检索结果-内蒙古大学图书馆

txnip Participated in NLRP3-Mediated Inflammation in a Rat Model of Cervical Spondylotic Myelopathy

JOURNAL OF INFLAMMATION RESEARCH 2022年 15卷 4547-4559页

作者： Liu, Peisheng Li, Xiaofeng Liu, Jing Zhang, Hengjia You, Zhitao Zhang, Jianfeng Yantaishan Hosp Dept Spinal Surg Yantai Peoples R China Yantai Vocat Coll Basic Dept Yantai Peoples R China Yantaishan Hosp Dept Spinal Surg 10087 Keji Ave Yantai Peoples R China

Background: Cervical spondylotic myelopathy (CSM) is a spinal cord disease caused by cervical disc degeneration and related pathological changes. Cervical spondylotic myelopathy may result from inflammation responses and neuronal damage. Thioredoxin-interacting protein (txnip)/NOD-like receptor protein 3 (NLRP3) signaling promotes inflammation. However, the effects of txnip/ NLRP3 on the pathogenesis of CSM have not been reported. Methods: A rat model of chronic cervical cord compression was established to observe changes in the levels of of TNXIP/NeuN and NLRP3/NeuN expression in the damaged anterior horn of the spinal cord following progression of CSM. Rats were injected with txnip small interfering RNA (siRNA) and scrambled control to determine the effects of txnip inhibition on NLRP3-mediated inflammation in rats with CSM. Behaviors effects and the expression of NLRP3 and pro-caspase-1 in the damaged spinal cord were ***: The expression levels of txnip and NLRP3 were significantly increased in the damaged anterior horn of the spinal cord following CSM. Injection of txnip siRNA significantly improved behavioral measures and decreased apoptosis in the damaged anterior horn of spinal cord. Furthermore, the levels of NLRP3 and pro-caspase-1 in the lesioned area were reduced by the txnip siRNA injection. Conclusion: Thioredoxin-interacting protein participated in NLRP3 mediated inflammation in a rat model of CSM, which indicated that txnip may be a potential therapeutic target in improving CSM.

关键词： neuroinflammation txnip NLRP3 spinal cord dysfunction pro-caspase-1

来源：评论

学校读者我要写书评

暂无评论

The Interaction of txnip and AFq1 Genes Increases the Susceptibility of Schizophrenia

引用

MOLECULAR NEUROBIOLOGY 2017年第6期54卷 4806-4812页

作者： Su, Yousong Ding, Wenhua Xing, Mengjuan Qi, Dake Li, Zezhi Cui, Donghong Shanghai Jiao Tong Univ Sch Med Shanghai Mental Hlth Ctr Shanghai Peoples R China Shanghai Key Lab Psychot Disorders Shanghai Peoples R China Mem Univ Newfoundland Fac Med St John NF Canada Shanghai Jiao Tong Univ Sch Med Dept Neurol Ren Ji Hosp Shanghai Peoples R China Shanghai Jiao Tong Univ Sch Med Key Lab Translat Psychiat Shanghai Peoples R China Shanghai Jiao Tong Univ Bio X Inst Shanghai Peoples R China

Although previous studies showed the reduced risk of cancer in patients with schizophrenia, whether patients with schizophrenia possess genetic factors that also contribute to tumor suppressor is still unknown. In the present study, based on our previous microarray data, we focused on the tumor suppressor genes txnip and AF1q, which differentially expressed in patients with schizophrenia. A total of 413 patients and 578 healthy controls were recruited. We found no significant differences in genotype, allele, or haplotype frequencies at the selected five single nucleotide polymorphisms (SNPs) (rs2236566 and rs7211 in txnip gene;rs10749659, rs2140709, and rs3738481 in AF1q gene) between patients with schizophrenia and controls. However, we found the association between the interaction of txnip and AF1q with schizophrenia by using the MDR method followed by traditional statistical analysis. The best gene-gene interaction model identified was a three-locus model txnip (rs2236566, rs7211)-AF1q (rs2140709). After traditional statistical analysis, we found the high-risk genotype combination was rs2236566 (GG)-rs7211(CC)-rs2140709(CC) (OR = 1.35 [1.03-1.76]). The low-risk genotype combination was rs2236566 (GT)-rs7211(CC)-rs2140709(CC) (OR = 0.67 [0.49-0.91]). Our finding suggested statistically significant role of interaction of txnip and AF1q polymorphisms (txnip-rs2236566, txnip-rs7211, and AF1q-rs2769605) in schizophrenia susceptibility.

