Importins and Exportins Regulating Allergic Immune Responses

Aggarwal, Ankita; Agrawal, Devendra K.

doi:10.1155/2014/476357

Cited by 23 publications

(20 citation statements)

References 86 publications

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“…Next, we examined whether the activation and translocation of NF-κB could be diminished by BIOGF1K using nuclear fractions, since the nuclear translocation of NF-κB is required for its activation [42]. As we expected, BIOGF1K suppressed the enhancement in the nuclear levels of the NF-κB p65 and p50 subunits at 30–60 min (Fig.…”

Section: Resultsmentioning

confidence: 74%

In vitro antioxidative and anti-inflammatory effects of the compound K-rich fraction BIOGF1K, prepared from Panax ginseng

Hossen

Hong

Baek

et al. 2017

Journal of Ginseng Research

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BackgroundBIOGF1K, a compound K-rich fraction prepared from the root of Panax ginseng, is widely used for cosmetic purposes in Korea. We investigated the functional mechanisms of the anti-inflammatory and antioxidative activities of BIOGF1K by discovering target enzymes through various molecular studies.MethodsWe explored the inhibitory mechanisms of BIOGF1K using lipopolysaccharide-mediated inflammatory responses, reporter gene assays involving overexpression of toll-like receptor adaptor molecules, and immunoblotting analysis. We used the 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay to measure the antioxidative activity. We cotransfected adaptor molecules, including the myeloid differentiation primary response gene 88 (MyD88) and Toll/interleukin-receptor domain containing adaptor molecule-inducing interferon-β (TRIF), to measure the activation of nuclear factor (NF)-κB and interferon regulatory factor 3 (IRF3).ResultsBIOGF1K suppressed lipopolysaccharide-triggered NO release in macrophages as well as DPPH-induced electron-donating activity. It also blocked lipopolysaccharide-induced mRNA levels of interferon-β and inducible nitric oxide synthase. Moreover, BIOGF1K diminished the translocation and activation of IRF3 and NF-κB (p50 and p65). This extract inhibited the upregulation of NF-κB-linked luciferase activity provoked by phorbal-12-myristate-13 acetate as well as MyD88, TRIF, and inhibitor of κB (IκBα) kinase (IKKβ), and IRF3-mediated luciferase activity induced by TRIF and TANK-binding kinase 1 (TBK1). Finally, BIOGF1K downregulated the NF-κB pathway by blocking IKKβ and the IRF3 pathway by inhibiting TBK1, according to reporter gene assays, immunoblotting analysis, and an AKT/IKKβ/TBK1 overexpression strategy.ConclusionOverall, our data suggest that the suppression of IKKβ and TBK1, which mediate transcriptional regulation of NF-κB and IRF3, respectively, may contribute to the broad-spectrum inhibitory activity of BIOGF1K.

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Section: Resultsmentioning

confidence: 74%

In vitro antioxidative and anti-inflammatory effects of the compound K-rich fraction BIOGF1K, prepared from Panax ginseng

Hossen

Hong

Baek

et al. 2017

Journal of Ginseng Research

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“…Indeed, the nuclear transport proteins, Ran and Crm1, have both recently been implicated as key proteins in the metastatic progression of cancer (21)(22)(23). Another role for Kpnb1 which has recently been highlighted is its role in inflammation (24). Kpnb1 has been shown to be a critical mediator of inflammation due to its nuclear import of many inflammatory-associated transcription factors, including NFkB (25), STAT family members (26), AP1 (27), and GATA-3 (28).…”

Section: Introductionmentioning

confidence: 99%

Targeting the Nuclear Import Receptor Kpnβ1 as an Anticancer Therapeutic

Watt

Chi

Stelma

et al. 2016

Molecular Cancer Therapeutics

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Karyopherin beta 1 (Kpnb1) is a nuclear transport receptor that imports cargoes into the nucleus. Recently, elevated Kpnb1 expression was found in certain cancers and Kpnb1 silencing with siRNA was shown to induce cancer cell death. This study aimed to identify novel small molecule inhibitors of Kpnb1, and determine their anticancer activity. An in silico screen identified molecules that potentially bind Kpnb1 and Inhibitor of Nuclear Import-43, INI-43

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“…Upon activation either by canonical or non-canonical pathways, IκBα is phosphorylated which leads to rapid, signal-induced polyubiquitination and degradation by the proteasome. The liberating NF-κB complex with unmasked NLSs binds to karyopherin alpha 4 (KPNA4) (also known importin α3), a nuclear membrane protein that functions as a part of the shuttling of protein nuclear translocation 19 . KPNA4- importin β complex recognizes and binds to NLSs in the NF-κB dimer, p65/p50.…”

Section: Introductionmentioning

confidence: 99%

Vitamin D Deficiency Accelerates Coronary Artery Disease Progression in Swine

Chen

Swier

Boosani

et al. 2016

ATVB

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Objective-The role of vitamin D deficiency in coronary artery disease (CAD) progression is uncertain. Chronic inflammation in epicardial adipose tissue (EAT) has been implicated in the pathogenesis of CAD. However, the molecular mechanism underlying vitamin D deficiency-enhanced inflammation in the EAT of diseased coronary arteries remains unknown. We examined a mechanistic link between 1,25-dihydroxyvitamin D-mediated suppression of nuclear factor-κB (NF-κB) transporter, karyopherin α4 (KPNA4) expression and NF-κB activation in preadipocytes. Furthermore, we determined whether vitamin D deficiency accelerates CAD progression by increasing KPNA4 and nuclear NF-κB levels in EAT. Approach and Results-Nuclear protein levels were detected by immunofluorescence and Western blot. Exogenous KPNA4 was transported into cells by a transfection approach and constituted lentiviral vector. Swine were administered vitamin D-deficient or vitamin D-sufficient hypercholesterolemic diet. After 1 year, the histopathology of coronary arteries and nuclear protein expression of EAT were assessed. 1,25-dihydroxyvitamin D inhibited NF-κB activation and reduced KPNA4 levels through increased vitamin D receptor expression. Exogenous KPNA4 rescued 1,25-dihydroxyvitamin D-dependent suppression of NF-κB nuclear translocation and activation. Vitamin D deficiency caused extensive CAD progression and advanced atherosclerotic plaques, which are linked to increased KPNA4 and nuclear NF-κB levels in the EAT. Conclusions-1,25-dihydroxyvitamin

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Importins and Exportins Regulating Allergic Immune Responses

Cited by 23 publications

References 86 publications

In vitro antioxidative and anti-inflammatory effects of the compound K-rich fraction BIOGF1K, prepared from Panax ginseng

In vitro antioxidative and anti-inflammatory effects of the compound K-rich fraction BIOGF1K, prepared from Panax ginseng

Targeting the Nuclear Import Receptor Kpnβ1 as an Anticancer Therapeutic

Vitamin D Deficiency Accelerates Coronary Artery Disease Progression in Swine

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