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Using TECHnology to predict the future of biomedical education 利用技术预测生物医学教育的未来。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-12 DOI: 10.1002/2211-5463.13953
Robert A. Harris, Hasan Kazdağlı
{"title":"Using TECHnology to predict the future of biomedical education","authors":"Robert A. Harris,&nbsp;Hasan Kazdağlı","doi":"10.1002/2211-5463.13953","DOIUrl":"10.1002/2211-5463.13953","url":null,"abstract":"<p>Biomedical research is currently benefiting from a technological revolution in which multiple forms of omics are permitting unprecedented characterization of molecular pathways. Likewise, medical device and Ai-assisted technologies now make diagnoses and medical imaging more accurate. The field of education is also starting to embrace how technology can promote pedagogical development and student learning. But how will this landscape look like in 2050? With the premise that collaboration will be central to teaching and learning practices, that Together, Everything Can Happen (TECH), we examine the emerging trends and innovations in biomedical education, exploring how they will influence the field's evolution and shape future teaching practices in the coming years.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"15 1","pages":"48-55"},"PeriodicalIF":2.8,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11705505/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Delta-9 desaturase reduction in gastrointestinal cells induced to senescence by doxorubicin. 阿霉素诱导胃肠道细胞衰老的δ -9去饱和酶降低。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-10 DOI: 10.1002/2211-5463.13945
Valentina De Nunzio, Emanuela Aloisio Caruso, Matteo Centonze, Giuliano Pinto, Miriam Cofano, Ilenia Saponara, Maria Notarnicola
{"title":"Delta-9 desaturase reduction in gastrointestinal cells induced to senescence by doxorubicin.","authors":"Valentina De Nunzio, Emanuela Aloisio Caruso, Matteo Centonze, Giuliano Pinto, Miriam Cofano, Ilenia Saponara, Maria Notarnicola","doi":"10.1002/2211-5463.13945","DOIUrl":"https://doi.org/10.1002/2211-5463.13945","url":null,"abstract":"<p><p>The condition of cellular senescence has specific features, including an altered lipid metabolism. Delta-9 desaturase (Δ9) catalyzes the conversion of saturated fatty acids, such as palmitic acid and stearic acid, into their monounsaturated forms, palmitoleic and oleic acid, respectively. Δ9 activity is important for most lipid functions, such as membrane fluidity, lipoprotein metabolism and energy storage. The present study aimed to investigate differences in the expression of Δ9 in senescence-induced pancreatic (MIA-PaCa-2 and PANC-1) and hepatic (Hepa-RG and HLF) cancer cell lines. Cellular senescence was induced by growing cells in the presence of the chemotherapic drug doxorubicin. Senescence status was determined by the senescence-associated beta-galactosidase activity assay kit combined with the p21 and senescence associated secretory phenotype protein assay. Δ9 was downregulated in all senescence-induced cell lines compared to control cells, in both the lipidomic analysis and when measuring protein levels via western blotting. Hence, our findings demonstrate that the study of membrane lipid composition and the expression levels of Δ9 could potentially form the basis for future applications investigating the state of cellular senescence.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
2-dodecyl-6-methoxycyclohexa-2,5-diene-1,4-dione mediates the effect of ROS-enhanced PI3K/Akt/mTOR pathway on autophagy in breast cancer. 2-十二烷基-6-甲氧基环己-2,5-二烯-1,4-二酮介导ros增强的PI3K/Akt/mTOR通路对乳腺癌自噬的影响。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-09 DOI: 10.1002/2211-5463.13940
Linqian Chen, Meifeng Chen, Yan Xie, Yuyan Zhang, Shutian Mo, Yongfei He, Tianyi Liang, Yuan Liao, Renbin Huang, Guodong Huang, Chuangye Han, Thi Thai Hoa Pham
