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Article ; Online: Emerging role of GCN5 in human diseases and its therapeutic potential.

Xiao, Hai-Tao / Jin, Jing / Zheng, Zu-Guo

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2023 Volume 165, Page(s) 114835

Abstract: As the first histone acetyltransferase to be cloned and identified in yeast, general control non-depressible 5 (GCN5) plays a crucial role in epigenetic and chromatin modifications. It has been extensively studied for its essential role in regulating and ...

Abstract	As the first histone acetyltransferase to be cloned and identified in yeast, general control non-depressible 5 (GCN5) plays a crucial role in epigenetic and chromatin modifications. It has been extensively studied for its essential role in regulating and causing various diseases. There is mounting evidence to suggest that GCN5 plays an emerging role in human diseases and its therapeutic potential is promising. In this paper, we begin by providing an introduction GCN5 including its structure, catalytic mechanism, and regulation, followed by a review of the current research progress on the role of GCN5 in regulating various diseases, such as cancer, diabetes, osteoporosis. Thus, we delve into the various aspects of GCN5 inhibitors, including their types, characteristics, means of discovery, activities, and limitations from a medicinal chemistry perspective. Our analysis highlights the importance of identifying and creating inhibitors that are both highly selective and effective inhibitors, for the future development of novel therapeutic agents aimed at treating GCN5-related diseases.
MeSH term(s)	Humans ; Histone Acetyltransferases/metabolism ; Neoplasms/drug therapy ; Neoplasms/genetics ; Saccharomyces cerevisiae/metabolism ; Acetylation ; Saccharomyces cerevisiae Proteins/metabolism
Chemical Substances	Histone Acetyltransferases (EC 2.3.1.48) ; GCN5 protein, S cerevisiae (EC 2.3.1.48) ; Saccharomyces cerevisiae Proteins
Language	English
Publishing date	2023-06-21
Publishing country	France
Document type	Journal Article ; Review
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2023.114835
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Article ; Online: Advancing targeted protein degradation for metabolic diseases therapy.

Zhou, Qian-Qian / Xiao, Hai-Tao / Yang, Fan / Wang, Yong-Dan / Li, Ping / Zheng, Zu-Guo

Pharmacological research

2022 Volume 188, Page(s) 106627

Abstract: The development and application of traditional drugs represented by small molecule chemical drugs and biological agents, especially inhibitors, have become the mainstream drug development. In recent years, targeted protein degradation (TPD) technology ... ...

Abstract	The development and application of traditional drugs represented by small molecule chemical drugs and biological agents, especially inhibitors, have become the mainstream drug development. In recent years, targeted protein degradation (TPD) technology has become one of the most promising methods to remove specific disease-related proteins using cell self-destruction mechanisms. Many different TPD strategies are emerging based on the ubiquitin-proteasome system (UPS) and the autophagy-lysosomal pathway (ALP), including but not limited to proteolysis-targeting chimeras (PROTAC), molecular glues (MG), lysosome targeting chimeras (LYTAC), chaperone-mediated autophagy (CMA)-targeting chimeras, autophagy-targeting chimera (AUTAC), autophagosome-tethering compound (ATTEC), and autophagy-targeting chimera (AUTOTAC). The advent of targeted degradation technology can change most protein targets in human cells from undruggable to druggable, greatly expanding the therapeutic prospect of refractory diseases such as metabolic syndrome. Here, we summarize the latest progress of major TPD technologies, especially in metabolic syndrome and look forward to providing new insights for drug discovery.
MeSH term(s)	Humans ; Proteolysis ; Metabolic Syndrome ; Proteasome Endopeptidase Complex/metabolism ; Proteins/metabolism ; Ubiquitin-Protein Ligases/metabolism
Chemical Substances	Proteasome Endopeptidase Complex (EC 3.4.25.1) ; Proteins ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2022-12-21
Publishing country	Netherlands
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1003347-6
ISSN	1096-1186 ; 0031-6989 ; 1043-6618
ISSN (online)	1096-1186
ISSN	0031-6989 ; 1043-6618
DOI	10.1016/j.phrs.2022.106627
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Article ; Online: Baohuoside I inhibits FXR signaling pathway to interfere with bile acid homeostasis via targeting ER α degradation.

