Early growth response 2 (Egr-2) expression is triggered by NF-κB activation

Nafez, Solmaz; Oikawa, Kensuke; Odero, Gary; Sproule, Michael K. J.; Ge, Ning; Schapansky, Jason; Abrenica, Bernard; Hatherell, Avril; Cadonic, Chris; Zhang, Shunzhen; Song, Xiaohua; Kauppinen, Tiina M.; Glazner, Gordon W.; Grilli, Mariagrazia; Czubryt, Michael P.; Eisenstat, David D.; Albensi, Benedict C.

doi:10.1016/j.mcn.2014.12.008

Cited by 15 publications

(17 citation statements)

References 52 publications

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“…In light of studies demonstrating enhanced cognition in cases of Egr2 deficiency, it would be interesting to evaluate basal levels of this Egr family member in animals exhibiting AD-associated cognitive dysfunction. Our laboratory has confirmed NF-κB-dependent upregulation of Egr2 after LTP in the hippocampus (Nafez et al, 2015). Whether this upregulation persists in the AD-like brain, however, is unknown.…”

Section: Early Growth Response (Egr) Factorssupporting

confidence: 56%

Section: Early Growth Response (Egr) Factorsmentioning

confidence: 99%

“…Krox20) has recently been confirmed as a gene target in neurons (Nafez et al, 2015). In mouse hippocampal slices, LTP upregulates Egr2 (Williams et al, 1995) in an NF-κB-dependent manner that requires p50 (Nafez et al, 2015). Studies of the behavioral impact of Egr2 regulation, however, have found a gain of function in Egr-2-conditional KO mice lacking forebrain expression, as reflected by improved motor skill learning and enhanced long-term memory (24 h) in an object recognition task (Poirier et al, 2007).…”

Section: Early Growth Response (Egr) Factorsmentioning

confidence: 99%

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Neuronal Gene Targets of NF-κB and Their Dysregulation in Alzheimer's Disease

Snow

Albensi

2016

Front. Mol. Neurosci.

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136

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Although, better known for its role in inflammation, the transcription factor nuclear factor kappa B (NF-κB) has more recently been implicated in synaptic plasticity, learning, and memory. This has been, in part, to the discovery of its localization not just in glia, cells that are integral to mediating the inflammatory process in the brain, but also neurons. Several effectors of neuronal NF-κB have been identified, including calcium, inflammatory cytokines (i.e., tumor necrosis factor alpha), and the induction of experimental paradigms thought to reflect learning and memory at the cellular level (i.e., long-term potentiation). NF-κB is also activated after learning and memory formation in vivo. In turn, activation of NF-κB can elicit either suppression or activation of other genes. Studies are only beginning to elucidate the multitude of neuronal gene targets of NF-κB in the normal brain, but research to date has confirmed targets involved in a wide array of cellular processes, including cell signaling and growth, neurotransmission, redox signaling, and gene regulation. Further, several lines of research confirm dysregulation of NF-κB in Alzheimer's disease (AD), a disorder characterized clinically by a profound deficit in the ability to form new memories. AD-related neuropathology includes the characteristic amyloid beta plaque formation and neurofibrillary tangles. Although, such neuropathological findings have been hypothesized to contribute to memory deficits in AD, research has identified perturbations at the cellular and synaptic level that occur even prior to more gross pathologies, including transcriptional dysregulation. Indeed, synaptic disturbances appear to be a significant correlate of cognitive deficits in AD. Given the more recently identified role for NF-κB in memory and synaptic transmission in the normal brain, the expansive network of gene targets of NF-κB, and its dysregulation in AD, a thorough understanding of NF-κB-related signaling in AD is warranted and may have important implications for uncovering treatments for the disease. This review aims to provide a comprehensive view of our current understanding of the gene targets of this transcription factor in neurons in the intact brain and provide an overview of studies investigating NF-κB signaling, including its downstream targets, in the AD brain as a means of uncovering the basic physiological mechanisms by which memory becomes fragile in the disease.

