BioEssays最新文献

筛选
英文 中文
Biosensors for Detecting Small Rho GTPases: Monitoring Expression and Activation. 用于检测小Rho gtpase的生物传感器:监测表达和激活。
IF 2.7 3区 生物学
BioEssays Pub Date : 2025-09-10 DOI: 10.1002/bies.70069
Nik Yasmin Umaira Hasnizan, Chong Chien Fung, Saw Keat Chuan, Nurul Syafawani Fizal, Noorhayati Idros, Ana Masara Ahmad Mokhtar
{"title":"Biosensors for Detecting Small Rho GTPases: Monitoring Expression and Activation.","authors":"Nik Yasmin Umaira Hasnizan, Chong Chien Fung, Saw Keat Chuan, Nurul Syafawani Fizal, Noorhayati Idros, Ana Masara Ahmad Mokhtar","doi":"10.1002/bies.70069","DOIUrl":"https://doi.org/10.1002/bies.70069","url":null,"abstract":"<p><p>Advanced biosensing technologies, such as Förster resonance energy transfer (FRET) and bioluminescence resonance energy transfer (BRET), have enabled real-time, high-resolution tracking of Rho GTPase activity, surpassing traditional methods like pull-down assays. However, current biosensors mainly detect the GTP-bound active state through effector interactions, without directly measuring Rho GTPase expression or identifying related biomarkers of abnormal activation. Small Rho GTPases are essential molecular switches that regulate key cellular processes such as cytoskeletal organization, cell movement, polarity, vesicle trafficking, and the cell cycle. Their precise activation and deactivation are critical for cellular balance, and disruptions in their signaling pathways are linked to diseases like cancer and immune disorders. Monitoring their activity is vital for understanding these processes and developing treatments. This study highlights the need for next-generation biosensors capable of directly monitoring expression levels and novel biomarkers, offering new avenues for research and therapeutic development targeting small Rho GTPases.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":" ","pages":"e70069"},"PeriodicalIF":2.7,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145028919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Emerging Perspectives on Gonadotropin Regulation in Vertebrates Revealed by the Discovery of FSH-RH in Teleosts. 硬骨鱼中FSH-RH的发现揭示了脊椎动物促性腺激素调节的新观点。
IF 2.7 3区 生物学
BioEssays Pub Date : 2025-09-10 DOI: 10.1002/bies.70066
Daichi Kayo, Shun Kenny Uehara, Muhammad Rahmad Royan, Shinji Kanda
{"title":"Emerging Perspectives on Gonadotropin Regulation in Vertebrates Revealed by the Discovery of FSH-RH in Teleosts.","authors":"Daichi Kayo, Shun Kenny Uehara, Muhammad Rahmad Royan, Shinji Kanda","doi":"10.1002/bies.70066","DOIUrl":"https://doi.org/10.1002/bies.70066","url":null,"abstract":"<p><p>Vertebrate gonadal function is regulated by pituitary gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH). These hormones are considered to be regulated by hypothalamic factor(s). Since the discovery of gonadotropin-releasing hormone (GnRH) in mammals, which stimulates the secretion of both FSH and LH, GnRH had been believed to be the sole gonadotropin-releasing hormone in vertebrates for more than 5 decades. However, recent studies have identified an alternative primary regulator of FSH in teleosts, leading to the hypothesis that FSH and LH are regulated by different factors in teleosts (dual GnRH model). This contrasts with the situation in mammals, where a single GnRH regulates both hormones (solo GnRH model). Importantly, although underlying mechanisms likely differ, both teleosts and mammals reproduce efficiently and have convergently evolved similar phenomena, including steroid feedback regulation. In this review, by comparing these taxa, we summarize mechanistic differences and propose an evolutionary scenario based on current experimental evidence.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":" ","pages":"e70066"},"PeriodicalIF":2.7,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145032816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Fusion Pores as Regulators of Quantal Size and Cellular Physiology. 融合孔作为量子大小和细胞生理的调节因子。
IF 2.7 3区 生物学
BioEssays Pub Date : 2025-09-07 DOI: 10.1002/bies.70064
Bhavya R Bhaskar, Shahina Mazumdar, Sruthilaya Dayanandan, Debasis Das
{"title":"Fusion Pores as Regulators of Quantal Size and Cellular Physiology.","authors":"Bhavya R Bhaskar, Shahina Mazumdar, Sruthilaya Dayanandan, Debasis Das","doi":"10.1002/bies.70064","DOIUrl":"https://doi.org/10.1002/bies.70064","url":null,"abstract":"<p><p>The timely release of chemical messengers is a crucial step in cell-to-cell communication. Does this release occur as a passive diffusion from the donor membrane or it is actively regulated? A series of studies indicated that chemical messengers' secretion is \"sub-quantal\". This mode of secretion demands a strongly regulated release mechanism and calls for a thorough characterization of the release sites. When secretory vesicles fuse with the plasma membrane, ephemeral fusion pores serve as the first aqueous connection between the lumen of secretory vesicle and the cell exterior through which chemical messengers are released. Here, we discuss the molecular players that directly regulate fusion pore properties. This has consequences in controlling the amount of chemical messengers' secretion, hence controlling the quantal size. A thorough understanding of the role of regulatory factors in controlling quantal size can help design potent therapeutics to alter vesicular secretion under pathological conditions.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":" ","pages":"e70064"},"PeriodicalIF":2.7,"publicationDate":"2025-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145008204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Shear Stress as a Danger Signal: Inducing Inflammation and Thrombosis via Mechanosensitive NETosis. 剪切应力作为危险信号:通过机械敏感性NETosis诱导炎症和血栓形成。
IF 2.7 3区 生物学
BioEssays Pub Date : 2025-09-04 DOI: 10.1002/bies.70065
