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Article ; Online: NRF2 and the Moirai: Life and Death Decisions on Cell Fates.

Yagishita, Yoko / Chartoumpekis, Dionysios V / Kensler, Thomas W / Wakabayashi, Nobunao

2023 Volume 38, Issue 7-9, Page(s) 684–708

Abstract: Significance: ...

Abstract	Significance:
MeSH term(s)	NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Cell Differentiation/genetics ; Gene Expression Regulation ; Signal Transduction/physiology ; Oxidation-Reduction ; Kelch-Like ECH-Associated Protein 1/metabolism
Chemical Substances	NF-E2-Related Factor 2 ; Kelch-Like ECH-Associated Protein 1
Language	English
Publishing date	2023-02-22
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2022.0200
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Article ; Online: Transcriptional Regulation of

Yagishita, Yoko / Joshi, Tanvi / Kensler, Thomas W / Wakabayashi, Nobunao

Molecular and cellular biology

2023 Volume 43, Issue 1, Page(s) 43–63

Abstract: The physiological roles of aryl hydrocarbon receptor (AhR) in the small intestine have been revealed as immunomodulatory and barrier functions. However, its contributions to cell fate regulation are incompletely understood. The Notch-activated signaling ... ...

Abstract	The physiological roles of aryl hydrocarbon receptor (AhR) in the small intestine have been revealed as immunomodulatory and barrier functions. However, its contributions to cell fate regulation are incompletely understood. The Notch-activated signaling cascade is a central component of intestinal cell fate determinations. The lateral inhibitory mechanism governed by Notch directs cell fates toward distinct cell lineages (i.e., absorptive and secretory cell lineages) through its downstream effector, mouse atonal homolog 1 (MATH1). An investigation employing cell lines and intestinal crypt cells revealed that AhR regulates
MeSH term(s)	Animals ; Mice ; Gene Expression Regulation ; Intestine, Small ; Intestines ; Receptors, Aryl Hydrocarbon/genetics ; Receptors, Aryl Hydrocarbon/metabolism ; Stem Cells
Chemical Substances	Receptors, Aryl Hydrocarbon ; Atoh1 protein, mouse
Language	English
Publishing date	2023-01-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	779397-2
ISSN	1098-5549 ; 0270-7306
ISSN (online)	1098-5549
ISSN	0270-7306
DOI	10.1080/10985549.2022.2160610
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Zs.A 1666: Show issues

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Article ; Online: Forced Hepatic Expression of NRF2 or NQO1 Impedes Hepatocyte Lipid Accumulation in a Lipodystrophy Mouse Model.

Wakabayashi, Nobunao / Yagishita, Yoko / Joshi, Tanvi / Kensler, Thomas W

International journal of molecular sciences

2023 Volume 24, Issue 17

Abstract: Lipodystrophy is a disorder featuring loss of normal adipose tissue depots due to impaired production of normal adipocytes. It leads to a gain of fat deposition in ectopic tissues such as liver and skeletal muscle that results in steatosis, dyslipidemia, ...

Abstract	Lipodystrophy is a disorder featuring loss of normal adipose tissue depots due to impaired production of normal adipocytes. It leads to a gain of fat deposition in ectopic tissues such as liver and skeletal muscle that results in steatosis, dyslipidemia, and insulin resistance. Previously, we established a
MeSH term(s)	Animals ; Mice ; Disease Models, Animal ; Fatty Liver/genetics ; Hepatocytes ; Hepatomegaly ; Kelch-Like ECH-Associated Protein 1/genetics ; Lipids ; NF-E2-Related Factor 2/genetics ; NAD(P)H Dehydrogenase (Quinone)/genetics ; Lipodystrophy/genetics ; Lipodystrophy/metabolism
Chemical Substances	Kelch-Like ECH-Associated Protein 1 ; Lipids ; NF-E2-Related Factor 2 ; Nqo1 protein, mouse (EC 1.6.5.2) ; NAD(P)H Dehydrogenase (Quinone) (EC 1.6.5.2)
Language	English
Publishing date	2023-08-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms241713345
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Article ; Online: Transcriptional Regulation of Math1 by Aryl Hydrocarbon Receptor: Effect on Math1⁺ Progenitor Cells in Mouse Small Intestine

