更新于：2024-05-01

SAT1

spermidine/spermine N1-acetyltransferase 1

更新于：2024-05-01

基本信息

别名

Diamine acetyltransferase 1、Polyamine N-acetyltransferase 1、Putrescine acetyltransferase

+ [6]

简介

Enzyme which catalyzes the acetylation of polyamines (PubMed:15283699, PubMed:16455797, PubMed:17516632). Substrate specificity: norspermidine = spermidine >> spermine > N(1)-acetylspermine (PubMed:17516632). This highly regulated enzyme allows a fine attenuation of the intracellular concentration of polyamines (PubMed:16455797). Also involved in the regulation of polyamine transport out of cells (PubMed:16455797). Also acts on 1,3-diaminopropane and 1,5-diaminopentane (PubMed:16455797, PubMed:17516632).

关联

100 项与 SAT1 相关的临床结果

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100 项与 SAT1 相关的转化医学

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0 项与 SAT1 相关的专利（医药）

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958

项与 SAT1 相关的文献（医药）

2024-02-22·International journal of biological macromolecules

Synergistic effect of spermidine and ciprofloxacin against Alzheimer's disease in male rat via ferroptosis modulation.

Article

作者: Menna Allah M Youssef ; Tarek M Mohamed ; Azza A Bakry ; Mai M El-Keiy

Alzheimer's disease (AD) is a prevalent form of neurodegenerative disease with a complex pathophysiology that remains not fully understood, and the exact mechanism of neurodegeneration is uncertain. Ferroptosis has been linked to the progression of degenerative diseases observed in AD models. The present study is designed to investigate the protective effects of spermidine, a potent antioxidant and iron chelator, and its synergistic interactions with ciprofloxacin, another iron chelator, in modulating ferroptosis and mitigating AD progression in rats. This study investigated AD-related biomarkers like neurotoxic amyloid beta (Aβ), arginase I, and serotonin. Spermidine demonstrated an anti-ferroptotic effect in the AD model, evident from the modulation of ferroptosis parameters such as hippocampus iron levels, reduced protein expression of transferrin receptor 1 (TFR1), and arachidonate 15-lipoxygenase (ALOX15). Additionally, the administration of spermidine led to a significant increase in protein expression of phosphorylated nuclear factor erythroid 2-related factor 2 (p-Nrf2) and upregulation of Cystine/glutamate transporter (SLC7A11) gene expression. Moreover, spermidine notably decreased p53 protein levels, acrolein, and gene expression of spermidine/spermine N1-acetyltransferase 1 (SAT1). Overall, our findings suggest that spermidine and/or ciprofloxacin may offer potential benefits against AD by modulating ferroptosis. Furthermore, spermidine enhanced the antioxidant efficacy of ciprofloxacin and reduced its toxic effects.

2024-02-02·Scientific reports

Characterization of antibiotic resistance genes and mobile genetic elements in Escherichia coli isolated from captive black bears.

Article

作者: Hang Liu ; Keyun Shi ; Yuhan Wang ; Wenhao Zhong ; Shulei Pan ; Lei Zhou ; Yuehong Cheng ; Yu Yuan ; Ziyao Zhou ; Haifeng Liu ; Shaqiu Zhang ; Guangneng Peng ; Qigui Yan ; Yan Luo ; Xiaoli Zhang ; Zhijun Zhong

The objective of this study was to analyze the antimicrobial resistance (AMR) characteristics produced by antibiotic resistance genes (ARGs), mobile genetic elements (MGEs) and gene cassettes in Escherichia coli isolated from the feces of captive black bears. Antimicrobial susceptibility testing was performed by using the disk diffusion method, and both MGEs and integron gene cassettes were detected by polymerase chain reaction. Our results showed that 43.7% (62/142) of the isolates were multidrug resistant strains and 97.9% (139/142) of the isolates were resistant to at least one antibiotic. The highest AMR phenotype was observed for tetracycline (79.6%, 113/142), followed by ampicillin (50.0%, 71/142), trimethoprim-sulfamethoxazole (43.7%, 62/142) and cefotaxime (35.9%, 51/142). However, all isolates were susceptible to tobramycin. tetA had the highest occurrence in 6 ARGs in 142 E. coli isolates (76.8%, 109/142). Ten mobile genetic elements were observed and IS26 was dominant (88.0%, 125/142). ISECP1 was positively associated with five β-lactam antibiotics. ISCR3/14, IS1133 and intI3 were not detected. Seventy-five E. coli isolates (65 intI1-positive isolates, 2 intI2-positive isolates and 8 intI1 + intI2-positive isolates) carried integrons. Five gene cassettes (dfrA1, aadA2, dfrA17-aadA5, aadA2-dfrA12 and dfrA1-aadA1) were identified in the intI1-positive isolates and 2 gene cassettes (dfrA1-catB2-sat2-aadA1 and dfrA1-catB2-sat1-aadA1) were observed in the intI2-positive isolates. Monitoring of ARGs, MGEs and gene cassettes is important to understand the prevalence of AMR, which may help to introduce measures to prevent and control of AMR in E. coli for captive black bears.