Zhao, Zhen / Yang, Lu-Lu / Wang, Qiao-Lei / Du, Jin-Fa / Zheng, Zu-Guo / Jiang, Yan / Li, Ping / Li, Hui-Jun

Cell biology and toxicology

2022 Volume 39, Issue 4, Page(s) 1215–1235

Abstract: Epimedii folium (EF) is an effective herbal medicine in osteoporosis treatment, but the clinical utilization of EF has been limited due to potential hepatotoxicity. The previous studies identified that baohuoside I (BI), the main active component of EF, ... ...

Abstract	Epimedii folium (EF) is an effective herbal medicine in osteoporosis treatment, but the clinical utilization of EF has been limited due to potential hepatotoxicity. The previous studies identified that baohuoside I (BI), the main active component of EF, was relevant to EF-induced liver injury. However, the mechanisms of BI causing direct injury to hepatocytes remain unclear. Here, we reveal that BI inhibits FXR-mediated signaling pathway via targeting estrogen receptor α (ER α), leading to the accumulation of bile acids (BAs). Targeted bile acid analyses show BI alters the BA composition and distribution, resulting in impaired BA homeostasis. Mechanistically, BI induces FXR-dependent hepatotoxicity at transcriptional level. Additionally, ER α is predicted to bind to the FXR promoter region based on transcription factor binding sites databases and we further demonstrate that ER α positively regulates FXR promoter activity and affects the expression of target genes involved in BA metabolism. Importantly, we discover that ER α and its mediated FXR transcription regulation might be involved in BI-induced liver injury via ligand-dependent ER α degradation. Collectively, our findings indicate that FXR is a newly discovered target gene of ER α mediated BI-induced liver injury, and suggest BI may be responsible for EF-induced liver injury.
MeSH term(s)	Humans ; Receptors, Cytoplasmic and Nuclear/genetics ; Receptors, Cytoplasmic and Nuclear/metabolism ; Receptors, Cytoplasmic and Nuclear/pharmacology ; Bile Acids and Salts/metabolism ; Bile Acids and Salts/pharmacology ; Estrogen Receptor alpha/genetics ; Estrogen Receptor alpha/metabolism ; Chemical and Drug Induced Liver Injury, Chronic/metabolism ; Liver ; Homeostasis ; Signal Transduction
Chemical Substances	baohuoside I (113558-15-9) ; Receptors, Cytoplasmic and Nuclear ; Bile Acids and Salts ; Estrogen Receptor alpha
Language	English
Publishing date	2022-07-08
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	48824-0
ISSN	1573-6822 ; 0742-2091
ISSN (online)	1573-6822
ISSN	0742-2091
DOI	10.1007/s10565-022-09737-x
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Article ; Online: Antidiabetic Effects and Mechanisms of Rosemary (

Bao, Tian-Qi / Li, Yi / Qu, Cheng / Zheng, Zu-Guo / Yang, Hua / Li, Ping

The American journal of Chinese medicine

2020 Volume 48, Issue 6, Page(s) 1353–1368

Abstract: Diabetes mellitus is a chronic endocrine disease result from absolute or relative insulin secretion deficiency, insulin resistance, or both, and has become a major and growing public healthy menace worldwide. Currently, clinical antidiabetic drugs still ... ...

Abstract	Diabetes mellitus is a chronic endocrine disease result from absolute or relative insulin secretion deficiency, insulin resistance, or both, and has become a major and growing public healthy menace worldwide. Currently, clinical antidiabetic drugs still have some limitations in efficacy and safety such as gastrointestinal side effects, hypoglycemia, or weight gain.
MeSH term(s)	Abietanes/isolation & purification ; Abietanes/pharmacology ; Abietanes/therapeutic use ; Animals ; Anti-Inflammatory Agents ; Antioxidants ; Cinnamates/isolation & purification ; Cinnamates/pharmacology ; Cinnamates/therapeutic use ; Depsides/isolation & purification ; Depsides/pharmacology ; Depsides/therapeutic use ; Diabetes Mellitus/drug therapy ; Glucose/metabolism ; Humans ; Lipid Metabolism/drug effects ; Phenols/isolation & purification ; Phenols/pharmacology ; Phenols/therapeutic use ; Phytotherapy ; Plant Extracts/chemistry ; Plant Extracts/isolation & purification ; Rosmarinus/chemistry ; Rosmarinic Acid
Chemical Substances	Abietanes ; Anti-Inflammatory Agents ; Antioxidants ; Cinnamates ; Depsides ; Phenols ; Plant Extracts ; carnosol (483O455CKD) ; Glucose (IY9XDZ35W2) ; salvin (LI791SXT24)
Language	English
Publishing date	2020-09-09
Publishing country	Singapore
Document type	Journal Article ; Review
ZDB-ID	193085-0
ISSN	1793-6853 ; 0090-2942 ; 0192-415X
ISSN (online)	1793-6853
ISSN	0090-2942 ; 0192-415X
DOI	10.1142/S0192415X20500664
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Article: [Advances in research on hypolipidemic mechanism of phytosterols].