Yagishita, Yoko / Joshi, Tanvi / Kensler, Thomas W. / Wakabayashi, Nobunao

Molecular and Cellular Biology. 2023 Jan. 2, v. 43, no. 1 p.43-63

2023

Abstract	The physiological roles of aryl hydrocarbon receptor (AhR) in the small intestine have been revealed as immunomodulatory and barrier functions. However, its contributions to cell fate regulation are incompletely understood. The Notch-activated signaling cascade is a central component of intestinal cell fate determinations. The lateral inhibitory mechanism governed by Notch directs cell fates toward distinct cell lineages (i.e., absorptive and secretory cell lineages) through its downstream effector, mouse atonal homolog 1 (MATH1). An investigation employing cell lines and intestinal crypt cells revealed that AhR regulates Math1 expression in a xenobiotic response element (XRE)-dependent manner. The AhR-Math1 axis was further addressed using intestinal organoids, where AhR-Math1 and HES1-Math1 axes appeared to coexist within the underlying Math1 transcriptional machinery. When the HES1-Math1 axis was pharmacologically suppressed, β-naphthoflavone-mediated AhR activation increased the number of goblet and Math1⁺ progenitor cells in the organoids. The same pharmacological dissection of the AhR-Math1 axis was applied in vivo, demonstrating an enhanced number of Math1⁺ progenitor cells in the small intestine following AhR activation. We report here that AhR-Math1 is a direct transcriptional axis with effects on Math1⁺ progenitor cells in the small intestine, highlighting a novel molecular basis for fine-tuning Notch-mediated cell fate regulation.
Keywords	aryl hydrocarbon receptors ; cell biology ; dissection ; mice ; organoids ; small intestine ; transcription (genetics) ; xenobiotics ; AhR ; Math1 ; intestinal organoids ; Math1+ progenitor cells ; goblet cells
Language	English
Dates of publication	2023-0102
Size	p. 43-63.
Publishing place	Taylor & Francis
Document type	Article ; Online
ZDB-ID	779397-2
ISSN	1098-5549 ; 0270-7306
ISSN (online)	1098-5549
ISSN	0270-7306
DOI	10.1080/10985549.2022.2160610
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: A Point Mutation at C151 of

Gatbonton-Schwager, Tonibelle / Yagishita, Yoko / Joshi, Tanvi / Wakabayashi, Nobunao / Srinivasan, Harini / Suzuki, Takafumi / Yamamoto, Masayuki / Kensler, Thomas W

Molecular pharmacology

2023 Volume 104, Issue 2, Page(s) 51–61

Abstract: Bardoxolone methyl (CDDO-Me) is an oleanane triterpenoid in late-stage clinical development for the treatment of patients with diabetic kidney disease. Preclinical studies in rodents demonstrate the efficacy of triterpenoids against carcinogenesis and ... ...

Abstract	Bardoxolone methyl (CDDO-Me) is an oleanane triterpenoid in late-stage clinical development for the treatment of patients with diabetic kidney disease. Preclinical studies in rodents demonstrate the efficacy of triterpenoids against carcinogenesis and other diseases, including renal ischemia-reperfusion injury, hyperoxia-induced acute lung injury, and immune hepatitis. Genetic disruption of
MeSH term(s)	Mice ; Animals ; Kelch-Like ECH-Associated Protein 1/genetics ; Kelch-Like ECH-Associated Protein 1/metabolism ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Point Mutation ; Cytoprotection ; Cysteine/metabolism ; Signal Transduction ; Oleanolic Acid/pharmacology ; Oleanolic Acid/therapeutic use ; Mice, Knockout ; Hepatitis
Chemical Substances	Kelch-Like ECH-Associated Protein 1 ; bardoxolone methyl (CEG1Q6OGU1) ; NF-E2-Related Factor 2 ; Cysteine (K848JZ4886) ; Oleanolic Acid (6SMK8R7TGJ) ; Keap1 protein, mouse
Language	English
Publishing date	2023-05-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	124034-1
ISSN	1521-0111 ; 0026-895X
ISSN (online)	1521-0111
ISSN	0026-895X
DOI	10.1124/molpharm.123.000671
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Article ; Online: Constitutive Activation of Nrf2 in Mice Expands Enterogenesis in Small Intestine Through Negative Regulation of Math1.

