Journal of Functional Foods
·
2023
·
IF 5.6
Shangyun Lu,Jiali Xu,Yang Xu,Yang Liu,Dongxing Shi,Jia Wang,Fubin Qiu
Maintaining the integrity and stability of the gut tract is essential for the health of the body. Autophagy is a promising target for balancing gut homeostasis, and numerous studies have focused on regulating autophagy to improve gut health. In this study, we found that glycyrol (GC), a representative coumarin compound isolated from Glycyrrhiza uralensis Fisch (used for medicine and food), can attenuate colon injury by activating autophagy. Specifically, we demonstrated that GC can act on ubiquitin-specific protease 8 (USP8), inhibit the interaction between SQSTM1/p62 and USP8, promote the ubiquitination of p62, and activate autophagy. Collectively, the findings of the present study suggest that GC is a novel and promising colon protector and deserves further investigation.
研究领域:
药理学
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胃肠病学
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分子生物学
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DOI
高影响因子
Autophagy
·
2023
·
IF 13.3
Jia Li,Yanrong Zhou,Wenkai Zhao,Jiao Liu,Rizwan Ullah,Puxian Fang,Liurong Fang,Shaobo Xiao
Porcine reproductive and respiratory syndrome virus (PRRSV) is a typical immunosuppressive virus devastating the global swine industry. DEAD-box helicases (DDXs) are a family of ATP-dependent RNA helicases that are predominantly implicated in modulating cellular RNA metabolism. Meanwhile, a growing number of studies have suggested that some DDXs are associated with innate immunity and virus infection, so they are considered potential antiviral targets. Herein, we screened 40 DDXs and found that ectopic expression of DDX10 exhibited a significant anti-PRRSV effect, while DDX10 knockdown promoted PRRSV proliferation. Further analysis revealed that DDX10 positively regulates type I interferon production, which may contribute to its anti-PRRSV effect. Interestingly, PRRSV infection promoted DDX10 translocation from the nucleus to the cytoplasm for macroautophagic/autophagic degradation to block the antiviral effect of DDX10. By screening PRRSV-encoded proteins, we found that the viral envelope (E) protein interacted with DDX10. In line with the autophagic degradation of DDX10 during PRRSV infection, E protein could induce autophagy and reduce DDX10 expression in wild-type cells, but not in ATG5 or ATG7 knockout (KO) cells. When further screening the cargo receptors for autophagic degradation, we found that SQSTM1/p62 (sequestosome 1) interacted with both DDX10 and E protein, and E protein-mediated DDX10 degradation was almost entirely blocked in SQSTM1 KO cells, demonstrating that E protein degrades DDX10 by promoting SQSTM1-mediated selective autophagy. Our study reveals a novel mechanism by which PRRSV escapes host antiviral innate immunity through selective autophagy, providing a new target for developing anti-PRRSV drugs.Abbreviations: ACTB: actin beta; ATG: autophagy related; co-IP: co-immunoprecipitation; CQ: chloroquine; DDX10: DEAD-box helicase 10; E: envelope; EGFP: enhanced green fluorescent protein; hpi: hours post infection; hpt: hours post transfection; IFA: indirect immunofluorescence assay; IFN-I: type I IFN; IFNB/IFN-β: interferon beta; IRF3: interferon regulatory factor 3; ISGs: interferon-stimulated genes; KO: knockout; MAP1LC3B/LC3: microtubule associated protein 1 light chain 3 beta; mAb: monoclonal antibody; MOI: multiplicity of infection; NBR1: NBR1 autophagy cargo receptor; NFKB/NF-κB: nuclear factor kappa B; OPTN: optineurin; ORF: open reading frame; PRRSV: porcine reproductive and respiratory syndrome virus; SeV: sendai virus; siRNA: small interfering RNA; SQSTM1/p62: sequestosome 1; TCID50: 50% tissue culture infective dose; WT: wild type.
