• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

相似文献

1
Oxidative stress, inflammation and carcinogenesis are controlled through the pentose phosphate pathway by transaldolase.通过转醛醇酶,氧化应激、炎症和致癌作用可通过戊糖磷酸途径得到控制。
Trends Mol Med. 2011 Jul;17(7):395-403. doi: 10.1016/j.molmed.2011.01.014. Epub 2011 Mar 2.
2
Prevention of hepatocarcinogenesis and increased susceptibility to acetaminophen-induced liver failure in transaldolase-deficient mice by N-acetylcysteine.N-乙酰半胱氨酸对转醛醇酶缺陷小鼠肝癌发生的预防作用及对乙酰氨基酚诱导的肝衰竭易感性增加
J Clin Invest. 2009 Jun;119(6):1546-57. doi: 10.1172/JCI35722. Epub 2009 May 11.
3
Transaldolase haploinsufficiency in subjects with acetaminophen-induced liver failure.翻译:对乙酰氨基酚诱导肝衰竭患者中 transaldolase 单倍体不足。
J Inherit Metab Dis. 2020 May;43(3):496-506. doi: 10.1002/jimd.12197. Epub 2020 Jan 1.
4
Cell type-specific regulation of the pentose phosphate pathway during development and metabolic stress-driven autoimmune diseases: Relevance for inflammatory liver, renal, endocrine, cardiovascular and neurobehavioral comorbidities, carcinogenesis, and aging.发育过程中以及代谢应激驱动的自身免疫性疾病中磷酸戊糖途径的细胞类型特异性调节:与炎症性肝脏、肾脏、内分泌、心血管和神经行为共病、致癌作用及衰老的相关性
Autoimmun Rev. 2025 Apr 30;24(5):103781. doi: 10.1016/j.autrev.2025.103781. Epub 2025 Feb 24.
5
mTOR-dependent loss of PON1 secretion and antiphospholipid autoantibody production underlie autoimmunity-mediated cirrhosis in transaldolase deficiency.转醛醇酶缺乏导致的自身免疫性疾病相关性肝硬化的发病机制与 mTOR 依赖性 PON1 分泌缺失和抗磷脂自身抗体产生有关。
J Autoimmun. 2023 Nov;140:103112. doi: 10.1016/j.jaut.2023.103112. Epub 2023 Sep 22.
6
The pathogenesis of transaldolase deficiency.转醛醇酶缺乏症的发病机制。
IUBMB Life. 2007 Jun;59(6):365-73. doi: 10.1080/15216540701387188.
7
Transaldolase deficiency influences the pentose phosphate pathway, mitochondrial homoeostasis and apoptosis signal processing.转醛醇酶缺乏会影响磷酸戊糖途径、线粒体稳态和凋亡信号处理。
Biochem J. 2008 Oct 1;415(1):123-34. doi: 10.1042/BJ20080722.
8
Molecular ordering in HIV-induced apoptosis. Oxidative stress, activation of caspases, and cell survival are regulated by transaldolase.HIV诱导凋亡中的分子有序化。转醛醇酶调节氧化应激、半胱天冬酶激活及细胞存活。
J Biol Chem. 1998 May 8;273(19):11944-53. doi: 10.1074/jbc.273.19.11944.
9
Cytosolic aldose metabolism contributes to progression from cirrhosis to hepatocarcinogenesis.细胞质醛糖代谢促进肝硬化向肝癌发生的进展。
Nat Metab. 2023 Jan;5(1):41-60. doi: 10.1038/s42255-022-00711-9. Epub 2023 Jan 19.
10
Untargeted metabolomics as an unbiased approach to the diagnosis of inborn errors of metabolism of the non-oxidative branch of the pentose phosphate pathway.非氧化戊糖磷酸途径的先天性代谢缺陷的非靶向代谢组学诊断方法。
Mol Genet Metab. 2020 Sep-Oct;131(1-2):147-154. doi: 10.1016/j.ymgme.2020.07.013. Epub 2020 Aug 5.