关键词： txnip AFq1 Interaction Schizophrenia

来源：评论

学校读者我要写书评

暂无评论

Identification of the txnip IRES and characterization of the impact of regulatory IRES trans-acting factors

引用

BIOCHIMICA ET BIOPHYSICA ACTA-GENE REGULATORY MECHANISMS 2018年第2期1861卷 147-157页

作者： Lampe, Sebastian Kunze, Michael Scholz, Anica Brauss, Thilo F. Winslow, Sofia Simm, Stefan Keller, Mario Heidler, Juliana Wittig, Ilka Bruene, Bernhard Schmid, Tobias Goethe Univ Frankfurt Fac Med Inst Biochem 1 Theodor Stern Kai 7 D-60590 Frankfurt Germany Goethe Univ Frankfurt Fac Biosci Dept Mol Cell Biol Plants D-60438 Frankfurt Germany Goethe Univ Frankfurt Fac Med SFB Core Unit 815 Funct Prote D-60590 Frankfurt Germany

Translation is a tightly regulated process and is predominantly controlled at the level of its initiation. Translation initiation mostly occurs in a cap-dependent manner. Under stress conditions when cap-dependent translation is hampered, internal ribosome entry sites (IRESes) allow for cap-independent translation of certain mRNAs. IRES-dependent translation is commonly regulated by RNA-interacting proteins, known as IRES trans-acting factors (ITAFs). In the present study, we found the 5' untranslated region (UTR) of the thioredoxin-interacting protein (txnip) mRNA to be bound by the ITAF hnRNPA1. Upon verification of an IRES element within the 5'UTR of txnip, we determined additional interacting proteins, which predominantly appeared to interact with the IRES-regulatory second half of the 5'UTR. Amongst these PTB emerged as an inhibitory ITAF, whereas FBP3 and GEMIN5 appeared to contain txnip IRES-enhancing properties. In summary, we identified and characterized a novel IRES within the 5'UTR of txnip, which is regulated by the ITAFs PTB, FBP3, and GEMIN5.

关键词： Cap-independent translation Internal ribosome entry site IRES trans-acting factor RNA-binding protein txnip

来源：评论

学校读者我要写书评

暂无评论

txnip interacts with hEcd to increase p53 stability and activity

引用

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2013年第2期438卷 264-269页

作者： Suh, Hyun-Woo Yun, Sohyun Song, Haeyoung Jung, Haiyoung Park, Young-Jun Kim, Tae-Don Yoon, Suk Ran Choi, Inpyo Korea Res Inst Biosci & Biotechnol Immunotherapy Res Ctr Taejon 305806 South Korea

The p53 protein plays a central role in cell cycle arrest and apoptosis in response to diverse stress stimuli. Human ecdysoneless (hEcd) is known for its role in stabilizing the p53 protein level and increasing p53-mediated transcription. Here, we report that thioredoxin interacting protein (txnip), a member of the tumor suppressor family, interacts with hEcd and decreases MDM2-mediated p53 ubiquitination, leading to p53 stabilization and an increase in p53 activity. The ectopic overexpression of both txnip and Ecd increased actinomycin D-mediated cell death in MCF-7 cells, whereas knockdown of txnip and Ecd decreased cell death. These results show that txnip is a new regulator of the Ecd-MDM2-p53 loop. (C) 2013 Elsevier Inc. All rights reserved.