研究领域:
病毒学
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免疫学
·
分子生物学
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细胞生物学
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DOI
PubMed
高影响因子
IUBMB LIFE
·
2023
·
IF 4.6
Le Chen,Hongmei Qiu,Qingqiu Chen,Peng Xiang,Jin Lei,Jun Zhang,Yining Lu,Xianmin Wang,Shengde Wu,Chao Yu,Limei Ma
Sialic acid (SIA) has been reported to be a risk factor for atherosclerosis (AS) due to its high plasma levels in such patients. However, the effect of increasing SIA in circulation on endothelial function during AS progression remains unclear. In the present study, ApoE −/− mice and endothelial cells line (HUVEC cells) were applied to investigate the effect of SIA on AS progression and its potential molecular mechanism. In vivo, mice were injected intraperitoneally with Neu5Ac (main form of SIA) to keep high-level SIA in circulation. ORO, H&E, and Masson staining were applied to detect the plaque progression. In vitro, HUVECs were treated with Neu5Ac at different times, CCK-8, RT-PCR, western blot, and immunoprecipitation methods were used to analyze its effects on endothelial function and the potential involved mechanism. Results from the present study showed that high plasma levels of Neu5Ac in ApoE −/− mice could aggravate the plaque areas as well as increase necrotic core areas and collagen fiber contents. Remarkably, Neu5Ac levels in circulation displayed a positive correlation with AS plaque areas. Furthermore, results from HUVECs showed that Neu5Ac inhibited cells viability in a time/dose-dependent manner, by then induced the activation of inflammation makers such as ICAM-1 and IL-1β. Mechanism study showed that the activation of excessive autophagy medicated by SQSTM1/p62 displayed an important role in endothelium inflammatory injury. Neu5Ac could modify SQSTM1/p62 as a sialylation protein, and then increase its level with ubiquitin binding, further inducing ubiquitination degradation and being involved in the excessive autophagy pathway. Inhibition of sialylation by P-3Fax-Neu5Ac, a sialyltransferase inhibitor, reduced the binding of SQSTM1/p62 to ubiquitin. Together, these findings indicated that Neu5Ac increased SQSTM1/p62-ubiquitin binding through sialylation modification, thereby inducing excessive autophagy and subsequent endothelial injury. Inhibition of SQSTM1/p62 sialylation might be a potential strategy for preventing such disease with high levels of Neu5Ac in circulation.
研究领域:
心血管疾病
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分子生物学
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细胞生物学
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病理学
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产品关联
DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2026
·
IF 5.6
Jian Yu,Jiangtao Wang,Ning Feng,Cancan Wang,Bohua Ma,Yuanming Zhang
Background Among the adverse effects of immunotherapy in cancer patients, immune checkpoint inhibitors (ICIs)-induced myocarditis is the most severe. Pyroptosis is involved in the pathogenesis of various cardiovascular diseases; however, its relationship with ICIs-related myocarditis remains unclear. Objective The purpose of this research is to characterize the critical genes mediating pyroptosis in myocarditis related to ICIs, with the goal of informing clinical practice. Materials and methods Based on single-cell RNA sequencing and bulk RNA sequencing, this study identified pyroptosis key genes in ICIs-related myocarditis and validated their expression levels and diagnostic value. Single-cell level validation of key genes, trajectory analysis and cellular interactions were also performed. Finally, ICIs-related myocarditis mouse model was established to verify the expression levels of key genes and pyroptosis-related markers. Results Integration of multiple bioinformatic analyses identified two pyroptosis key genes in ICIs-related myocarditis: Myd88 and Sqstm1. The expression levels of pyroptosis key genes were significantly higher in the ICIs-related myocarditis group compared to the normal group ( P < 0.05 or P < 0.01), and both demonstrated high diagnostic value. Trajectory analysis and cell interaction analysis revealed the interaction strength and relative expression patterns between these two pyroptosis key genes. In the ICIs-related myocarditis mouse model, cardiac injury markers were significantly elevated ( P < 0.001 or P < 0.0001), while cardiac function indices were significantly decreased ( P < 0.01) compared to the normal group. Quantitative real time polymerase chain reaction and western blot analyses revealed that the expression levels of Myd88 and Sqstm1 were significantly upregulated in the myocarditis group compared to the normal group, at both the mRNA and protein expression levels ( P < 0.05 or P < 0.01 or P < 0.0001). Compared with the normal group, the expression levels of pyroptosis-related markers Caspase-1, IL-1β, and GSDMD-N were significantly elevated in the myocarditis group ( P < 0.05 or P < 0.01). Conclusion Pyroptosis is involved in the pathogenesis of ICIs-related myocarditis, and Myd88 and Sqstm1 may serve as potential biomarkers for future clinical application.