2024-01-17·International immunopharmacology

METTL14 depletion ameliorates ferroptosis in severe acute pancreatitis by increasing the N6-methyladenosine modification of ACSL4 and STA1.

Article

作者: Feng Chen ; Minghua Su ; Dong Han ; Yifan Wang ; Menglong Song

Methyltransferase-like 14 (METTL14) is implicated in the regulation of various inflammatory disorders. However, its function and molecular mechanism in severe acute pancreatitis (SAP) remains unrevealed. Here we reported an increase in METTL14 in the pancreas of SAP mice and cerulein-LPS-treated AR42J cells. METTL14 depletion reversed inflammatory response and ferroptosis by reducing the expression of SAT1 (spermidine/spermine N1-acetyltransferase 1) and ACSL4 (acyl-CoA synthetase long chain family member 4) in an m6A-dependent manner. IGF2BP2 (insulin like growth factor 2 mRNA binding protein 2) could recognize m6A-modified SAT1 and ACSL4 mRNA and enhance their stability. Moreover, METTL14 depletion ameliorated pancreatic injury, inflammation, and ferroptosis induced by SAP. METTL14 overexpression aggravated SAP by promoting ferroptosis in vivo. Therefore, these results demonstrated that METTL14-induced ferroptosis promoted the progression of SAP, and targeting METTL14 or ferroptosis could be a potential strategy for the prevention and treatment of SAP.

项与 SAT1 相关的新闻（医药）

2024-03-08

·奇点网

醋酸，又是你！

*仅供医学专业人士阅读参考去年奇点糕有一回曾经吐槽过，癌细胞们都是爱消耗醋酸的“醋精”，而以癌细胞的狡诈和刁钻本性，它们绝对不会满足于仅仅享用自身产生的醋酸，还会想办法巧取豪夺，那在肿瘤微环境里，哪种细胞会成为癌细胞“吃醋”行为的帮凶呢？近日，美国内布拉斯加大学研究团队在《自然·细胞生物学》（Nature Cell Biology）上发表的最新研究成果，就发现帮“癌王”胰腺癌吃醋的还是熟面孔——肿瘤相关成纤维细胞（CAFs）：由CAFs分泌的醋酸会通过表观遗传机制（乙酰化），增强癌细胞内关键转录因子SP1稳定性及转录活性，进而上调对胰腺癌细胞生存和增殖极为重要的SAT1表达[1]。论文核心内容总结胰腺癌最知名的特征之一就是存在大量细胞外基质，而CAFs是其中的重要组分，因此如果要查一查胰腺导管腺癌（PDAC）细胞消耗的醋酸从何而来，CAFs肯定第一批被写进嫌疑人名单。借助同位素示踪技术和基于核磁共振的代谢组学分析，研究者们首先评估了胰腺癌细胞与CAFs前体细胞，即胰腺星状细胞（PSCs）共培养时的代谢物交换情况。分析显示，由PSCs分泌的大量醋酸，是PDAC细胞在低pH条件下加速生长的关键动力，将PSCs中调节醋酸分泌的关键酶——ATP柠檬酸裂解酶（ACLY）水平敲低，即可使PSCs的促癌作用明显减弱，PDAC细胞也更难在低pH条件下存活。值得一提的是，虽然奇点糕常说CAFs的异质性问题，但它们在帮PDAC细胞吃醋方面却非常团结一致。PSCs分泌的大量醋酸可帮助PDAC细胞在低pH条件下存活下一个问题：醋酸进入PDAC细胞后，是如何帮它们存活并加速癌症发展的呢？此前有研究显示，醋酸会在乏氧条件下通过表观遗传机制促进癌细胞的脂质代谢，但本次研究中研究者们未能观察到相似的改变[2]；不过在醋酸处理后，PDAC细胞内的组蛋白乙酰化标志物，如H3K9/H3K18/H3K27等均明显上调，说明相关调控机制也与表观遗传有关。与组蛋白乙酰化同步发生的，还有乙酰辅酶合成酶2（ACSS2）这个关键醋酸代谢酶的mRNA表达水平显著上调，而且ACSS2的表达上调仅发生在肿瘤低pH区域即酸性区域，其存在也是PDAC细胞在低pH条件下存活的必要条件；在PDAC细胞与PSCs共培养时，将PDAC细胞的ACSS2表达敲低，会明显抑制PDAC细胞增殖速度、减轻肿瘤负荷。回头再来看醋酸对PDAC细胞的表观遗传调控，在醋酸处理后表达显著改变的基因中，有48个是ACSS2依赖性的，里面有多个抑癌和促癌基因，其中促癌性的SAT1基因启动子区域在低pH时，有明显的H3K27乙酰化富集，被研究者们定为了后续分析重点；敲低SAT1水平后，PDAC细胞生长速率立马被踩了刹车，也更难在低pH条件下存活。SAT1对PDAC细胞的生长和在酸性条件中存活起到关键作用在SAT1基因的启动子区域，研究者们又发现了转录因子SP1的富集，它的存在也与H3K27乙酰化修饰水平高度相关，而SP1同样是醋酸处理后被乙酰化修饰的蛋白质之一，其赖氨酸19残基（Lysine 19）位点是乙酰化修饰位点。总而言之，ACSS2–SP1–SAT1这条调控轴是CAFs分泌醋酸，助力PDAC细胞生存和加速生长的关键环节，值得开展治疗干预。ACSS2–SP1–SAT1调控轴汇总参考文献：[1]Murthy D, Attri K S, Shukla S K, et al. Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism via the ACSS2–SP1–SAT1 axis[J]. Nature Cell Biology, 2024.[2]Gao X, Lin S H, Ren F, et al. Acetate functions as an epigenetic metabolite to promote lipid synthesis under hypoxia[J]. Nature communications, 2016, 7: 11960.本文作者丨谭硕