关键词： txnip hEcd p53 Cell death

来源：评论

学校读者我要写书评

暂无评论

txnip contributes to impaired glucose tolerance by upregulating the expression of genes involved in hepatic gluconeogenesis in mice

引用

DIABETOLOGIA 2013年第12期56卷 2723-2732页

作者： Jo, Seong Ho Kim, Mi Young Park, Joo Man Kim, Tae Hyun Ahn, Yong Ho Yonsei Univ Coll Med Dept Biochem & Mol Biol Seoul 120752 South Korea Yonsei Univ Coll Med Brain Korea Project Med Sci 21 Seoul 120752 South Korea

Thioredoxin-interacting protein (txnip) is upregulated in the hyperglycaemic state and represses glucose uptake, resulting in imbalanced glucose homeostasis. In this study, we propose a mechanism of how txnip impairs hepatic glucose tolerance at the transcriptional level. We administered adenoviral txnip (Ad-txnip) to normal mice and performed intraperitoneal glucose tolerance tests (IPGTT), insulin tolerance tests (ITT) and pyruvate tolerance tests (PTT). After Ad-txnip administration, the expression of genes involved in glucose metabolism, including G6pc and Gck, was analysed using quantitative real-time PCR and western blot. To understand the increased G6pc expression in liver resulting from txnip overexpression, we performed pull-down assays for txnip and small heterodimer partner (SHP). Luciferase reporter assays and chromatin immunoprecipitation using the txnip promoter were performed to elucidate the interrelationship between carbohydrate response element-binding protein (ChREBP) and transcription factor E3 (TFE3) in the regulation of txnip expression. Overabundance of txnip resulted in impaired glucose, insulin and pyruvate tolerance in normal mice. Ad-txnip transduction upregulated G6pc expression and caused a decrease in Gck levels in the liver of normal mice and primary hepatocytes. txnip increased G6pc expression by forming a complex with SHP, which is known to be a negative modulator of gluconeogenesis. txnip expression in mouse models of diabetes was decreased by Ad-Tfe3 administration, suggesting that TFE3 may play a negative role through competition with ChREBP at the E-box of the txnip promoter. We demonstrated that txnip impairs glucose and insulin tolerance in mice by upregulating G6pc through interaction with SHP.

关键词： db/db mice GCK G6PC SHP Streptozotocin Transcriptional regulation txnip

来源：评论

学校读者我要写书评

暂无评论

txnip Regulates NLRP3 Inflammasome-Induced Pyroptosis Related to Aging via cAMP/PKA and PI3K/Akt Signaling Pathways

引用

MOLECULAR NEUROBIOLOGY 2024年第10期61卷 8051-8068页

作者： Xi, Xiaoshuang Zhang, Rong Chi, Yijia Zhu, Ziman Sun, Ruifeng Gong, Weijun Capital Med Univ Beijing Rehabil Hosp Beijing Peoples R China Capital Med Univ Beijing Rehabil Med Acad Beijing Peoples R China Yunnan Univ Chinese Med Clin Med Coll 2 Kunming Yunnan Peoples R China Capital Med Univ Beijing Rehabil Hosp Dept Neurol Rehabil Beijing Peoples R China

Aging is an inevitable natural process with time-dependent dysfunction and the occurrence of various diseases, which impose heavy burdens on individuals, families, and society. It has been reported that NLRP3 inflammasome-induced pyroptosis contributes significantly to age-related diseases and aging, while txnip is suggested to be involved in regulating pyroptosis mediated by NLRP3. However, the mechanism between txnip and NLRP3 inflammasome is still unclear. In this study, we used HT-22 cells to explore the effect of txnip on pyroptosis and its potential association with the aging. Also, we delved into the underlying mechanisms. Our findings revealed that txnip significantly augmented pyroptosis in HT-22 cells, primarily by enhancing the activation of the NLRP3 inflammasome and promoting the release of proinflammatory cytokines. Remarkably, as txnip levels increased, we observed a corresponding rise in the number of p16-positive cells, which is indicative of aging. Furthermore, we conducted experiments to modulate the improvement of txnip on NLRP3 inflammasome-induced pyroptosis, that is, the PI3K activator 740 Y-P and the PKA activator DC2797 inhibited the effect, while the PI3K inhibitor LY294002 and the PKA inhibitor H89 enhanced the effect. In conclusion, our study demonstrated that txnip regulates NLRP3 inflammasome-induced pyroptosis in HT-22 cells related to aging via the PI3K/Akt and cAMP/PKA pathways.

