FEBS Letters最新文献_第10页

Keep calm and reboot - how cells restart transcription after DNA damage and DNA repair. 保持冷静，重新启动--细胞如何在 DNA 损伤和 DNA 修复后重新启动转录。

IF 3.5 4区生物学

FEBS Letters Pub Date : 2024-07-11 DOI: 10.1002/1873-3468.14964

Lise-Marie Donnio, Giuseppina Giglia-Mari

{"title":"Keep calm and reboot - how cells restart transcription after DNA damage and DNA repair.","authors":"Lise-Marie Donnio, Giuseppina Giglia-Mari","doi":"10.1002/1873-3468.14964","DOIUrl":"https://doi.org/10.1002/1873-3468.14964","url":null,"abstract":"The effects of genotoxic agents on DNA and the processes involved in their removal have been thoroughly studied; however, very little is known about the mechanisms governing the reinstatement of cellular activities after DNA repair, despite restoration of the damage-induced block of transcription being essential for cell survival. In addition to impeding transcription, DNA lesions have the potential to disrupt the precise positioning of chromatin domains within the nucleus and alter the meticulously organized architecture of the nucleolus. Alongside the necessity of resuming transcription mediated by RNA polymerase 1 and 2 transcription, it is crucial to restore the structure of the nucleolus to facilitate optimal ribosome biogenesis and ensure efficient and error-free translation. Here, we examine the current understanding of how transcriptional activity from RNA polymerase 2 is reinstated following DNA repair completion and explore the mechanisms involved in reassembling the nucleolus to safeguard the correct progression of cellular functions. Given the lack of information on this vital function, this Review seeks to inspire researchers to explore deeper into this specific subject and offers essential suggestions on how to investigate this complex and nearly unexplored process further.","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2024-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141589965","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

The ERK5 pathway in BRAFV600E melanoma cells plays a role in development of acquired resistance to dabrafenib but not vemurafenib BRAFV600E黑色素瘤细胞中的ERK5通路在达拉非尼获得性抗药性的形成过程中发挥了作用，但在维莫非尼获得性抗药性的形成过程中并未发挥作用。

IF 3.5 4区生物学

FEBS Letters Pub Date : 2024-07-08 DOI: 10.1002/1873-3468.14960

Anil Kumar Mondru, Beth Wilkinson, Mohammad A. Aljasir, Ahmed Alrumayh, Georgia Greaves, Maxine Emmett, Saad Albohairi, Rowan Pritchard-Jones, Michael J. Cross

{"title":"The ERK5 pathway in BRAFV600E melanoma cells plays a role in development of acquired resistance to dabrafenib but not vemurafenib","authors":"Anil Kumar Mondru, Beth Wilkinson, Mohammad A. Aljasir, Ahmed Alrumayh, Georgia Greaves, Maxine Emmett, Saad Albohairi, Rowan Pritchard-Jones, Michael J. Cross","doi":"10.1002/1873-3468.14960","DOIUrl":"10.1002/1873-3468.14960","url":null,"abstract":"Malignant melanoma, an aggressive skin cancer with a poor prognosis, frequently features BRAFV600E mutation resulting in activation of the MAPK pathway and melanocyte proliferation and survival. BRAFV600E inhibitors like vemurafenib and dabrafenib have enhanced patient survival, yet drug resistance remains a significant challenge. We investigated the role of the ERK5 pathway in BRAFV600E melanoma cells and cells with acquired resistance to PLX4720 (vemurafenib) and dabrafenib. In BRAFV600E melanoma, ERK5 inhibition minimally affected viability compared to ERK1/2 inhibition. In vemurafenib-resistant cells, ERK5 inhibition alone didn't impact viability or restore drug sensitivity to vemurafenib. However, in dabrafenib-resistant cells, ERK5 inhibition reduced viability and enhanced the anti-proliferative effect of MEK1/2 inhibition. Targeting the ERK5 pathway may represent a therapeutic opportunity in dabrafenib-resistant melanoma.","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"598 16","pages":"2011-2027"},"PeriodicalIF":3.5,"publicationDate":"2024-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.14960","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141558430","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

The HPE1 RNA-binding protein modulates chloroplast RNA editing to promote photosynthesis under cold stress in Arabidopsis HPE1 RNA 结合蛋白调节叶绿体 RNA 编辑，促进拟南芥在冷胁迫下的光合作用。

IF 3.5 4区生物学

FEBS Letters Pub Date : 2024-07-08 DOI: 10.1002/1873-3468.14969

Yajun Zeng, Jie Dong, Danni Fu, Meihui Shi, Zhifeng Zheng, Mingxi Zhong, Hong-Bin Wang, Su-Juan Duan, Hong-Lei Jin

引用次数: 0

Identifying actionable synthetically lethal cancer gene pairs using mutual exclusivity 利用互斥性识别可操作的合成致命癌症基因对。

IF 3.5 4区生物学

FEBS Letters Pub Date : 2024-07-08 DOI: 10.1002/1873-3468.14950

Sarah K. Wooller, Laurence H. Pearl, Frances M. G. Pearl

引用次数: 0

SARS-CoV-2-derived protein Orf9b enhances MARK2 activity via interaction with the autoinhibitory KA1 domain 源自 SARS-CoV-2 的蛋白 Orf9b 通过与自抑制 KA1 结构域相互作用增强 MARK2 的活性。