Yagishita, Yoko / McCallum, Melissa L / Kensler, Thomas W / Wakabayashi, Nobunao

Cellular and molecular gastroenterology and hepatology

2020 Volume 11, Issue 2, Page(s) 503–524

Abstract: Background & aims: Notch signaling coordinates cell differentiation processes in the intestinal epithelium. The transcription factor Nrf2 orchestrates defense mechanisms by regulating cellular redox homeostasis, which, as shown previously in murine ... ...

Abstract	Background & aims: Notch signaling coordinates cell differentiation processes in the intestinal epithelium. The transcription factor Nrf2 orchestrates defense mechanisms by regulating cellular redox homeostasis, which, as shown previously in murine liver, can be amplified through signaling crosstalk with the Notch pathway. However, interplay between these 2 signaling pathways in the gut is unknown. Methods: Mice modified genetically to amplify Nrf2 in the intestinal epithelium (Keap1 Results: Constitutive activation of Nrf2 signaling caused increased intestinal length along with expanded cell number and thickness of enterocytes without any alterations of secretory lineage, outcomes abrogated by concomitant disruption of Nrf2. The Nrf2 and Notch pathways in epithelium showed inverse spatial profiles, where Nrf2 activity in crypts was lower than villi. In progenitor cells of Keap1 Conclusions: Activation of Nrf2 perturbed the dialog of the Notch cascade though negative regulation of Math1 in progenitor cells, leading to enhanced enterogenesis. The crosstalk between the Nrf2 and Notch pathways could be critical for fine-tuning intestinal homeostasis and point to new approaches for the pharmacological management of absorptive deficiencies.
MeSH term(s)	Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Cell Differentiation/drug effects ; Cell Differentiation/genetics ; Cell Line ; Enterocytes/drug effects ; Enterocytes/physiology ; Female ; Intestinal Mucosa/drug effects ; Intestinal Mucosa/growth & development ; Intestine, Small/drug effects ; Intestine, Small/growth & development ; Male ; Mice ; Models, Animal ; NF-E2-Related Factor 2/agonists ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Regeneration/drug effects ; Regeneration/genetics ; Stem Cells/drug effects ; Stem Cells/physiology
Chemical Substances	Atoh1 protein, mouse ; Basic Helix-Loop-Helix Transcription Factors ; NF-E2-Related Factor 2 ; Nfe2l2 protein, mouse
Language	English
Publishing date	2020-09-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2819778-1
ISSN	2352-345X ; 2352-345X
ISSN (online)	2352-345X
ISSN	2352-345X
DOI	10.1016/j.jcmgh.2020.08.013
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Article ; Online: Keap1/Nrf2 pathway in the frontiers of cancer and non-cancer cell metabolism.

Chartoumpekis, Dionysios V / Wakabayashi, Nobunao / Kensler, Thomas W

Biochemical Society transactions

2015 Volume 43, Issue 4, Page(s) 639–644

Abstract: Cancer cells adapt their metabolism to their increased needs for energy and substrates for protein, lipid and nucleic acid synthesis. Nuclear erythroid factor 2-like 2 (Nrf2) pathway is usually activated in cancers and has been suggested to promote ... ...

Abstract	Cancer cells adapt their metabolism to their increased needs for energy and substrates for protein, lipid and nucleic acid synthesis. Nuclear erythroid factor 2-like 2 (Nrf2) pathway is usually activated in cancers and has been suggested to promote cancer cell survival mainly by inducing a large battery of cytoprotective genes. This mini review focuses on metabolic pathways, beyond cytoprotection, which can be directly or indirectly regulated by Nrf2 in cancer cells to affect their survival. The pentose phosphate pathway (PPP) is enhanced by Nrf2 in cancers and aids their growth. PPP has also been found to be up-regulated in non-cancer tissues and other pathways, such as de novo lipogenesis, have been found to be repressed after activation of the Nrf2 pathway. The importance of these Nrf2-regulated metabolic pathways in cancer compared with non-cancer state remains to be determined. Last but not least, the importance of context about Nrf2 and cancer is highlighted as the Nrf2 pathway may be activated in cancers but its pharmacological activators are useful in chemoprevention.
MeSH term(s)	Cell Proliferation ; Cell Survival ; Gene Expression Regulation, Neoplastic ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Kelch-Like ECH-Associated Protein 1 ; NF-E2-Related Factor 2/metabolism ; Neoplasms/metabolism ; Pentose Phosphate Pathway ; Signal Transduction
Chemical Substances	Intracellular Signaling Peptides and Proteins ; KEAP1 protein, human ; Kelch-Like ECH-Associated Protein 1 ; NF-E2-Related Factor 2 ; NFE2L2 protein, human
Language	English
Publishing date	2015-08
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	184237-7
ISSN	1470-8752 ; 0300-5127
ISSN (online)	1470-8752
ISSN	0300-5127
DOI	10.1042/BST20150049
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Article ; Online: Crosstalk between Nrf2 and Notch signaling.