Lu, Jing-Xia / Zheng, Zu-Guo / Xu, Zhi-Meng / Yang, Hua / Li, Ping

Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica

2019 Volume 44, Issue 21, Page(s) 4552–4559

Abstract: Hyperlipidemia,as one of the severe risk factors of cardiovascular disease,could easily trigger atherosclerosis,coronary heart disease,peripheral vascular disease,pancreatitis,etc.,and could also increase the incidence of type 2 diabetes and fatty liver ... ...

Abstract	Hyperlipidemia,as one of the severe risk factors of cardiovascular disease,could easily trigger atherosclerosis,coronary heart disease,peripheral vascular disease,pancreatitis,etc.,and could also increase the incidence of type 2 diabetes and fatty liver disease. Improving dyslipidemia could slow down the progression of atherosclerosis and reduce the risk of coronary heart disease. This is of great importance for prevention and treatment of cardiovascular disease. Phytosterols are natural active ingredients in plants. Many researches have shown that phytosterols have significant lipid-lowering activity,which could effectively lower blood cholesterol and triglyceride levels. Foods containing phytosterols have been widely used as therapeutic diets for improving dyslipidemia. In the early years,it was believed that the lipid-lowering effect of phytosterols was achieved by competitively inhibiting the absorption of dietary cholesterol in the intestine since phytosterols had similar chemical structures with cholesterol. In further researches in recent years,more progress has been made in the lipid-lowering mechanisms of phytosterols. In this paper,PubMed and Web of Science were used to review the cholesterol-lowering and triglyceride-lowering mechanisms of phytosterols according to the available data published,so as to use phytosterols more rationally in clinical application to improve hyperlipidemia and other induced diseases.
MeSH term(s)	Cholesterol ; Diabetes Mellitus, Type 2 ; Humans ; Hyperlipidemias ; Hypolipidemic Agents/pharmacology ; Phytosterols/pharmacology ; Triglycerides
Chemical Substances	Hypolipidemic Agents ; Phytosterols ; Triglycerides ; Cholesterol (97C5T2UQ7J)
Language	Chinese
Publishing date	2019-12-23
Publishing country	China
Document type	Journal Article
ZDB-ID	1004649-5
ISSN	1001-5302 ; 0254-0029
ISSN	1001-5302 ; 0254-0029
DOI	10.19540/j.cnki.cjcmm.20190424.401
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Article ; Online: Discovery of a potent allosteric activator of DGKQ that ameliorates obesity-induced insulin resistance via the sn-1,2-DAG-PKCε signaling axis.

Zheng, Zu-Guo / Xu, Yin-Yue / Liu, Wen-Ping / Zhang, Yang / Zhang, Chong / Liu, Han-Ling / Zhang, Xiao-Yu / Liu, Run-Zhou / Zhang, Yi-Ping / Shi, Meng-Ying / Yang, Hua / Li, Ping

Cell metabolism

2022 Volume 35, Issue 1, Page(s) 101–117.e11

Abstract: sn-1,2-diacylglycerol (sn-1,2-DAG)-mediated activation of protein kinase Cε (PKCε) is a key pathway that is responsible for obesity-related lipid metabolism disorders, which induces hepatic insulin resistance and type 2 diabetes. No small molecules have ... ...