引用本文的文献

1
Gut microbiota alterations modulate high-fat diet-induced precocious puberty.肠道微生物群的改变调节高脂饮食诱导的性早熟。
Microbiol Spectr. 2025 Sep 2;13(9):e0326424. doi: 10.1128/spectrum.03264-24. Epub 2025 Aug 12.
2
Mitochondrial mass and mitochondrial membrane potential of peripheral lymphocytes: promising biomarkers of systemic lupus erythematosus.外周淋巴细胞的线粒体质量和线粒体膜电位:系统性红斑狼疮有前景的生物标志物。
Front Mol Biosci. 2025 Jun 6;12:1585847. doi: 10.3389/fmolb.2025.1585847. eCollection 2025.
3
Glioma stem cells: drivers of tumor progression and recurrence.胶质瘤干细胞:肿瘤进展和复发的驱动因素。
Stem Cell Res Ther. 2025 Jun 7;16(1):293. doi: 10.1186/s13287-025-04352-z.
4
OsLC1, a transaldolase, regulates cell patterning and leaf morphology through modulation of secondary metabolism.OsLC1是一种转醛醇酶,通过调节次生代谢来调控细胞模式和叶片形态。
Plant Biotechnol J. 2025 May;23(5):1751-1767. doi: 10.1111/pbi.70004. Epub 2025 Feb 14.
5
The Pentose Phosphate Pathway: From Mechanisms to Implications for Gastrointestinal Cancers.磷酸戊糖途径:从机制到对胃肠道癌症的影响
Int J Mol Sci. 2025 Jan 13;26(2):610. doi: 10.3390/ijms26020610.
6
Insights into the molecular underpinning of type 2 diabetes complications.对2型糖尿病并发症分子基础的见解。
Hum Mol Genet. 2025 Mar 7;34(6):469-480. doi: 10.1093/hmg/ddae203.
7
Oxidative Stress, Inflammation and Altered Glucose Metabolism Contribute to the Retinal Phenotype in the Choroideremia Zebrafish.氧化应激、炎症和葡萄糖代谢改变促成了脉络膜视网膜病变斑马鱼的视网膜表型。
Antioxidants (Basel). 2024 Dec 23;13(12):1587. doi: 10.3390/antiox13121587.
8
Chaperones vs. oxidative stress in the pathobiology of ischemic stroke.伴侣蛋白与氧化应激在缺血性脑卒中病理生物学中的作用
Front Mol Neurosci. 2024 Dec 11;17:1513084. doi: 10.3389/fnmol.2024.1513084. eCollection 2024.
9
Exploring novel markers for coronary heart disease associated with systemic lupus erythematosus: A review.探索与系统性红斑狼疮相关的冠心病新标志物:综述
Medicine (Baltimore). 2024 Dec 13;103(50):e40773. doi: 10.1097/MD.0000000000040773.
10
Identification of the serum metabolomic profile for acute ischemic preconditioning in athletes.运动员急性缺血预处理血清代谢组学特征的鉴定。
Front Physiol. 2024 Nov 6;15:1492202. doi: 10.3389/fphys.2024.1492202. eCollection 2024.