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PubMed
高影响因子
Scientific Reports
·
2019
·Vol. 9
·期 1
·1-13
·
IF 4.011
Hou Bolin,Wang Gang,Gao Quan,Wei Yanjie,Zhang Caining,Wang Yange,Huo Yuqing,Yang Huaiyi,Jiang Xuejun,Xi Zhijun
Sunitinib (ST), a multitargeted receptor tyrosine kinase inhibitor, has been demonstrated to be effective for the treatment of renal carcinoma. It has been reported that ST is involved in the mediation of autophagy; however, its regulatory role in the autophagic process remains controversial. Furthermore, the mechanism by which activated AMP-activated protein kinase (AMPK) negatively regulates autophagy remains nearly unexplored. In the present study, we revealed that ST inhibited AMPK activity and regulated autophagy in a cell type- and dose-dependent manner. In a number of cell lines, ST was demonstrated to inhibit H 2 O 2 -induced autophagy and the phosphorylation of acetyl-CoA carboxylase (ACC), whereas alone it could block the autophagic flux concurrent with increased expression of p62. An immunoprecipitation assay revealed that LC3 directly interacted with p62, whereas ST increased punctate LC3 staining, which was well colocalized with p62. Taken together, we reveal a previously unnoticed pathway for ST to regulate the autophagic process, and p62, although often utilized as a substrate in autophagy, plays a critical role in regulating the inhibition of ST in both basal and induced autophagy.
研究领域:
肿瘤学
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细胞生物学
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药理学
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产品关联
DOI
PubMed
高影响因子
Toxics
·
2026
·Vol. 14
·期 9
·814
·
IF 4.9
Huijie Chen,Yitong Wang,Zhenkai Yao,Jing Li,Peng Li,Lei Diao
The neonicotinoid insecticide imidacloprid (IMD), widely used in agriculture, poses potential risks to aquatic ecosystems, yet its hepatotoxic mechanisms in freshwater fish remain poorly understood. This study investigates the roles of ferroptosis, mitochondrial dysfunction, inflammation, and the miR-153c/SQSTM1-mediated ferritinophagy pathway in IMD-induced hepatotoxicity in carp ( Cyprinus carpio ) hepatocytes. Using the CCK-8 assay, 0.6 μM IMD was selected for subsequent experiments. IMD exposure triggered ferroptosis, evidenced by increased intracellular Fe 2+ accumulation, upregulated pro-ferroptotic gene and protein expression, and downregulated ferroptosis inhibitors (SLC7A11 and GPX4). Mitochondrial dysfunction was confirmed by reduced ATP content, decreased mtDNA levels, and a lowered NADPH/NADP + ratio, along with aberrant expression of mitochondrial fission (Fis1 and Drp1) and fusion (Mfn1 and TFAM) genes. Additionally, IMD induced oxidative stress (elevated ROS and MDA; decreased T-AOC, CAT, and SOD activities) and a pronounced inflammatory response with upregulated pro-inflammatory cytokines. Mechanistically, IMD downregulated miR-153c, with concomitant upregulation of SQSTM1 at both the mRNA and protein levels, and dual-luciferase assays validated SQSTM1 as a direct target of miR-153c. miR-153c overexpression attenuated IMD-induced ferritinophagy, ferroptosis, and inflammation via the miR-153c/SQSTM1 axis. Collectively, these findings demonstrate that IMD induces hepatotoxicity in carp by triggering ferroptosis, mitochondrial dysfunction, and inflammation through the miR-153c/SQSTM1-mediated ferritinophagy pathway, providing mechanistic insights and potential targets for mitigating IMD’s ecological risks.