{"title":"2-dodecyl-6-methoxycyclohexa-2,5-diene-1,4-dione mediates the effect of ROS-enhanced PI3K/Akt/mTOR pathway on autophagy in breast cancer.","authors":"Linqian Chen, Meifeng Chen, Yan Xie, Yuyan Zhang, Shutian Mo, Yongfei He, Tianyi Liang, Yuan Liao, Renbin Huang, Guodong Huang, Chuangye Han, Thi Thai Hoa Pham","doi":"10.1002/2211-5463.13940","DOIUrl":"https://doi.org/10.1002/2211-5463.13940","url":null,"abstract":"<p><p>Several studies have suggested a potential antitumor effect of 2-dodecyl-6-methoxycyclohexa-2,5-diene-1,4-dione (DMDD). To further understand the mechanism of action of this compound, we investigated its effect on the phosphatidylinositol-3-kinase (PI3K)/serine-threonine kinase (Akt)/mammalian target of rapamycin (mTOR) signaling pathway. We show that DMDD application significantly inhibited the proliferation of breast cancer cell lines MDA-MB-231 and ER-α positive MCF-7. Furthermore, DMDD application resulted in increased intracellular reactive oxygen species (ROS) levels, apoptosis and autophagy, whereas it downregulated the expression of PI3K, Akt and mTOR mRNA and proteins, and increased the expression of LC3II/I and p62 proteins. In a mouse breast cancer xenograft model, DMDD inhibited tumor growth. Expression analyses suggest that ROS levels were higher in DMDD treated tumor tissues, whereas immunohistochemical analyses suggest that apoptotic cells were more prevalent in the DMDD treated group compared to the control group. Taken together, our results suggest that the molecular mechanism of action of DMDD may involve the enhancement of breast cancer autophagy through the PI3K/Akt/mTOR signaling pathway by mediating ROS expression.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
RETRACTION: NGF Protects Neuroblastoma Cells Against β-Amyloid-Induced Apoptosis via the Nrf2/HO-1 pathway. 结论:NGF通过Nrf2/HO-1途径保护神经母细胞瘤细胞免受β-淀粉样蛋白诱导的凋亡。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-06 DOI: 10.1002/2211-5463.13950
{"title":"RETRACTION: NGF Protects Neuroblastoma Cells Against β-Amyloid-Induced Apoptosis via the Nrf2/HO-1 pathway.","authors":"","doi":"10.1002/2211-5463.13950","DOIUrl":"https://doi.org/10.1002/2211-5463.13950","url":null,"abstract":"<p><strong>Retraction: </strong>R. Su, W. Su, and Q. Jiao, \"NGF Protects Neuroblastoma Cells Against β-Amyloid-Induced Apoptosis via the Nrf2/HO-1 pathway,\" FEBS Open Bio 9, no. 12 (2019): 2063-2071, https://doi.org/10.1002/2211-5463.12742. The above article, published online on 01 November 2019, in Wiley Online Library (wileyonlinelibrary.com), and its correction (https://doi.org/10.1002/2211-5463.12782) has been retracted by agreement between the journal Editor-in-Chief, Miguel A. De la Rosa; FEBS Press; and John Wiley and Sons Ltd. The retraction has been agreed upon following an investigation into concerns raised by a third party, which revealed inappropriate image duplications between this (Figure 2A, 3A, 5A and 6E) and other articles that were previously published or published in the same or following year. Given the extent of the identified issues, the editors have lost confidence in the data presented and consider the conclusions of this manuscript substantially compromised.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
RETRACTION: LKB1 Suppresses Androgen Synthesis in a Mouse Model of Hyperandrogenism via IGF-1 Signaling. 撤回:LKB1通过IGF-1信号抑制高雄激素血症小鼠模型中的雄激素合成。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-06 DOI: 10.1002/2211-5463.13948
{"title":"RETRACTION: LKB1 Suppresses Androgen Synthesis in a Mouse Model of Hyperandrogenism via IGF-1 Signaling.","authors":"","doi":"10.1002/2211-5463.13948","DOIUrl":"https://doi.org/10.1002/2211-5463.13948","url":null,"abstract":"<p><strong>Retraction: </strong>Y. Xu, Y. Gao, Z. Huang, Y. Zheng, W. Teng, D. Zheng, and X. Zheng, \"LKB1 Suppresses Androgen Synthesis in a Mouse Model of Hyperandrogenism via IGF-1 Signaling,\" FEBS Open Bio 9, no. 10 (2019): 1817-1825, https://doi.org/10.1002/2211-5463.12723. The above article, published online on 12 September 2019, in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Miguel A. De la Rosa; FEBS Press; and John Wiley and Sons Ltd. The retraction has been agreed upon following an investigation into concerns raised by a third party, which revealed inappropriate image duplications between this (Figure 1C, 1H) and other articles that were previously published or published in the same or following year. Given the extent of the identified issues, the editors have lost confidence in the data presented and consider the conclusions of this manuscript substantially compromised.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
RETRACTION: MicroRNA-498 Reduces the Proliferation and Invasion of Colorectal Cancer Cells via Targeting Bcl-2. 撤回:MicroRNA-498通过靶向Bcl-2抑制结直肠癌细胞的增殖和侵袭。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-06 DOI: 10.1002/2211-5463.13949