Abstract	sn-1,2-diacylglycerol (sn-1,2-DAG)-mediated activation of protein kinase Cε (PKCε) is a key pathway that is responsible for obesity-related lipid metabolism disorders, which induces hepatic insulin resistance and type 2 diabetes. No small molecules have been previously reported to ameliorate these diseases through this pathway. Here, we screened and identified the phytochemical atractylenolide II (AT II) that reduces the hepatic sn-1,2-DAG levels, deactivates PKCε activity, and improves obesity-induced hyperlipidemia, hepatosteatosis, and insulin resistance. Furthermore, using the ABPP strategy, the diacylglycerol kinase family member DGKQ was identified as a direct target of AT II. AT II may act on a novel drug-binding pocket in the CRD and PH domains of DGKQ to thereby allosterically regulate its kinase activity. Moreover, AT II also increases weight loss by activating DGKQ-AMPK-PGC1α-UCP-1 signaling in adipose tissue. These findings suggest that AT II is a promising lead compound to improve obesity-induced insulin resistance.
MeSH term(s)	Humans ; Protein Kinase C-epsilon/metabolism ; Insulin Resistance ; Diabetes Mellitus, Type 2/drug therapy ; Diglycerides/metabolism ; Obesity/drug therapy
Chemical Substances	Protein Kinase C-epsilon (EC 2.7.11.13) ; 1,2-diacylglycerol ; Diglycerides
Language	English
Publishing date	2022-12-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2022.11.012
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Article ; Online: Statins induce skeletal muscle atrophy via GGPP depletion-dependent myostatin overexpression in skeletal muscle and brown adipose tissue.

Wang, Lai / Zheng, Zu-Guo / Meng, Lingchang / Zhu, Lijun / Li, Ping / Chen, Jun / Yang, Hua

Cell biology and toxicology

2020 Volume 37, Issue 3, Page(s) 441–460

Abstract: Myopathy is the major adverse effect of statins. However, the underlying mechanism of statin-induced skeletal muscle atrophy, one of statin-induced myopathy, remains to be elucidated. Myostatin is a negative regulator of skeletal muscle mass and ... ...

Abstract	Myopathy is the major adverse effect of statins. However, the underlying mechanism of statin-induced skeletal muscle atrophy, one of statin-induced myopathy, remains to be elucidated. Myostatin is a negative regulator of skeletal muscle mass and functions. Whether myostatin is involved in statin-induced skeletal muscle atrophy remains unknown. In this study, we uncovered that simvastatin administration increased serum myostatin levels in mice. Inhibition of myostatin with follistatin, an antagonist of myostatin, improved simvastatin-induced skeletal muscle atrophy. Simvastatin induced myostatin expression not only in skeletal muscle but also in brown adipose tissue (BAT). Mechanistically, simvastatin inhibited the phosphorylation of forkhead box protein O1 (FOXO1) in C2C12 myotubes, promoting the nuclear translocation of FOXO1 and thereby stimulating the transcription of myostatin. In differentiated brown adipocytes, simvastatin promoted myostatin expression mainly by inhibiting the expression of interferon regulatory factor 4 (IRF4). Moreover, the stimulative effect of simvastatin on myostatin expression was blunted by geranylgeranyl diphosphate (GGPP) supplementation in both myotubes and brown adipocytes, suggesting that GGPP depletion was attributed to simvastatin-induced myostatin expression. Besides, the capacities of statins on stimulating myostatin expression were positively correlated with the lipophilicity of statins. Our findings provide new insights into statin-induced skeletal muscle atrophy. Graphical headlights 1. Simvastatin induces skeletal muscle atrophy via increasing serum myostatin levels in mice; 2. Simvastatin promotes myostatin expression in both skeletal muscle and brown adipose tissue through inhibiting GGPP production; 3. The stimulating effect of statins on myostatin expression is positively correlated with the lipophilicity of statins.
MeSH term(s)	Adipose Tissue, Brown/drug effects ; Adipose Tissue, Brown/metabolism ; Adipose Tissue, Brown/pathology ; Animals ; Forkhead Box Protein O1/genetics ; Gene Expression Regulation/drug effects ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/adverse effects ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology ; Interferon Regulatory Factors/genetics ; Mice ; Muscle, Skeletal/drug effects ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Muscular Atrophy/chemically induced ; Muscular Atrophy/genetics ; Muscular Atrophy/metabolism ; Muscular Atrophy/pathology ; Muscular Diseases/chemically induced ; Muscular Diseases/genetics ; Muscular Diseases/pathology ; Myostatin/blood ; Myostatin/genetics ; Polyisoprenyl Phosphates/pharmacology ; Simvastatin/adverse effects ; Simvastatin/pharmacology
Chemical Substances	Forkhead Box Protein O1 ; Foxo1 protein, mouse ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Interferon Regulatory Factors ; Myostatin ; Polyisoprenyl Phosphates ; interferon regulatory factor-4 ; Simvastatin (AGG2FN16EV) ; geranylgeranyl pyrophosphate (N21T0D88LX)
Language	English
Publishing date	2020-10-09
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	48824-0
ISSN	1573-6822 ; 0742-2091
ISSN (online)	1573-6822
ISSN	0742-2091
DOI	10.1007/s10565-020-09558-w
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Article ; Online: Dual targeting of SREBP2 and ERRα by carnosic acid suppresses RANKL-mediated osteoclastogenesis and prevents ovariectomy-induced bone loss.