Wakabayashi, Nobunao / Chartoumpekis, Dionysios V / Kensler, Thomas W

Free radical biology & medicine

2015 Volume 88, Issue Pt B, Page(s) 158–167

Abstract: The transcription factor Nrf2 (nuclear factor, erythroid derived 2, like 2) belongs to the CNC-bZip protein family, forming a transcriptosome with its direct heterodimer partner, sMaf, and co-factors such as CBP/p300. Nrf2 binds to one or more AREs ( ... ...

Abstract	The transcription factor Nrf2 (nuclear factor, erythroid derived 2, like 2) belongs to the CNC-bZip protein family, forming a transcriptosome with its direct heterodimer partner, sMaf, and co-factors such as CBP/p300. Nrf2 binds to one or more AREs (antioxidant response elements) that are located in the gene regulatory regions of the hundreds of Nrf2 target genes. The AREs are key enhancers that are activated in response to endogenous or exogenous stresses to maintain cellular and tissue homeostasis. Data emanating from gene expression microarray analyses comparing Nrf2-disrupted and wild-type mouse embryonic fibroblasts (MEF) showed that expression of Notch1 and Notch-signaling-related genes were decreased in Nrf2-disrupted cells. This observation triggered our research on Nrf2-Notch crosstalk. A functional ARE has been identified upstream of the Notch1 major transcription start site. Furthermore, an Rbpjκ binding site is conserved on the promoters of Nrf2 among animal species. Notch1 is one of the transmembrane Notch family receptors that drive Notch signaling, together with the Rbpjκ transcription factor. After canonically accepting ligands such as Jags and Deltas, the receptor undergoes cleavage to yield the Notch intracellular domain, which translocates to the nucleus. Recent studies using conditional knockout mice indicate that Notch1 as well as Notch2 plays an important role postnatally in liver development and in maintenance of hepatic function. In this review, we summarize current understanding of the role of reciprocal transcriptional regulation between Nrf2 and Notch in adult liver from studies using Nrf2, Keap1, and Notch1 genetically engineered mice.
MeSH term(s)	Animals ; Liver/metabolism ; Mice ; NF-E2-Related Factor 2/metabolism ; Receptor Cross-Talk/physiology ; Receptors, Notch/metabolism ; Signal Transduction/physiology
Chemical Substances	NF-E2-Related Factor 2 ; Nfe2l2 protein, mouse ; Receptors, Notch
Language	English
Publishing date	2015-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2015.05.017
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Article ; Online: Nrf2 through Aryl Hydrocarbon Receptor Regulates IL-22 Response in CD4

Lin, Xun / Tawch, Suzanne / Wong, Hoi Tong / Roy, Suyasha / Gaudino, Stephen / Castillo, Patricia / Elsegeiny, Waleed / Wakabayashi, Nobunao / Oury, Tim D / Pociask, Derek / Chen, Kong / McLinskey, Nancy / Melville, Patricia / Syritsyna, Olga / Coyle, Patricia / Good, Misty / Awasthi, Amit / Kolls, Jay K / Kumar, Pawan

Journal of immunology (Baltimore, Md. : 1950)

2021 Volume 206, Issue 7, Page(s) 1540–1548

Abstract: IL-17A and IL-22 derived from Th17 cells play a significant role in mucosal immunity and inflammation. TGF-β and IL-6 promote Th17 differentiation; however, these cytokines have multiple targets. The identification and screening of additional molecules ... ...