核酸药物信使RNA

2023-12-04

·BioSpace

BioMark Announces Recent New Patent Granted in Canada to Support Its Liquid Biopsy Based Legacy Assay

Vancouver, British Columbia--(News - December 4, 2023) - BioMark Diagnostics Inc. (CSE: BUX) (FSE: 20B) (OTC Pink: BMKDF) ("BioMark" or the "Company") a clinical and diagnostic laboratory developing a liquid biopsy molecular diagnostic tests with a focus on hard to detect and treat cancers, is pleased to announce today that the Canadian Intellectual Property Office (CIPO) has granted patent N° 2.906.236, on October 31, 2023. This patent entitled "Detection and Quantification of Acetylamantadine in Urine Sample" belongs to our legacy assay and its claims cover BioMark's response to treatment assay. Rashid Ahmed, President and CEO, says, "Granting of this patent expands and strengthens our metabolite measurement capabilities by offering options to cost-effectively and reliably quantify the substrate of interest (acetyl amantadine) in a biological sample for our legacy SSAT1 urine-based assay using Raman spectroscopy. The patent has also been issued in the United States and China. The current application for our legacy SSAT1 assay includes measuring response to treatment and monitoring for recurrence, especially for hard-to-detect and treat cancers. The company is currently conducting 2 prospective clinical studies that include measuring response to treatment following treatment for glioblastoma and assessing response to treatment following immunotherapy for patients with advanced-stage lung cancer. Results are anticipated early in 2024. Once the assay is approved by regulators, this technology can be used as a point-of-care tool in economically and resource-challenged environments on a global basis." He further adds, "BioMark's portfolio of patents are testament to the robustness of its scientific and technology team that has over the years channeled targeted resources to ensure that we lead in the development of robust metabolites that can revolutionize early detection and diagnosis of lung cancer and other hard to detect cancers. More positive patent news is anticipated shortly following our recent breakthrough discoveries. We remain optimistic that adding critical patents would enhance the commercial value of BioMark's technology platform." About BioMark Diagnostics Inc. BioMark is an oncology-focused company with advanced near-to-market liquid biopsy diagnostic technologies. BioMark's cancer diagnostics technology platform leverages the power of metabolomics and machine learning algorithms to bring new cancer diagnostics to market and improve cancer prognosis by allowing physicians to detect carcinomas in the pre-symptomatic stages. The technology can also be used for measuring response to treatment and potentially for serial monitoring of cancer survivors. While the Company's current focus is on the commercialization of its liquid biopsy test for early detection of lung, it has a plan to expand into other hard-to-detect and treat cancers such as brain, ovarian, and pancreatic. Further information about BioMark is available under its pro the SEDAR+ website and on the CSE website . For further information on BioMark, please Contact: Rashid Ahmed Bux President & CEO BioMark Diagnostics Inc. Tel. 604-370-0779 Email: info@biomarkdiagnostics.com Forward-Looking Information: This press release may include forward-looking information within the meaning of Canadian securities legislation, concerning the business of BioMark. Forward-looking information is based on certain key expectations and assumptions made by the management of BioMark. Although BioMark believes that the expectations and assumptions on which such forward-looking information is based are reasonable, undue reliance should not be placed on the forward-looking information because BioMark can give no assurance that they will prove to be correct. Forward-looking statements contained in this press release are made as of the date of this press release. BioMark disclaims any intent or obligation to update publicly any forward-looking information, whether as a result of new information, future events, or results or otherwise, other than as required by applicable securities laws. The CSE has not reviewed, approved, or disapproved the content of this press release. To view the source version of this press release, please visit