IF 3.5 4区生物学

FEBS Letters Pub Date : 2024-07-05 DOI: 10.1002/1873-3468.14975

Daiki Homma, Sophia Jobien M. Limlingan, Taro Saito, Kanae Ando

引用次数: 0

Multiplexed imaging to reveal tissue dendritic cell spatial localisation and function. 通过多重成像揭示组织树突状细胞的空间定位和功能。

IF 3.5 4区生物学

FEBS Letters Pub Date : 2024-07-05 DOI: 10.1002/1873-3468.14962

Giuseppe Rocca, Marco Galli, Anna Celant, Giulia Stucchi, Laura Marongiu, Stefano Cozzi, Metello Innocenti, Francesca Granucci

引用次数: 0

Sphingosine-1-phosphate signalling in the heart: exploring emerging perspectives in cardiopathology 心脏中的鞘氨醇-1-磷酸信号：探索心脏病理学的新视角。

IF 3.5 4区生物学

FEBS Letters Pub Date : 2024-07-04 DOI: 10.1002/1873-3468.14973

Franck Phan, Olivier Bourron, Fabienne Foufelle, Hervé Le Stunff, Eric Hajduch

{"title":"Sphingosine-1-phosphate signalling in the heart: exploring emerging perspectives in cardiopathology","authors":"Franck Phan, Olivier Bourron, Fabienne Foufelle, Hervé Le Stunff, Eric Hajduch","doi":"10.1002/1873-3468.14973","DOIUrl":"10.1002/1873-3468.14973","url":null,"abstract":"Cardiometabolic disorders contribute to the global burden of cardiovascular diseases. Emerging sphingolipid metabolites like sphingosine-1-phosphate (S1P) and its receptors, S1PRs, present a dynamic signalling axis significantly impacting cardiac homeostasis. S1P's intricate mechanisms extend to its transportation in the bloodstream by two specific carriers: high-density lipoprotein particles and albumin. This intricate transport system ensures the accessibility of S1P to distant target tissues, influencing several physiological processes critical for cardiovascular health. This review delves into the diverse functions of S1P and S1PRs in both physiological and pathophysiological conditions of the heart. Emphasis is placed on their diverse roles in modulating cardiac health, spanning from cardiac contractility, angiogenesis, inflammation, atherosclerosis and myocardial infarction. The intricate interplays involving S1P and its receptors are analysed concerning different cardiac cell types, shedding light on their respective roles in different heart diseases. We also review the therapeutic applications of targeting S1P/S1PRs in cardiac diseases, considering existing drugs like Fingolimod, as well as the prospects and challenges in developing novel therapies that selectively modulate S1PRs.","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"598 21","pages":"2641-2655"},"PeriodicalIF":3.5,"publicationDate":"2024-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.14973","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141534035","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

Unlocking the biochemical secrets of longevity: balancing healthspan and lifespan 揭开长寿的生化秘密：平衡健康寿命和寿命。

IF 3.5 4区生物学

FEBS Letters Pub Date : 2024-07-02 DOI: 10.1002/1873-3468.14963

Jose Viña, Consuelo Borrás

引用次数: 0

Poliovirus capsid protein VP3 can penetrate vascular endothelial cells 脊髓灰质炎病毒壳蛋白 VP3 可以穿透血管内皮细胞。

IF 3.5 4区生物学

FEBS Letters Pub Date : 2024-07-02 DOI: 10.1002/1873-3468.14974

Taketoshi Mizutani, Aya Ishizaka

引用次数: 0

Host–diet–microbiota interplay in intestinal nutrition and health 肠道营养与健康中的宿主-饮食-微生物群相互作用。

IF 3.5 4区生物学

FEBS Letters Pub Date : 2024-06-30 DOI: 10.1002/1873-3468.14966

Anastasia Ignatiou, Chrysoula Pitsouli

{"title":"Host–diet–microbiota interplay in intestinal nutrition and health","authors":"Anastasia Ignatiou, Chrysoula Pitsouli","doi":"10.1002/1873-3468.14966","DOIUrl":"10.1002/1873-3468.14966","url":null,"abstract":"The intestine is populated by a complex and dynamic assortment of microbes, collectively called gut microbiota, that interact with the host and contribute to its metabolism and physiology. Diet is considered a key regulator of intestinal microbiota, as ingested nutrients interact with and shape the resident microbiota composition. Furthermore, recent studies underscore the interplay of dietary and microbiota-derived nutrients, which directly impinge on intestinal stem cells regulating their turnover to ensure a healthy gut barrier. Although advanced sequencing methodologies have allowed the characterization of the human gut microbiome, mechanistic studies assessing diet–microbiota–host interactions depend on the use of genetically tractable models, such as Drosophila melanogaster. In this review, we first discuss the similarities between the human and fly intestines and then we focus on the effects of diet and microbiota on nutrient-sensing signaling cascades controlling intestinal stem cell self-renewal and differentiation, as well as disease. Finally, we underline the use of the Drosophila model in assessing the role of microbiota in gut-related pathologies and in understanding the mechanisms that mediate different whole-body manifestations of gut dysfunction.","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"598 20","pages":"2482-2517"},"PeriodicalIF":3.5,"publicationDate":"2024-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.14966","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141467202","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