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Section: Early Growth Response (Egr) Factorssupporting

confidence: 56%

Section: Early Growth Response (Egr) Factorsmentioning

confidence: 99%

Section: Early Growth Response (Egr) Factorsmentioning

confidence: 99%

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Neuronal Gene Targets of NF-κB and Their Dysregulation in Alzheimer's Disease

Snow

Albensi

2016

Front. Mol. Neurosci.

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136

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“…Plenty of document information included findings that endogenous EGR2 was significantly low expression in various cancer cell lines and primary cancers [54–57]. Egr2 can be induced by a variety of extracellular signal molecules, such as cytokines and kinase, and combine with gene promoters and affect the expression of the downstream genes [58–60]. Evidence showed that dysregulation of Egr2 was found in chronic lymphocytic leukemia and miRNA-150 promoted the proliferation of gastric cancer through negative regulating Egr2 [61, 62].…”

Section: Discussionmentioning

confidence: 99%

LncRNA-AF113014 promotes the expression of Egr2 by interaction with miR-20a to inhibit proliferation of hepatocellular carcinoma cells

et al. 2017

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Long non-coding RNAs (lncRNAs), tentatively identified as non-protein coding RNA, are transcripts more than 200nt in length and accounting for 98% of the whole genome of human being. Accumulating evidence showed aberrant expressions of lncRNAs are strongly correlated to the development of cancers. In this study, AF113014 is a new lncRNA identified from Microarray. We found AF113014 is differentially expressed between HCC cell lines and normal hepatocytes. Functionally, AF113014 inhibited proliferation of HCC cells both in vitro and in vivo, whereas the opposite effect was observed when AF113014 knockdown. Moreover, we identified that Egr2, a tumor suppressor gene, was a downstream target gene of AF113014. Furthermore, we discovered that AF113014 up-regulated Egr2 expression through interacting with miR-20a by using dual-luciferase reporter assay, qRT-PCR and Western blotting analysis. Our data provides a new insight for understanding the mechanisms of HCC.

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“…Human LAG3 + Tregs also suppress antibody production and SLE is correlated with both decreased EGR2 expression and decreased LAG3+ Treg numbers [99, 100]. While the molecular mechanisms controlling EGR2/3 expression are not fully elucidated, NF-κB binding to its recognition sequence in the proximal promoter of EGR2 has been observed [89, 101]. Further, Ca 2+ dependent expression of EGR2 and EGR3 has been observed [39].…”

Section: Cooperativity Of Transcription Factors In T Cell Activationmentioning

confidence: 99%

EGR-mediated control of STIM expression and function

Gross

Hooper

et al. 2019

Cell Calcium

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Summary Ca2+ is a ubiquitous, dynamic and pluripotent second messenger with highly context-dependent roles in complex cellular processes such as differentiation, proliferation, and cell death [1]. These Ca2+ signals are generated by Ca2+-permeable channels located on the plasma membrane (PM) and endoplasmic reticulum (ER) and shaped by PM- and ER-localized pumps and transporters. Differences in the expression of these Ca2+ homeostasis proteins contribute to cell and context-dependent differences in the spatiotemporal organization of Ca2+ signals and, ultimately, cell fate. This review focuses on the Early Growth Response (EGR) family of zinc finger transcription factors and their role in the transcriptional regulation of Stromal Interaction Molecule (STIM1), a critical regulator of Ca2+ entry in both excitable and non-excitable cells.

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Early growth response 2 (Egr-2) expression is triggered by NF-κB activation

Cited by 15 publications

References 52 publications

Neuronal Gene Targets of NF-κB and Their Dysregulation in Alzheimer's Disease

Neuronal Gene Targets of NF-κB and Their Dysregulation in Alzheimer's Disease

LncRNA-AF113014 promotes the expression of Egr2 by interaction with miR-20a to inhibit proliferation of hepatocellular carcinoma cells

EGR-mediated control of STIM expression and function

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