New Frontiers for the NFIL3 bZIP Transcription Factor in Cancer, Metabolism and Beyond

Keniry, Megan; Dearth, Robert K.; Persans, Michael W.; Parsons, Ramon

doi:10.15190/d.2014.7

Cited by 29 publications

(22 citation statements)

References 78 publications

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“…The b-ZIP transcription factor, E4BP4, is abundantly expressed in immune cells, liver, and bone (35). We previously reported an elevated level of E4bp4 mRNA in the refed liver and its induction by insulin in hepatocytes (39).…”

Section: Discussionmentioning

confidence: 99%

“…The b-ZIP transcription repressor, E4-binding protein 4 (E4BP4), also called nuclear factor interleukin-3-regulated (NFIL3), plays an essential role in innate immunity (34,35). The mRNA oscillations of E4bp4 were detected in the suprachiasmatic nuclei, liver, adipose tissues, aorta, skeletal muscles, and adrenal glands (36,37).…”

Section: Generation Of Adenovirusesmentioning

confidence: 99%

“…Until now, E4BP4's biological actions have been shown to depend on its DNA-binding ability to regulate transcription (35,54). Whether E4BP4 can regulate transcription via protein-protein interaction has not been demonstrated.…”

Section: E4bp4 Regulates Nuclear Srebp-1c Acetylation Ubiquitinationmentioning

confidence: 99%

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E4BP4 is an insulin-induced stabilizer of nuclear SREBP-1c and promotes SREBP-1c-mediated lipogenesis

Tong

Zhang

et al. 2016

Journal of Lipid Research

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Section: Discussionmentioning

confidence: 99%

Section: Generation Of Adenovirusesmentioning

confidence: 99%

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E4BP4 is an insulin-induced stabilizer of nuclear SREBP-1c and promotes SREBP-1c-mediated lipogenesis

Tong

Zhang

et al. 2016

Journal of Lipid Research

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“…As a b-ZIP transcription factor, E4BP4 is ubiquitously expressed in various tissues, particularly abundant in the liver, spleen, and adipose tissue. 22 Although E4BP4 is well-known for its critical role in NK cell development and lymphocytes 23,24 and has been recently implicated in hepatic gluconeogenesis and the regulation of body composition, 25,26 the involvement of E4BP4 in lipid metabolism remains largely unexplored. We previously reported that potent induction of E4BP4 by insulin contributes to the postprandial de novo lipogenesis in an SREBP-1c-dependent manner.…”

Section: Introductionmentioning

confidence: 99%

Hepatic E4BP4 induction promotes lipid accumulation by suppressing AMPK signaling in response to chemical or diet‐induced ER stress

et al. 2020

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Prolonged ER stress has been known to be one of the major drivers of impaired lipid homeostasis during the pathogenesis of non‐alcoholic liver disease (NAFLD). However, the downstream mediators of ER stress pathway in promoting lipid accumulation remain poorly understood. Here, we present data showing the b‐ZIP transcription factor E4BP4 in both the hepatocytes and the mouse liver is potently induced by the chemical ER stress inducer tunicamycin or by high‐fat, low‐methionine, and choline‐deficient (HFLMCD) diet. We showed that such an induction is partially dependent on CHOP, a known mediator of ER stress and requires the E‐box element of the E4bp4 promoter. Tunicamycin promotes the lipid droplet formation and alters lipid metabolic gene expression in primary mouse hepatocytes from E4bp4flox/flox but not E4bp4 liver‐specific KO (E4bp4‐LKO) mice. Compared with E4bp4flox/flox mice, E4bp4‐LKO female mice exhibit reduced liver lipid accumulation and partially improved liver function after 10‐week HFLMCD diet feeding. Mechanistically, we observed elevated AMPK activity and the AMPKβ1 abundance in the liver of E4bp4‐LKO mice. We have evidence supporting that E4BP4 may suppress the AMPK activity via promoting the AMPKβ1 ubiquitination and degradation. Furthermore, acute depletion of the Ampkβ1 subunit restores lipid droplet formation in E4bp4‐LKO primary mouse hepatocytes. Our study highlighted hepatic E4BP4 as a key factor linking ER stress and lipid accumulation in the liver. Targeting E4BP4 in the liver may be a novel therapeutic avenue for treating NAFLD.

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“…Figure 3E, F shows the top 5 transcription factors predicted to regulate genes within 5 kb of the transcription start site of up-regulated or down-regulated genes, respectively. Ctcf is involved in gene regulation of multiple cell types, whereas the transcription factor families of IRF, Nfil3, and Stat are enriched in inflammatory cells and related processes (27)(28)(29). Gabpa, aka NRF2, is involved in metabolism and survival (30).…”

Section: Sca-1 + Reconstitution Induces Dramatic Transcriptional Chanmentioning

confidence: 99%

Dual roles for bone marrow‐derived Sca‐1 cells in cardiac function

Tobin

et al. 2017

FASEB j.

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Recruitment of stem cells from the bone marrow (BM) is an important aspect of cardiac healing that becomes inefficient with age. We investigated the role of young stem cell antigen 1 (Sca-1)-positive BM cells on the aged heart by microarray analysis after BM reconstitution. Sca-1 and Sca-1 BM cells from young green fluorescent protein (GFP)-positive mice were used to reconstitute the BM of aged mice. Myocardial infarction (MI) was induced 3 mo later. GFP cells were more abundant in the BM, blood, and heart of Sca-1 mice, which corresponded to preserved cardiac function after MI. At baseline, Sca-1 BM reconstitution increased cardiac expression of serum response factor, vascular endothelial growth factor A, and myogenic genes, but reduced the expression of After MI, inflammation was identified as a key difference between Sca-1 and Sca-1 groups, as cytokine expression and cell surface markers associated with inflammatory cells were up-regulated with Sca-1 reconstitution. Mac-3 and F4/80 staining showed that the postinfarction heart was composed of a mixture of GFP (donor) macrophages, GFP (host) macrophages, and GFP cells that did not contribute to the macrophage population. This study demonstrates that Sca-1 BM cells regulate cardiac healing though an acute inflammatory response and also before injury by stimulating formation of a beneficial cardiac niche.-Tobin, S. W., Li, S.-H., Li, J., Wu, J., Yeganeh, A., Yu, P., Weisel, R. D., Li, R.-K. Dual roles for bone marrow-derived Sca-1 cells in cardiac function.

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New Frontiers for the NFIL3 bZIP Transcription Factor in Cancer, Metabolism and Beyond

Cited by 29 publications

References 78 publications

E4BP4 is an insulin-induced stabilizer of nuclear SREBP-1c and promotes SREBP-1c-mediated lipogenesis

E4BP4 is an insulin-induced stabilizer of nuclear SREBP-1c and promotes SREBP-1c-mediated lipogenesis

Hepatic E4BP4 induction promotes lipid accumulation by suppressing AMPK signaling in response to chemical or diet‐induced ER stress

Dual roles for bone marrow‐derived Sca‐1 cells in cardiac function

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