本文引用的文献

1
Autophagy and metabolism.自噬和代谢。
Science. 2010 Dec 3;330(6009):1344-8. doi: 10.1126/science.1193497.
2
The control of the metabolic switch in cancers by oncogenes and tumor suppressor genes.癌基因和抑癌基因对代谢开关的控制。
Science. 2010 Dec 3;330(6009):1340-4. doi: 10.1126/science.1193494.
3
Novel heterozygous mutations in TALDO1 gene causing transaldolase deficiency and early infantile liver failure.TALDO1基因的新型杂合突变导致转醛醇酶缺乏和早期婴儿肝功能衰竭。
J Pediatr Gastroenterol Nutr. 2011 Jan;52(1):113-6. doi: 10.1097/MPG.0b013e3181f50388.
4
mTOR signaling: a central pathway to pathogenesis in systemic lupus erythematosus?mTOR信号传导:系统性红斑狼疮发病机制的核心途径?
Discov Med. 2010 Mar;9(46):173-8.
5
Cleavage of transaldolase by granzyme B causes the loss of enzymatic activity with retention of antigenicity for multiple sclerosis patients.颗粒酶 B 切割醛缩酶导致其酶活性丧失,同时保留了多发性硬化症患者的抗原性。
J Immunol. 2010 Apr 1;184(7):4025-32. doi: 10.4049/jimmunol.0804174. Epub 2010 Mar 1.
6
Peroxisomes are oxidative organelles.过氧化物酶体是氧化细胞器。
Antioxid Redox Signal. 2010 Aug 15;13(4):525-37. doi: 10.1089/ars.2009.2996.
7
Identification of seroreactive proteins in the culture filtrate antigen of Mycobacterium avium ssp. paratuberculosis human isolates to sera from Crohn's disease patients.鉴定鸟分枝杆菌副结核亚种人分离株培养滤液抗原中与克罗恩病患者血清发生反应的蛋白。
FEMS Immunol Med Microbiol. 2010 Feb;58(1):128-37. doi: 10.1111/j.1574-695X.2009.00617.x. Epub 2009 Oct 1.
8
Prevention of hepatocarcinogenesis and increased susceptibility to acetaminophen-induced liver failure in transaldolase-deficient mice by N-acetylcysteine.N-乙酰半胱氨酸对转醛醇酶缺陷小鼠肝癌发生的预防作用及对乙酰氨基酚诱导的肝衰竭易感性增加
J Clin Invest. 2009 Jun;119(6):1546-57. doi: 10.1172/JCI35722. Epub 2009 May 11.
9
Transaldolase: from biochemistry to human disease.转醛醇酶:从生物化学到人类疾病
Int J Biochem Cell Biol. 2009 Jul;41(7):1482-94. doi: 10.1016/j.biocel.2009.02.001. Epub 2009 Feb 11.
10
Transaldolase deficiency in two new patients with a relative mild phenotype.两名具有相对轻度表型的新患者存在转醛醇酶缺乏症。
Mol Genet Metab. 2009 May;97(1):15-7. doi: 10.1016/j.ymgme.2009.01.016. Epub 2009 Feb 10.

通过转醛醇酶,氧化应激、炎症和致癌作用可通过戊糖磷酸途径得到控制。

Oxidative stress, inflammation and carcinogenesis are controlled through the pentose phosphate pathway by transaldolase.

机构信息

Department of Medicine, State University of New York Upstate Medical University, College of Medicine, 750 East Adams Street, Syracuse, NY 13210, USA.

出版信息

Trends Mol Med. 2011 Jul;17(7):395-403. doi: 10.1016/j.molmed.2011.01.014. Epub 2011 Mar 2.

DOI:10.1016/j.molmed.2011.01.014
PMID:21376665
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3116035/
Abstract

Metabolism of glucose through the pentose phosphate pathway (PPP) influences the development of diverse pathologies. Hemolytic anemia due to deficiency of PPP enzyme glucose 6-phosphate dehydrogenase is the most common genetic disease in humans. Recently, inactivation of another PPP enzyme, transaldolase (TAL), has been implicated in male infertility and fatty liver progressing to steatohepatitis and cancer. Hepatocarcinogenesis was associated with activation of aldose reductase and redox-sensitive transcription factors and prevented by N-acetylcysteine. In this paper, we discuss how alternative formulations of the PPP with and without TAL reflect cell type-specific metabolic control of oxidative stress, a crucial source of inflammation and carcinogenesis. Ongoing studies of TAL deficiency will identify new molecular targets for diagnosis and treatment in clinical practice.

摘要

通过戊糖磷酸途径(PPP)代谢葡萄糖会影响多种病理的发展。由于 PPP 酶葡萄糖 6-磷酸脱氢酶缺乏导致的溶血性贫血是人类最常见的遗传疾病。最近,另一种 PPP 酶转醛醇酶(TAL)的失活与男性不育以及进展为脂肪性肝炎和肝癌的脂肪肝有关。醛还原酶和氧化还原敏感转录因子的激活与肝癌的发生有关,而 N-乙酰半胱氨酸可预防其发生。本文中,我们将讨论有/无 TAL 的 PPP 替代途径如何反映细胞类型特异性的氧化应激代谢控制,这是炎症和癌变的关键来源。对 TAL 缺乏的持续研究将为临床实践中的诊断和治疗确定新的分子靶点。