关键词： txnip NLRP3 Pyroptosis PI3K/Akt cAMP/PKA Aging

来源：评论

学校读者我要写书评

暂无评论

txnip induced by MondoA, rather than ChREBP, suppresses cervical cancer cell proliferation, migration and invasion

引用

JOURNAL OF BIOCHEMISTRY 2020年第4期167卷 371-378页

作者： Zhang, Junhua Tian, Xingbo Yin, Huifang Xiao, Songshu Yi, Shuijing Zhang, Youzhong Zeng, Fei Shandong Univ Dept Gynecol & Obstet Qilu Hosp 107 West Wenhua Rd Jinan 250012 Shandong Peoples R China Cent South Univ Xiangya Hosp 3 Dept Gynecol & Obstet 138 Tongzipo Rd Changsha 410013 Hunan Peoples R China

Evidence has indicated the associations between thioredoxin-interacting protein (txnip) and cancers. However, the role of txnip in cervical cancer remains unclear. Hence, this study aims to investigate the role of txnip in regulating cervical cancer cell proliferation, migration and invasion. txnip expression can be regulated by either MondoA or ChREBP in a cell- or tissue- dependent manner. Thus, we also explored whether txnip expression in cervical cancer can be regulated by MondoA or ChREBP. Our results showed that txnip expression was decreased in cervical cancer cells (HeLa, SiHa, CaSki, MS751, C-33A). Furthermore, txnip overexpression inhibited cell proliferation, migration and invasion in HeLa cells, whereas txnip silencing exerted the opposite effect in C-33A cells. Moreover, txnip expression could be induced by MondoA, rather than ChREBP in HeLa cells. Additionally, MondoA overexpression inhibited cell proliferation, migration and invasion through upregulating txnip in HeLa cells. In summary, txnip induced by MondoA, rather than ChREBP, suppresses cervical cancer cell proliferation, migration and invasion. Our findings provide new ideas for the prevention and treatment of cervical cancer.

关键词： cervical cancer ChREBP MondoA txnip

来源：评论

学校读者我要写书评

暂无评论

txnip gene not associated with familial combined hyperlipidemia in the NHLBI Family Heart Study

引用

ATHEROSCLEROSIS 2004年第2期174卷 357-362页

作者： Coon, H Singh, N Dunn, D Eckfeldt, JH Province, MA Hopkins, PN Weiss, R Hunt, SC Leppert, MF Univ Utah Neurodev Genet Project Salt Lake City UT 84108 USA Univ Utah Dept Human Genet Salt Lake City UT 84108 USA Univ Minnesota Sch Med Dept Lab Med & Pathol Minneapolis MN 55455 USA Washington Univ Div Biostat St Louis MO 63110 USA Univ Utah Dept Internal Med Salt Lake City UT 84108 USA

Familial combined hyperlipidemia (FCHL) is the most common familial dyslipidemia, and is implicated in up to 20% of cases of premature coronary heart disease. Positive linkage to chromosome 1q was found in FCHL families participating in the NHLBI Family Heart Study (FHS), replicating linkage found in other studies. The HcB-19 mouse, which shares phenotypes with FCHL, was shown in other studies to have a nonsense mutation in the thioredoxin interacting protein gene (txnip). txnip is a gene on mouse chromosome 3 in a region syntenic with the 1q human FCHL linkage region. We re-sequenced the human homolog of mouse txnip in the FHS sample and identified nine single nucleotide polymorphisms (SNPs). We did not observe the nonsense mutation found in the HcB-19 mouse, and only three of the SNPs discovered were sufficiently polymorphic for analysis. No association between FCHL and the txnip gene was found. Within FCHL cases, presence of variants also did not significantly affect body mass index or levels of lipids, insulin, or glucose. Our results suggest that in this sample, txnip does not play a major role in FCHL or related traits, and is unlikely to account for the positive evidence of linkage in this region. (C) 2004 Elsevier Ireland Ltd. All rights reserved.