Abstract	IL-17A and IL-22 derived from Th17 cells play a significant role in mucosal immunity and inflammation. TGF-β and IL-6 promote Th17 differentiation; however, these cytokines have multiple targets. The identification and screening of additional molecules that regulate IL-17A and IL-22 responses in certain inflammatory conditions is of great clinical significance. In this study, we show that CDDO-Im, a specific Nrf2 activator, promotes IL-17A and IL-22 responses in murine Th17 cells. In contrast, CDDO-Im inhibits IL-17A response in multiple sclerosis patient-derived PBMCs. However, Nrf2 specifically regulates IL-22 response in vivo. Nrf2 acts through the regulation of antioxidant response element (ARE) binding motifs in target genes to induce or repress transcription. Promoter analysis revealed that
MeSH term(s)	Animals ; Azo Compounds/metabolism ; CD4-Positive T-Lymphocytes/immunology ; Gene Expression Regulation ; Humans ; Imidazoles/metabolism ; Interleukin-17/genetics ; Interleukin-17/metabolism ; Interleukins/metabolism ; Lymphocyte Activation ; Mice ; Mice, Knockout ; Multiple Sclerosis/immunology ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Nuclear Receptor Subfamily 1, Group F, Member 3/genetics ; Oleanolic Acid/analogs & derivatives ; Oleanolic Acid/metabolism ; Promoter Regions, Genetic/genetics ; Pyrazoles/metabolism ; Receptors, Aryl Hydrocarbon/genetics ; Receptors, Aryl Hydrocarbon/metabolism ; Signal Transduction ; Th17 Cells/immunology ; Interleukin-22
Chemical Substances	1-(2-cyano-3,12-dioxooleana-1,9-dien-28-oyl) imidazole ; 2-methyl-2H-pyrazole-3-carboxylic acid (2-methyl-4-o-tolylazophenyl)amide ; Azo Compounds ; Imidazoles ; Interleukin-17 ; Interleukins ; NF-E2-Related Factor 2 ; Nfe2l2 protein, mouse ; Nuclear Receptor Subfamily 1, Group F, Member 3 ; Pyrazoles ; Receptors, Aryl Hydrocarbon ; Rorc protein, mouse ; Oleanolic Acid (6SMK8R7TGJ)
Language	English
Publishing date	2021-03-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1900656
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Article ; Online: Nrf2: friend or foe for chemoprevention?

Kensler, Thomas W / Wakabayashi, Nobunao

Carcinogenesis

2009 Volume 31, Issue 1, Page(s) 90–99

Abstract: Health reflects the ability of an organism to adapt to stress. Stresses--metabolic, proteotoxic, mitotic, oxidative and DNA-damage stresses--not only contribute to the etiology of cancer and other chronic degenerative diseases but are also hallmarks of ... ...

Abstract	Health reflects the ability of an organism to adapt to stress. Stresses--metabolic, proteotoxic, mitotic, oxidative and DNA-damage stresses--not only contribute to the etiology of cancer and other chronic degenerative diseases but are also hallmarks of the cancer phenotype. Activation of the Kelch-like ECH-associated protein 1 (KEAP1)-NF-E2-related factor 2 (NRF2)-signaling pathway is an adaptive response to environmental and endogenous stresses and serves to render animals resistant to chemical carcinogenesis and other forms of toxicity, whilst disruption of the pathway exacerbates these outcomes. This pathway can be induced by thiol-reactive small molecules that demonstrate protective efficacy in preclinical chemoprevention models and in clinical trials. However, mutations and epigenetic modifications affecting the regulation and fate of NRF2 can lead to constitutive dominant hyperactivation of signaling that preserves rather than attenuates cancer phenotypes by providing selective resistance to stresses. This review provides a synopsis of KEAP1-NRF2 signaling, compares the impact of genetic versus pharmacologic activation and considers both the attributes and concerns of targeting the pathway in chemoprevention.
MeSH term(s)	Chemoprevention ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Kelch-Like ECH-Associated Protein 1 ; NF-E2-Related Factor 2/metabolism ; NF-E2-Related Factor 2/physiology ; Signal Transduction
Chemical Substances	Intracellular Signaling Peptides and Proteins ; KEAP1 protein, human ; Kelch-Like ECH-Associated Protein 1 ; NF-E2-Related Factor 2 ; NFE2L2 protein, human
Language	English
Publishing date	2009-09-30
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	603134-1
ISSN	1460-2180 ; 0143-3334
ISSN (online)	1460-2180
ISSN	0143-3334
DOI	10.1093/carcin/bgp231
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