathology. The first four involve carefully tuned molecular processes; pathology is the loss of control.
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The αvβ3 Integrin, NF-κB, Osteoprotegerin Endothelial Cell Survival Pathway Potential Role in AngiogenesisTcm

Trends in Cardiovascular Medicine, 2002
The growth and survival of many cell types requires integrin-mediated adhesion to the extracellular matrix (ECM). Physiologically, the prerequisite of cell-ECM adhesion interaction for cell cycle progression and cell survival is likely to be important in tissue morphology and regression as a mechanism to regulate tissue architecture and cell number ...
Marta Scatena, Cecilia M. Giachelli
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Physiological functions for brain NF-κB

Trends in Neurosciences, 2005
Members of the nuclear factor kappaB (NF-kappaB) family of transcription factors are activated within the CNS in pathological settings of apoptosis and neurological disease. Recent work using several model systems provides accumulating evidence that these transcription factors also participate in the regulation of neuronal activity-dependent ...
Meffert, Mollie K., Baltimore, David
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MicroRNAs, new effectors and regulators of NF‐κB

Immunological Reviews, 2012
Summary:  Since its discovery 25 years ago, nuclear factor‐κB (NF‐κB) has emerged as a transcription factor that controls diverse biological functions, ranging from inflammation to learning and memory. Activation of NF‐κB initiates an elaborate genetic program. Some of the NF‐κB‐driven genes do not encode proteins but rather are precursors to microRNAs.
Boldin, Mark P., Baltimore, David
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miR-675 promotes disease progression of non-small cell lung cancer via activating NF-κB signaling pathway

Cellular and Molecular Biology, 2017
Non-small cell lung cancer (NSCLC) is a major type of lung cancer significantly affected human life. Current studies have revealed potential role of miR-675 in the etiology of lung cancer. Therefore, in this study, we aimed to investigate the role of miR-675 in NSCLC cell line.
Xinghuan Wang, D. Hu, C. Yang, X. Liu, Y. Feng   +4 more
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Hypericin as a Non-Antioxidant Inhibitor of NF-κB

Planta Medica, 1999
NF-kappa B is a transcription factor involved in immune and inflammatory responses. Here we show that micromolar concentrations of hypericin inhibited the PMA- and TNF-alpha-induced activation of NF-kappa B in HeLa and TC10 cells, respectively. In contrast, NF-kappa B activated by H2O2 was not influenced by hypericin, indicating a pathway-specificity ...
Bork, PM M, Bacher, S, Schmitz, ML L, Kaspers, U, Heinrich, M.   +4 more
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An Essential Role for NF-κB in Preventing TNF-α-Induced Cell Death

Science, 1996
Studies on mice deficient in nuclear factor kappa B (NF-κB) subunits have shown that this transcription factor is important for lymphocyte responses to antigens and cytokine-inducible gene expression. In particular, the RelA (p65) subunit is required for induction of tumor necrosis factor-α (TNF-α)-dependent genes.
Beg, Amer A,, Baltimore, David
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