关键词： hyperlipiderma FCHL txnip association linkage

来源：评论

学校读者我要写书评

暂无评论

METTL3-mediated m6A modification of pri-miR-148a-3p affects prostate cancer progression by regulating txnip

引用

ENVIRONMENTAL TOXICOLOGY 2023年第10期38卷 2377-2390页

作者： Li, Guoqiang Liu, Junwen Wang, Yinhuai Liu, Hanqi Fu, Jianhan Zhao, Yuanqiao Huang, Yanqing Cent South Univ Xiangya Hosp 2 Dept Urol Changsha Peoples R China Cent South Univ Xiangya Sch Med Dept Histol & Embryol 172 Tongzipo Rd Changsha 410000 Peoples R China

ObjectiveProstate cancer (PCa) severely affects men's health worldwide. The mechanism of methyltransferase-like 3 (METTL3) in affecting PCa development by regulating miR-148a-3p expression via N6-methyladenosine (m6A) modification was investigated. MethodsMETTL3, miR-148a-3p, and thioredoxin interacting protein (txnip) levels were determined using RT-qPCR and Western blotting. The m6A modification level of miR-148a-3p was observed by Me-RIP assay. Bioinformatics website predicted miR-148a-3p and txnip levels in PCa and their correlation, and the binding site between them was verified by dual-luciferase assay. The proliferation, migration, invasion, and apoptosis of PCa cells were examined by CCK-8 assay, Transwell assay, and flow cytometry. A transplanted tumor model was established in nude mice to observe the tumor growth ability, followed by determination of txnip levels in tumor tissues by immunohistochemistry. ResultsMETTL3 interference restrained the proliferation, migration, and invasion and promoted apoptosis of PCa cells. METTL3 up-regulated miR-148a-3p by promoting the m6A modification of pri-miR-148a-3p in PCa cells. miR-148a-3p overexpression nullified the inhibitory actions of silencing METTL3 on PCa cell growth. miR-148a-3p facilitated PCa cell growth by silencing txnip. METTL3 interference inhibited tumor growth by down-regulating miR-148a-3p and up-regulating txnip. ConclusionMETTL3 promoted miR-148a-3p by mediating the m6A modification of pri-miR-148a-3p, thereby targeting txnip, interfering with METTL3 to inhibit the proliferation, migration and invasion of PCa cells, promote apoptosis, and inhibit tumor growth in nude mice.

关键词： epigenetics m6A METTL3 miR-148a-3p pri-miR-148a-3p prostate cancer txnip

来源：评论

学校读者我要写书评

暂无评论

Ginsenoside Compound K Ameliorates Osteoarthritis by Inhibiting the Chondrocyte Endoplasmic Reticulum Stress-Mediated IRE1α-txnip-NLRP3 Axis and Pyroptosis

引用

JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY 2023年第3期71卷 1499-1509页

作者： Tian, Yicheng Feng, Xinyuan Zhou, Zimo Qin, Sen Chen, Senxiang Zhao, Jihui Hou, Jianglin Liu, Da China Med Univ Dept Orthoped Shengjing Hosp Shenyang 110004 Liaoning Peoples R China

Osteoarthritis (OA) is a common joint disease, and studies have reported that the endoplasmic reticulum stress (ERS) in chondrocytes caused by the cartilage tissue damage could mediate the activation of Nod-like receptor protein 3 (NLRP3) inflammasomes through inositol-requiring enzyme 1 alpha (IRE1a) and thioredoxin interacting protein (txnip). Ginsenoside compound K (CK) has an inhibitory effect on IRE1a activation. However, the role of IRE1 alpha-txnip and its interaction with CK are still unclear. In this study, we examined the role and mechanism of action of CK in OA. We found that CK ameliorated OA and ERS in IL-1 beta-treated chondrocytes and a monoiodoacetate-induced rat OA model. The effect of CK on inflammation, pyroptosis, and ERS was blocked by the ERS inducer tunicamycin. In conclusion, CK hindered OA progression by inhibiting the ERS-IRE1atxnip-NLRP3 axis. Overall, our data indicate that CK could be useful in the treatment of OA and other chronic inflammatory diseases.

关键词： compound K osteoarthritis endoplasmic reticulum stress txnip

来源：评论

学校读者我要写书评

暂无评论

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

请选择保存的检索档案：

请选择收藏分类：

通借通还

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：