{"title":"RETRACTION: MicroRNA-498 Reduces the Proliferation and Invasion of Colorectal Cancer Cells via Targeting Bcl-2.","authors":"","doi":"10.1002/2211-5463.13949","DOIUrl":"https://doi.org/10.1002/2211-5463.13949","url":null,"abstract":"<p><strong>Retraction: </strong>T. Wang, L. Ma, W. Li, L. Ding, and H. Gao, \"MicroRNA-498 Reduces the Proliferation and Invasion of Colorectal Cancer Cells via Targeting Bcl-2,\" FEBS Open Bio 10, no. 1 (2020): 168-175, https://doi.org/10.1002/2211-5463.12767. The above article, published online on 17 December 2019, in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Miguel A. De la Rosa; FEBS Press; and John Wiley and Sons Ltd. The retraction has been agreed upon following an investigation into concerns raised by a third party, which revealed inappropriate image duplications between this (Figure 3A and B, 5E and F) and other articles that were previously published or published in the same or following year. Given the extent of the identified issues, the editors have lost confidence in the data presented and consider the conclusions of this manuscript substantially compromised.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
RETRACTION: XBP1 Inhibits Mesangial Cell Apoptosis in Response to Oxidative Stress via the PTEN/AKT Pathway in Diabetic Nephropathy. 回顾:XBP1通过PTEN/AKT通路抑制糖尿病肾病中氧化应激反应中的系膜细胞凋亡。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-06 DOI: 10.1002/2211-5463.13947
{"title":"RETRACTION: XBP1 Inhibits Mesangial Cell Apoptosis in Response to Oxidative Stress via the PTEN/AKT Pathway in Diabetic Nephropathy.","authors":"","doi":"10.1002/2211-5463.13947","DOIUrl":"https://doi.org/10.1002/2211-5463.13947","url":null,"abstract":"<p><strong>Retraction: </strong>Y. Wang, Z. He, Q. Yang, and G. Zhou, \"XBP1 Inhibits Mesangial Cell Apoptosis in Response to Oxidative Stress via the PTEN/AKT Pathway in Diabetic Nephropathy,\" FEBS Open Bio 9, no. 7 (2019): 1249-1258, https://doi.org/10.1002/2211-5463.12655. The above article, published online on 02 June 2019, in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Miguel A. De la Rosa; FEBS Press; and John Wiley and Sons Ltd. The retraction has been agreed upon following an investigation into concerns raised by a third party, which revealed inappropriate image duplications between this (Figure 1C-F, 3A and C) and other articles that were previously published or published in the same or following year. Given the extent of the identified issues, the editors have lost confidence in the data presented and consider the conclusions of this manuscript substantially compromised.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
RETRACTION: CDKL5 Promotes Proliferation, Migration, and Chemotherapeutic Drug Resistance of Glioma Cells via Activation of the PI3K/AKT Signaling Pathway. 回顾:CDKL5通过激活PI3K/AKT信号通路促进胶质瘤细胞的增殖、迁移和化疗耐药。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-06 DOI: 10.1002/2211-5463.13946
{"title":"RETRACTION: CDKL5 Promotes Proliferation, Migration, and Chemotherapeutic Drug Resistance of Glioma Cells via Activation of the PI3K/AKT Signaling Pathway.","authors":"","doi":"10.1002/2211-5463.13946","DOIUrl":"https://doi.org/10.1002/2211-5463.13946","url":null,"abstract":"<p><strong>Retraction: </strong>Z. Jiang, T. Gong, and H. Wei, \"CDKL5 Promotes Proliferation, Migration, and Chemotherapeutic Drug Resistance of Glioma Cells via Activation of the PI3K/AKT Signaling Pathway,\" FEBS Open Bio 10, no. 2 (2020): 268-277, https://doi.org/10.1002/2211-5463.12780. The above article, published online on 21 January 2020, in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Miguel A. De la Rosa; FEBS Press; and John Wiley and Sons Ltd. The retraction has been agreed upon following an investigation into concerns raised by a third party, which revealed inappropriate image duplications between this (Figure 3E, 4A and E, 5B and E) and other articles that were previously published or published in the same or following year. Given the extent of the identified issues, the editors have lost confidence in the data presented and consider the conclusions of this manuscript substantially compromised.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Using a 'Students as Partners' model to develop an authentic assessment promoting employability skills in undergraduate life science education. 使用“学生作为伙伴”模式,开发一个真实的评估,以促进本科生命科学教育中的就业技能。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-05 DOI: 10.1002/2211-5463.13941
Kelsey Van, Sana Tasawar, Elaina B K Brendel, Camille Law, Anisha Mahajan, Carissa Brownell-Riddell, Natalia Diamond, Kerry Ritchie, Jennifer M Monk