Zheng, Zu-Guo / Cheng, Hui-Min / Zhou, Ya-Ping / Zhu, Si-Tong / Thu, Pyone Myat / Li, Hui-Jun / Li, Ping / Xu, Xiaojun

Cell death and differentiation

2020 Volume 27, Issue 7, Page(s) 2048–2065

Abstract: Osteoporosis develops because of impaired bone formation and/or excessive bone resorption. Several pharmacological treatment of osteoporosis has been developed; however, new treatments are still necessary. Cholesterol and estrogen receptor-related ... ...

Abstract	Osteoporosis develops because of impaired bone formation and/or excessive bone resorption. Several pharmacological treatment of osteoporosis has been developed; however, new treatments are still necessary. Cholesterol and estrogen receptor-related receptor alpha (ERRα) promote osteoclasts formation, survival, and cellular fusion and thus become high risk factors of osteoporosis. In this study, we identified that carnosic acid (CA) suppressed bone loss by dual-targeting of sterol regulatory element-binding protein 2 (SREBP2, a major regulator that regulates cholesterol synthesis) and ERRα. Mechanistically, CA reduced nuclear localization of mature SREBP2 and suppressed de novo biogenesis of cholesterol. CA subsequently decreased the interaction between ERRα and peroxisome proliferator-activated receptor gamma coactivator 1-beta (PGC1β), resulting in decreased the transcription activity of ERRα and its target genes expression. Meanwhile, CA directly bound to the ligand-binding domain of ERRα and significantly promoted its ubiquitination and proteasomal degradation. Subsequently, STUB1 was identified as the E3 ligase of ERRα. The lysine residues (K51 and K68) are essential for ubiquitination and proteasomal degradation of ERRα by CA. In conclusion, CA dually targets SREBP2 and ERRα, thus inhibits the RANKL-induced osteoclast formation and improves OVX-induced bone loss. CA may serve as a lead compound for pharmacological control of osteoporosis.
MeSH term(s)	Abietanes/pharmacology ; Animals ; Bone Resorption/diagnostic imaging ; Bone Resorption/etiology ; Bone Resorption/pathology ; Bone Resorption/prevention & control ; Cell Differentiation/drug effects ; Cell Line ; Cholesterol/metabolism ; Female ; Humans ; Luciferases/metabolism ; Lysine/metabolism ; Mice, Inbred C57BL ; Nuclear Proteins/metabolism ; Osteoclasts/drug effects ; Osteoclasts/metabolism ; Osteogenesis/drug effects ; Osteoporosis/blood ; Osteoporosis/diagnostic imaging ; Osteoporosis/etiology ; Ovariectomy ; Proteasome Endopeptidase Complex/metabolism ; Proteolysis/drug effects ; RANK Ligand/pharmacology ; Receptors, Estrogen/metabolism ; Sterol Regulatory Element Binding Protein 2/metabolism ; Tartrate-Resistant Acid Phosphatase/metabolism ; Transcription Factors/metabolism ; Ubiquitin-Protein Ligases ; Ubiquitination/drug effects ; ERRalpha Estrogen-Related Receptor
Chemical Substances	Abietanes ; Nuclear Proteins ; Ppargc1b protein, mouse ; RANK Ligand ; Receptors, Estrogen ; Sterol Regulatory Element Binding Protein 2 ; Transcription Factors ; Cholesterol (97C5T2UQ7J) ; Luciferases (EC 1.13.12.-) ; STUB1 protein, human (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Tartrate-Resistant Acid Phosphatase (EC 3.1.3.2) ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; Lysine (K3Z4F929H6) ; salvin (LI791SXT24)
Language	English
Publishing date	2020-01-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1225672-9
ISSN	1476-5403 ; 1350-9047
ISSN (online)	1476-5403
ISSN	1350-9047
DOI	10.1038/s41418-019-0484-5
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Article ; Online: Correction: Praeruptorin B improves diet-induced hyperlipidemia and alleviates insulin resistance