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DOI
PubMed
高影响因子
ENVIRONMENTAL RESEARCH
·
2026
·
IF 8.2
Minming Chen,Yongjie Liu,Wenwen Qu,Qianlong Zhang,Fei Li,Yi Wang,Xuan Zhai
Per- and polyfluoroalkyl substances (PFASs) are persistent environmental contaminants closely linked to metabolic liver disease; however, the transgenerational hepatotoxicity and underlying mechanisms of emerging PFAS substitutes remain poorly understood. Herein, we focused on 6:2 polyfluoroalkyl phosphate diester (6:2 diPAP), a prominent PFAS substitute, to evaluate its developmental hepatotoxicity. By integrating zebrafish phenotyping, transcriptomic feature selection, virtual gene knockout, and experimental validation, we characterized the candidate molecular events through which 6:2 diPAP triggers non-alcoholic fatty liver disease (NAFLD)-like injury in offspring. Early-life exposure to environmentally relevant concentrations of 6:2 diPAP from 0 to 5 dpf, particularly 500 ng/L, induced persistent hepatic lipid accumulation, hepatic vacuolation, and metabolic disturbances in zebrafish at 28 dpf. Integrated network and transcriptomic analyses identified sequestosome 1 (SQSTM1) as a key stress-responsive hub associated with pathological hepatocyte remodeling. Quantitative real-time polymerase chain reaction (RT-qPCR) and immunofluorescence analyses further demonstrated exposure-responsive increases in sqstm1 expression and SQSTM1/p62 protein fluorescence intensity, with the strongest changes observed in the 500 ng/L group. Human single-nucleus RNA-seq and pseudotime analyses revealed that SQSTM1-high hepatocytes were enriched in injury-associated and senescence-associated states during NAFLD progression, suggesting a link between SQSTM1 activation and hepatocyte-state deterioration. Furthermore, virtual SQSTM1 knockout in NASH hepatocytes predicted oxidative stress, xenobiotic metabolic, and inflammatory rewiring. Molecular docking predicted a feasible 6:2 diPAP-SQSTM1 interaction with a binding affinity of −6.0 kcal/mol, and 200 ns molecular dynamics simulation supported the structural plausibility of the ligand-protein complex. Collectively, this study proposes a 6:2 diPAP-SQSTM1-hepatocyte remodeling axis and provides a comprehensive framework linking early-life PFAS exposure with hepatocyte-state transition and NAFLD-like metabolic dysfunction.
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高影响因子
Cell Death & Disease
·
2024
·Vol. 15
·期 7
·1-17
·
IF 8.1
Wang Yuying,Su Kunqi,Wang Chang,Deng Tao,Liu Xiaofeng,Sun Shiqi,Jiang Yang,Zhang Chunfeng,Xing Baocai,Du Xiaojuan
Chemotherapeutic efficacy is seriously impeded by chemoresistance in more than half of hepatocellular carcinoma (HCC) patients. However, the mechanisms involved in chemotherapy-induced upregulation of chemoresistant genes are not fully understood. Here, this study unravels a novel mechanism controlling nuclear acetyl-CoA production to activate the transcription of chemoresistant genes in HCC. NAT10 is upregulated in HCC tissues and its upregulation is correlated with poor prognosis of HCC patients. NAT10 is also upregulated in chemoresistant HCC cells. Targeting NAT10 increases the cytotoxicity of chemotherapy in HCC cells and mouse xenografts. Upon chemotherapy, NAT10 translocates from the nucleolus to the nucleus to activate the transcription of CYP2C9 and PIK3R1 . Additionally, nuclear acetyl-CoA is specifically upregulated by NAT10. Mechanistically, NAT10 binds with ACLY in the nucleus and acetylates ACLY at K468 to counteract the SQSTM1-mediated degradation upon chemotherapy. ACLY K468-Ac specifically accumulates in the nucleus and increases nuclear acetyl-CoA production to activate the transcription of CYP2C9 and PIK3R1 through enhancing H3K27ac. Importantly, K468 is required for nuclear localization of ACLY. Significantly, ACLY K468-Ac is upregulated in HCC tissues, and ablation of ACLY K468-Ac sensitizes HCC cells and mouse xenografts to chemotherapy. Collectively, these findings identify NAT10 as a novel chemoresistant driver and the blockage of NAT10-mediated ACLY K468-Ac possesses the potential to attenuate HCC chemoresistance.