{"title":"Using a 'Students as Partners' model to develop an authentic assessment promoting employability skills in undergraduate life science education.","authors":"Kelsey Van, Sana Tasawar, Elaina B K Brendel, Camille Law, Anisha Mahajan, Carissa Brownell-Riddell, Natalia Diamond, Kerry Ritchie, Jennifer M Monk","doi":"10.1002/2211-5463.13941","DOIUrl":"https://doi.org/10.1002/2211-5463.13941","url":null,"abstract":"<p><p>Authentic assessments (AA) include three principles, realism, cognitive challenge, and evaluative judgment, and replicate professional workplace expectations. Developing AA in undergraduate life science education is necessary to promote critical skill development and adequately prepare students for the workplace. Using a 'Students-as-Partners' (SAP) approach, five students, an educational developer and the instructor codeveloped an AA requiring students to utilize scientific literacy (SL) and critical thinking (CT) skills to develop a data extraction table and generate communication outputs for scientific and nonscientific audiences. Subsequently, the SAP-developed AA was completed by students (n = 173) enrolled in a fourth-year life sciences and pathophysiology course who completed an online survey providing feedback about their perceived development of critical skills and the relevance of the assignment to the workplace. The top transferable skills students reported the greatest growth in were SL (41.6%, n = 72), communication (34.7%, n = 60), CT (16.2%, n = 28), and problem-solving (7.5%, n = 13). Student self-assessed and instructor-assessed grades were positively correlated, wherein 60.6% of students assessed their AA grades below the instructor's assessment and 4.7% of students assigned themselves the same grade as the instructor. Students' perceived stress levels were (a) negatively correlated with assignment grades and feelings of enjoyment, hope and pride, and (b) positively correlated with feelings of anger, anxiety, shame, and hopelessness while working on the assignment. This study demonstrates the impact of AA on the student learning experience and the relevance of AA to help prepare students for life science careers.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Antitubercular potential and pH-driven mode of action of salicylic acid derivatives. 水杨酸衍生物的抗结核潜能和ph驱动作用模式。
IF 2.8 4区 生物学
FEBS Open Bio Pub Date : 2024-12-03 DOI: 10.1002/2211-5463.13944
Janïs Laudouze, Thomas Francis, Emma Forest, Frédérique Mies, Jean-Michel Bolla, Céline Crauste, Stéphane Canaan, Vadim Shlyonsky, Pierre Santucci, Jean-François Cavalier
{"title":"Antitubercular potential and pH-driven mode of action of salicylic acid derivatives.","authors":"Janïs Laudouze, Thomas Francis, Emma Forest, Frédérique Mies, Jean-Michel Bolla, Céline Crauste, Stéphane Canaan, Vadim Shlyonsky, Pierre Santucci, Jean-François Cavalier","doi":"10.1002/2211-5463.13944","DOIUrl":"https://doi.org/10.1002/2211-5463.13944","url":null,"abstract":"<p><p>In the search for new antituberculosis drugs with novel mechanisms of action, we evaluated the antimycobacterial activity of a panel of eight phenolic acids against four pathogenic mycobacterial model species, including Mycobacterium tuberculosis. We demonstrated that salicylic acid (SA), as well as the iodinated derivatives 5-iodo-salicylic acid (5ISA) and 3,5-diiodo-salicylic acid (3,5diISA), displayed promising antitubercular activities. Remarkably, using a genetically encoded mycobacterial intrabacterial pH reporter, we describe for the first time that SA, 5ISA, 3,5diISA, and the anti-inflammatory drug aspirin (ASP) act by disrupting the intrabacterial pH homeostasis of M. tuberculosis in a dose-dependent manner under in vitro conditions mimicking the endolysosomal pH of macrophages. In contrast, the structurally related second-line anti-TB drug 4-aminosalicylic acid (PAS) had no pH-dependent activity and was strongly antagonized by l-methionine supplementation, thereby suggesting distinct modes of action. Finally, we propose that SA, ASP, and its two iodinated derivatives could restrict M. tuberculosis growth in a pH-dependent manner by acidifying the cytosol of the bacilli, therefore making such compounds very attractive for further development of antibacterial agents.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142767678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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