Zheng, Zu-Guo / Lu, Chong / Thu, Pyone Myat / Zhang, Xin / Li, Hui-Jun / Li, Ping / Xu, Xiaojun

RSC advances

2019 Volume 9, Issue 11, Page(s) 6101

Abstract: This corrects the article DOI: 10.1039/C7RA11797C.]. ...

Abstract	[This corrects the article DOI: 10.1039/C7RA11797C.].
Language	English
Publishing date	2019-02-19
Publishing country	England
Document type	Published Erratum
ISSN	2046-2069
ISSN (online)	2046-2069
DOI	10.1039/c9ra90010a
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Article ; Online: Discovery of a potent SCAP degrader that ameliorates HFD-induced obesity, hyperlipidemia and insulin resistance via an autophagy-independent lysosomal pathway.

Zheng, Zu-Guo / Zhu, Si-Tong / Cheng, Hui-Min / Zhang, Xin / Cheng, Gang / Thu, Pyone Myat / Wang, Supeng Perry / Li, Hui-Jun / Ding, Ming / Qiang, Lei / Chen, Xiao-Wei / Zhong, Qing / Li, Ping / Xu, Xiaojun

Autophagy

2020 Volume 17, Issue 7, Page(s) 1592–1613

Abstract: SCAP (SREBF chaperone) regulates SREBFs (sterol regulatory element binding transcription factors) processing and stability, and, thus, becomes an emerging drug target to treat dyslipidemia and fatty liver disease. However, the current known SCAP ... ...

Abstract	SCAP (SREBF chaperone) regulates SREBFs (sterol regulatory element binding transcription factors) processing and stability, and, thus, becomes an emerging drug target to treat dyslipidemia and fatty liver disease. However, the current known SCAP inhibitors, such as oxysterols, induce endoplasmic reticulum (ER) stress and NR1H3/LXRα (nuclear receptor subfamily 1 group H member 3)-SREBF1/SREBP-1 c-mediated hepatic steatosis, which severely limited the clinical application of this inhibitor. In this study, we identified a small molecule, lycorine, which binds to SCAP, which suppressed the SREBF pathway without inducing ER stress or activating NR1H3. Mechanistically, lycorine promotes SCAP lysosomal degradation in a macroautophagy/autophagy-independent pathway, a mechanism completely distinct from current SCAP inhibitors. Furthermore, we determined that SQSTM1 captured SCAP after its exit from the ER. The interaction of SCAP and SQSTM1 requires the WD40 domain of SCAP and the TB domain of SQSTM1. Interestingly, lycorine triggers the lysosome translocation of SCAP independent of autophagy. We termed this novel protein degradation pathway as the SQSTM1-mediated autophagy-independent lysosomal degradation (SMAILD) pathway.
MeSH term(s)	Amaryllidaceae Alkaloids/pharmacology ; Animals ; Diet, High-Fat/adverse effects ; Down-Regulation ; HEK293 Cells ; Hep G2 Cells ; Humans ; Hyperlipidemias/etiology ; Hyperlipidemias/metabolism ; Hyperlipidemias/physiopathology ; Insulin Resistance/physiology ; Intracellular Signaling Peptides and Proteins/antagonists & inhibitors ; Intracellular Signaling Peptides and Proteins/physiology ; Lysosomes/metabolism ; Lysosomes/physiology ; Male ; Membrane Proteins/antagonists & inhibitors ; Membrane Proteins/physiology ; Mice ; Mice, Inbred C57BL ; Obesity/etiology ; Obesity/metabolism ; Obesity/physiopathology ; Phenanthridines/pharmacology ; Sequestosome-1 Protein/metabolism ; Signal Transduction/drug effects
Chemical Substances	Amaryllidaceae Alkaloids ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins ; Phenanthridines ; SQSTM1 protein, human ; SREBP cleavage-activating protein ; Sequestosome-1 Protein ; lycorine (I9Q105R5BU)
Language	English
Publishing date	2020-05-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2020.1757955
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