诊断试剂免疫疗法

2023-04-03

·生物谷

Cell子刊：房静远团队揭示肠道菌群调控结直肠癌发生发展新机制

房静远教授团队揭示了具核梭杆菌（Cell, 2017；Gut 2021）和产肠毒素脆弱拟杆菌（Gastroenterology, 2021）等肠道细菌通过促进炎症、破坏肠道微环境、加剧代谢紊乱等途径促世界卫生组织国际癌症研究署（IARC）公布的数据显示，结直肠癌在我国发病率呈现迅猛增长态势，每年新发人数达55万。对于结直肠癌的发生机制，目前大多数学者公认腺瘤-腺癌序列学说，约85%的散发型结直肠癌是由腺瘤进展而来。结肠镜检查广泛用于人群筛查和监测，是结直肠癌和腺瘤诊断的金标准。内镜下切除腺瘤可以将结直肠癌的发病率降低76%-90%。然而，息肉切除术后仍有相当高的复发概率。对于腺瘤复发和癌变的判断，目前主要依赖于解剖和组织学特征，包括息肉的大小、数量和是否存在异型增生。然而，这些特征并不具有特异性，亟需更加精确的临床指标用于判断腺瘤-腺癌的恶性转化。既往研究表明，宿主-微生物群相互作用在结直肠癌的发生发展中起重要作用。结直肠癌患者常常表现为肠道菌群失调的特征。近年来，房静远教授团队揭示了具核梭杆菌（Cell, 2017；Gut 2021）和产肠毒素脆弱拟杆菌（Gastroenterology, 2021）等肠道细菌通过促进炎症、破坏肠道微环境、加剧代谢紊乱等途径促进结直肠癌的发生发展。然而，肠道菌群与宿主代谢互作导致结直腺瘤-腺癌转变的作用机制仍不清楚。近日，上海交通大学医学院附属仁济医院消化科房静远教授团队在 Cell 子刊 Cell Metabolism 上发表了题为：Urea cycle activation triggered by host-microbiota maladaptation driving colorectal tumorigenesis 的研究论文。该研究首次揭示了肠道菌群能够介导宿主尿素循环代谢途径，与宿主形成免疫-微生物代谢轴，进而调节宿主免疫代谢与功能，影响结直肠癌的发生。这一研究成果为干预结直肠腺瘤-腺癌进程提供了潜在的诊断、预警及治疗靶点。在这项研究中，研究团队聚焦于肠道微生态与宿主代谢之间的相互作用机制，通过对结直肠腺瘤和结直肠癌的单细胞转录组、微生物组、代谢组和临床队列数据的整合分析，证实在结直肠腺瘤-腺癌进展过程中，宿主尿素循环代谢途径显著激活，并伴随着以双歧杆菌为代表的具有尿素降解功能的肠道共生菌的缺失。尿素高负荷可通过抑制巨噬细胞中p-STAT1和SAT1启动子区域的结合效率，促进巨噬细胞向向免疫抑制性亚型分化进而破坏肠道免疫稳态。进一步动物干预实验提示尿素循环通路的抑制剂及富含尿素酶的益生菌有可能成为预防肠道腺瘤复发及癌变的有效干预制剂。这项基础结合临床验证的研究确定了尿素循环通路作为宿主-微生物共代谢途径参与结直肠癌发生的新机制，首次提出“肠菌和宿主共代谢调控肠道免疫微环境”的全新观点，从全新的理论层面补充和完善了肠道细菌影响大肠腺瘤进展癌变的知识概念体系，也为干预结直肠腺瘤-腺癌进程提供潜在的诊断、预警及潜在治疗策略。该论文共同第一作者为附属仁济医院消化科陈豪燕研究员、博士研究生童天颖、博士研究生陆诗媛及胃肠外科季林华医师，消化科房静远教授、洪洁研究员及陈豪燕研究员为论文共同通讯作者。该论文也是附属仁济医院消化科与胃肠外科携手推进深度合作后的丰硕产出。