研究领域:
肿瘤学
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分子生物学
·
细胞生物学
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DOI
PubMed
高影响因子
MOLECULES
·
2020
·Vol. 25
·期 22
·5302
·
IF 3.267
Lili Qin,Tianfeng Lu,Yao Qin,Yiwei He,Ningxin Cui,Ai Du,Jingyu Sun
Resveratrol (RSV) is a natural flavonoid polyphenol compound extracted from the plants which shows various biological activities. However, the clinical application of RSV is limited by its poor aqueous solubility, rapid metabolism and poor bioavailability. In this study, resveratrol-loaded solid lipid nanoparticles (RSV- SLNs) was design as a nano-antioxidant against the physical fatigue. The resultant RSV-SLNs were characterized by photon correlation spectroscopy (PCS), transmission electron micrographs (TEM), zeta potential, differential scanning calorimetry (DSC) and Raman spectroscopy pattern. Furthermore, the in vivo anti-fatigue effect assays showed that RSV-SLNs prolonged the mice exhausted time and running distance. The biochemical parameters of blood related to fatigue suggested that RSV-SLNs have potential applications to improve the antioxidant defense of the mice after extensive exercise and confer anti-fatigue capability. Furthermore, the molecular mechanisms of antioxidant by RSV-SLNs supplementation was investigated through the analysis of silent information regulator 2 homolog 1 (SIRT1) protein expression, which demonstrated that it could downregulate the expression of SIRT1 and increase autophagy markers, microtubule-associated protein 1 light chain 3-II (LC3-II) and sequestosome-1 (SQSTM1/p62). These results reveal that the RSV-SLNs may have great potential used as a novel anti-fatigue sports nutritional supplement.Keywords:solid lipid nanoparticles (SLNs);resveratrol;drug delivery;anti-fatigue;nutrition supplements
研究领域:
药理学
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纳米技术
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运动科学
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营养学
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产品关联
DOI
PubMed
高影响因子
MOLECULES
·
2022
·Vol. 27
·期 23
·8475
·
IF 4.927
Lanxin Bao,Jing Ye,Nannan Liu,Yubao Shao,Wenhao Li,Xuefei Fan,Dahai Zhao,Hongzhi Wang,Xiaoyu Chen
Interstitial lung disease associated with rheumatoid arthritis (RA-ILD) can lead to interstitial fibrosis and even lung failure as a complication of rheumatoid arthritis (RA), and there is currently no effective treatment and related basic research. Studies have found that resveratrol (Res) can improve the progression of RA by regulating autophagy, and increasing evidence supports the connection between autophagy and common interstitial lung disease (ILD). We explored changes in autophagy levels in fibrotic lungs in RA-ILD and found that the level of autophagy is enhanced in the early stage but inhibited in the late stage. However, resveratrol treatment improved the level of autophagy and reversed the inhibition of autophagy, and attenuated fibrosis. We created corresponding cell models that exhibited the same phenotypic changes as animal models; under the effect of resveratrol, the level of fibrosis changed accordingly, and the fusion process of lysosomes and autophagosomes in autophagy was liberated from the inhibition state. Resveratrol effects were reversed by the addition of the late autophagy inhibitor chloroquine. These results suggest that resveratrol attenuates pulmonary fibrosis, increases autophagic flux, and modulates the autophagy–lysosome pathway, and particularly it may work by improving the formation of autophagic lysosomes, which may be an effective treatment for induced RA-ILD.Keywords:RA-ILD;resveratrol;autophagy;fibrosis;P62/SQSTM1
研究领域:
药理学
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免疫学
·
肺病学
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风湿病学
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产品关联
DOI
PubMed
高影响因子
BIOMATERIALS
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2021
·
IF 12.479
Qi Xu,Hao Zhang,Hanghang Liu,Yaobao Han,Weibao Qiu,Zhen Li
Radio-resistance of glioblastoma (GBM) remains a leading cause of radiotherapy failure because of the protective autophagy induced by X-Ray irradiation and tumor cells’ strong capability of repairing damaged DNA . It is of great importance to overcome the radio-resistance for improving the efficacy of radiotherapy. Herein, we report the novel mechanism of core-shell copper selenide coated gold nanoparticles ( [email protected] 2- x Se NPs) inhibiting the protective autophagy and DNA repair of tumor cells to drastically boost the radiotherapy efficacy of glioblastoma. We reveal that the core-shell [email protected] 2- x Se NPs can inhibit the autophagy flux by effectively alkalizing lysosomes . They can increase the SQSTM1/p62 protein levels of tumor cells without influencing their mRNA. We also reveal that [email protected] 2- x Se NPs can increase the ubiquitination of DNA repair protein Rad51, and promote the degradation of Rad51 by proteasomes to prevent the DNA repair. The simultaneous inhibition of protective autophagy and DNA repair significantly suppress the growth of orthotopic GBM by using radiotherapy and our novel [email protected] 2- x Se NPs. Our work provides a new insight and paradigm to significantly improve the efficacy of radiotherapy by rationally designing theranostic nano-agents to simultaneously inhibit protective autophagy and DNA repair of tumor cells.
