Ezrin-Radixin-Moesin-binding Phosphoprotein 50 (EBP50) and Nuclear Factor-κB (NF-κB)

Leslie, Kristen L; Song, Gyun Jee; Barrick, Stacey; Wehbi, Vanessa L.; Vilardaga, Jean-Pierre; Bauer, Philip M.; Bisello, Alessandro

doi:10.1074/jbc.m113.483339

Cited by 24 publications

(22 citation statements)

References 48 publications

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“…The levels of EBP50 expressed under these conditions were approximately three times higher than primary VSMC (Fig. 2D), and were similar to those observed under inflammatory conditions (27) and in vessels (23,24). Cells were incubated with FBS after overnight serum starvation to induce Akt activation (Fig.…”

Section: Skp2 Binds the Pdz1 Domain Of Ebp50 -Ebp50supporting

confidence: 73%

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Phosphorylation of Ezrin-Radixin-Moesin-binding Phosphoprotein 50 (EBP50) by Akt Promotes Stability and Mitogenic Function of S-phase Kinase-associated Protein-2 (Skp2)

Song

Barrick²,

Mamonova³

et al. 2015

Journal of Biological Chemistry

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Background:The PDZ scaffolding protein EBP50 promotes Akt-dependent cell proliferation through the S-phase kinase associated protein-2 Skp2. Results: Akt phosphorylates threonine 156 of EBP50, allosterically promoting the binding of Skp2 to the first PDZ domain of EBP50. Conclusion:The interaction with EBP50 regulates the localization and stability of Skp2 and promotes cell proliferation. Significance: These studies define a regulatory mechanism contributing to Akt-dependent cell proliferation.

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Section: Skp2 Binds the Pdz1 Domain Of Ebp50 -Ebp50supporting

confidence: 73%

“…In addition to the effect on cell proliferation, EBP50 promotes VSMC motility (38) and the production of pro-inflammatory mediators in macrophages and of adhesion molecules in VSMC and endothelial cells (27). Collectively, these studies support the notion that EBP50 is a critical regulator of vascular remodeling.…”

Section: Ebp50 Stabilizes Skp2supporting

confidence: 58%

Phosphorylation of Ezrin-Radixin-Moesin-binding Phosphoprotein 50 (EBP50) by Akt Promotes Stability and Mitogenic Function of S-phase Kinase-associated Protein-2 (Skp2)

Song

Barrick²,

Mamonova³

et al. 2015

Journal of Biological Chemistry

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“…In addition, the recent study showed that the expression of NHERF1 was increased by nuclear transcription factor NF-κB in the primary macrophages and vascular smooth muscle cells [36]. In colon cancer cells, NHERF1 expression could be increased by the activation of NF-κB signaling and/or the multiple downstream signaling pathway of HIF-1α/VEGF-A induced in the hypoxia microenvironment.…”

Section: Discussionmentioning

confidence: 99%

NHERF1 regulates the progression of colorectal cancer through the interplay with VEGFR2 pathway

Hao

et al. 2016

Oncotarget

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The oncogenic role of ectopic expression of Na+/H+ exchanger regulatory factor 1 (NHERF1) was recently suggested in colorectal cancer, where it was implicated in playing a role in the tumor hypoxia microenvironment. Here we showed that a high level expression of NHERF1 was found in colorectal cancer tissues and that the expression of NHERF1 was positively correlated with VEGFR2 expression. The prognostic value of VEGFR2 expression in colorectal cancer relied on the expression of NHERF1. The up-regulation of NHERF1 induced by the exposure to hypoxia in colon cancer cells depended on the activation of VEGFR2 signaling. NHERF1 in turn inhibited the activation of VEGFR2 signaling which could be regulated by the interaction between NHERF1 and VEGFR2, resulting in the reduction of migration and invasion of colon cancer cells. These results suggest a dynamic interplay between NHERF1 and VEGFR2 signaling in colorectal cancer, which could explain the contribution of NHERF1 to the regulation of tumor cell responses to the hypoxia microenvironment.

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“…Multiple studies have shown various mechanisms of NHERF1’s involvement in NF-kB activation. For example, NHERF1 is a positive regulator of NF-kB activation in vascular inflammation by recruiting PKCζ at the cell membrane, resulting in activation of NF-kB [ 14 ]. NHERF1 maintains cyclic amino monophosphate (cAMP) and PKA signaling and regulates interleukin (IL)-6 production in human airway smooth muscle cells [ 15 ] and promotes mast cell activation via the C3a complement receptor (C3aR) pathway [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

Sodium Hydrogen Exchanger Regulatory Factor-1 (NHERF1) Regulates Fetal Membrane Inflammation

Kammala

Sheller‐Miller

Radnaa

et al. 2020

IJMS

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The fetal inflammatory response, a key contributor of infection-associated preterm birth (PTB), is mediated by nuclear factor kappa B (NF-kB) activation. Na+/H+ exchanger regulatory factor-1 (NHERF1) is an adapter protein that can regulate intracellular signal transduction and thus influence NF-kB activation. Accordingly, NHERF1 has been reported to enhance proinflammatory cytokine release and amplify inflammation in a NF-kB-dependent fashion in different cell types. The objective of this study was to examine the role of NHERF1 in regulating fetal membrane inflammation during PTB. We evaluated the levels of NHERF1 in human fetal membranes from term labor (TL), term not in labor (TNIL), and PTB and in a CD1 mouse model of PTB induced by lipopolysaccharide (LPS). Additionally, primary cultures of fetal membrane cells were treated with LPS, and NHERF1 expression and cytokine production were evaluated. Gene silencing methods using small interfering RNA targeting NHERF1 were used to determine the functional relevance of NHERF1 in primary cultures. NHERF1 expression was significantly (p < 0.001) higher in TL and PTB membranes compared to TNIL membranes, and this coincided with enhanced (p < 0.01) interleukin (IL)-6 and IL-8 expression levels. LPS-treated animals delivering PTB had increased levels of NHERF1, IL-6, and IL-8 compared to phosphate-buffered saline (PBS; control) animals. Silencing of NHERF1 expression resulted in a significant reduction in NF-kB activation and IL-6 and IL-8 production as well as increased IL-10 production. In conclusion, downregulation of NHERF1 increased anti-inflammatory IL-10, and reducing NHERF1 expression could be a potential therapeutic strategy to reduce the risk of infection/inflammation associated with PTB.

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Ezrin-Radixin-Moesin-binding Phosphoprotein 50 (EBP50) and Nuclear Factor-κB (NF-κB)

Cited by 24 publications

References 48 publications

Phosphorylation of Ezrin-Radixin-Moesin-binding Phosphoprotein 50 (EBP50) by Akt Promotes Stability and Mitogenic Function of S-phase Kinase-associated Protein-2 (Skp2)

Phosphorylation of Ezrin-Radixin-Moesin-binding Phosphoprotein 50 (EBP50) by Akt Promotes Stability and Mitogenic Function of S-phase Kinase-associated Protein-2 (Skp2)

NHERF1 regulates the progression of colorectal cancer through the interplay with VEGFR2 pathway

Sodium Hydrogen Exchanger Regulatory Factor-1 (NHERF1) Regulates Fetal Membrane Inflammation

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