研究领域:
肿瘤学
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纳米技术
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放射生物学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
Autophagy
·
2020
·
IF 9.77
Zu-Guo Zheng,Si-Tong Zhu,Hui-Min Cheng,Xin Zhang,Gang Cheng,Pyone Myat Thu,Supeng Perry Wang,Hui-Jun Li,Ming Ding,Lei Qiang,Xiao-Wei Chen,Qing Zhong,Ping Li,Xiaojun Xu
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. In vivo, lycorine ameliorates high-fat diet-induced hyperlipidemia, hepatic steatosis, and insulin resistance in mice. Our study demonstrated that the inhibition of SCAP through the SMAILD pathway could be employed as a useful therapeutic strategy for treating metabolic diseases.Abbreviation: 25-OHD: 25-hydroxyvitamin D; 3-MA: 3-methyladenine; ABCG5: ATP binding cassette subfamily G member 5; ABCG8: ATP binding cassette subfamily G member 8; ACACA: acetyl-CoA carboxylase alpha; AEBSF: 4-(2-aminoethyl) benzenesulfonyl fluoride hydrochloride; AHI: anhydroicaritin; AKT/protein kinase B: AKT serine/threonine kinase; APOE: apolipoprotein E; ATF6: activating transcription factor 6; ATG: autophagy-related; BAT: brown adipose tissue; CD274/PD-L1: CD274 molecule; CETSA: cellular thermal shift assay; CMA: chaperone-mediated autophagy; COPII: cytoplasmic coat protein complex-II; CQ: chloroquine; DDIT3/CHOP: DNA damage inducible transcript 3; DNL: de novo lipogenesis; EE: energy expenditure; EGFR: epithelial growth factor receptor; eMI: endosomal microautophagy; ERN1/IRE1α: endoplasmic reticulum to nucleus signaling 1; FADS2: fatty acid desaturase 2; FASN: fatty acid synthase; GOT1/AST: glutamic-oxaloacetic transaminase 1; GPT/ALT: glutamic-pyruvate transaminase; HMGCR: 3-hydroxy-3-methylglutaryl-CoA reductase; HMGCS1: 3-hydroxy-3-methylglutaryl-CoA synthase 1; HSP90B1/GRP94: heat shock protein 90 beta family member 1; HSPA5/GRP78: heat hock protein family A (Hsp70) member 5; HSPA8/HSC70: heat shock protein family A (Hsp70) member 8; INSIG1: insulin induced gene 1; LAMP2A: lysosomal associated membrane protein 2A; LDLR: low density lipoprotein receptor; LyTACs: lysosome targeting chimeras; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MBTPS1: membrane bound transcription factor peptidase, site 1; MEF: mouse embryonic fibroblast; MST: microscale thermophoresis; MTOR: mechanistic target of rapamycin kinase; MVK: mevalonate kinase; PROTAC: proteolysis targeting chimera; RQ: respiratory quotient; SCAP: SREBF chaperone; SCD1: stearoyl-coenzemy A desaturase 1; SMAILD: sequestosome 1 mediated autophagy-independent lysosomal degradation; SQSTM1: sequestosome 1; SREBF: sterol regulatory element binding transcription factor; TNFRSF10B/DR5: TNF receptor superfamily member 10b; TRAF6: TNF receptor associated factor 6; UPR: unfolded protein response; WAT: white adipose tissue; XBP1: X-box binding protein 1
研究领域:
药理学
·
代谢
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分子生物学
·
内分泌学
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PubMed
高影响因子
危险品化学品经营许可证（带存储）