Sara Baratchi, Karlheinz Peter
{"title":"Shear Stress as a Danger Signal: Inducing Inflammation and Thrombosis via Mechanosensitive NETosis.","authors":"Sara Baratchi, Karlheinz Peter","doi":"10.1002/bies.70065","DOIUrl":"https://doi.org/10.1002/bies.70065","url":null,"abstract":"<p><p>Neutrophil extracellular traps (NETs)-web-like DNA structures extruded by neutrophils in response to various stimuli, including pathogens, sterile inflammation, and mechanical stress-play a dual role in immunity and disease. While NETs serve to trap and neutralize pathogens during host defense, excessive or dysregulated NET formation, known as NETosis, can amplify inflammation and contribute to thrombotic complications such as atherosclerosis and valve disease. Increasing evidence supports that NETosis is a regulated, signaling-driven process, and that mechanical forces-including shear stress, tensile force, and matrix stiffness-can act as noncanonical danger signals capable of inducing NETosis. Mechanosensitive ion channels such as Piezo1, have emerged as key transducers of these biophysical cues, enabling cells to convert changes in shear stress levels into intracellular calcium flux, cytoskeletal remodeling, and ultimately NET release. Furthermore, exposure to pathologically high levels of shear stress may improve the sensitivity of neutrophils to secondary stimuli, lowering their activation threshold and amplifying inflammatory and thrombotic cascades. This mechanosensitive framework highlights shear-induced NETosis as a critical pathway by which neutrophils contribute to inflammation and thrombosis in mechanically stressed vascular environments.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":" ","pages":"e70065"},"PeriodicalIF":2.7,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144999744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Conformational Rearrangement of Fission DSPs. 裂变dsp的构象重排。
IF 2.7 3区 生物学
BioEssays Pub Date : 2025-09-01 DOI: 10.1002/bies.70062
Anelise N Hutson, Kristy Rochon, Jason A Mears
{"title":"Conformational Rearrangement of Fission DSPs.","authors":"Anelise N Hutson, Kristy Rochon, Jason A Mears","doi":"10.1002/bies.70062","DOIUrl":"https://doi.org/10.1002/bies.70062","url":null,"abstract":"<p><p>Dynamin superfamily proteins (DSPs) are large GTPases that play crucial roles in membrane remodeling processes, including vesicle uptake, mitochondrial fission, and opposing fusion events. Among them, dynamin and dynamin-related protein 1 (Drp1) share a conserved domain architecture, yet exhibit unique structural and regulatory features that tailor their functions. This review explores the conformational rearrangements of the mammalian fission DSPs, dynamin and Drp1, focusing on their dimeric and tetrameric structures, lipid-bound assemblies, and key regulatory elements that drive membrane constriction. Structural biology methods, including x-ray crystallography and cryo-electron microscopy, have provided insight into the mechanism of activation and constriction of these DSPs, revealing how domain interactions and intrinsically disordered regions regulate self-assembly and enzymatic activity. We briefly examine the role of sequence modifications and partner proteins in modulating DSP function, highlighting the impact of regulatory factors on their respective cellular functions. An ongoing goal is to better understand the molecular mechanisms governing the transitions from a pre-assembled cytosolic state to a self-assembled state for dynamin and Drp1 on membranes, which provides a foundation for studying subsequent helical constriction. This insight will enhance our knowledge of organelle dynamics and provide new avenues for therapeutic interventions targeting DSP-related pathologies.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":" ","pages":"e70062"},"PeriodicalIF":2.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144943697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Taking Down the Primary Cilium: Pathways for Disassembly in Differentiating Cells. 初级纤毛的脱落:分化细胞的拆卸途径。
IF 2.7 3区 生物学
BioEssays Pub Date : 2025-09-01 DOI: 10.1002/bies.70060
Carolyn M Ott, Saikat Mukhopadhyay
{"title":"Taking Down the Primary Cilium: Pathways for Disassembly in Differentiating Cells.","authors":"Carolyn M Ott, Saikat Mukhopadhyay","doi":"10.1002/bies.70060","DOIUrl":"https://doi.org/10.1002/bies.70060","url":null,"abstract":"<p><p>Primary cilia are customized subcellular signaling compartments leveraged to detect signals in diverse physiological contexts. Although prevalent throughout mammalian tissues, primary cilia are not universal. Many non-ciliated cells derive from developmental lineages that include ciliated progenitors; however, little is known about how primary cilia are lost as cells differentiate. Here, we examine how ciliated and non-ciliated states emerge during development and are actively maintained. We highlight several pathways for primary cilia loss, including cilia resorption in pre-mitotic cells, cilia deconstruction in post-mitotic cells, cilia shortening via remodeling, and cilia disassembly preceding multiciliogenesis. Lack of ciliogenesis is known to decrease primary cilia frequency and cause ciliopathies. Failure to maintain cilia can also cause primary cilia to be absent. Conversely, defects in primary cilia suppression or disassembly can lead to the presence of primary cilia in non-ciliated cells. We examine how changes in ciliation states could contribute to tumorigenesis and neurodegeneration.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":" ","pages":"e70060"},"PeriodicalIF":2.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144943726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
When the Clock Is Ticking: The Role of Mitotic Duration in Cell Fate Determination. 当时钟滴答作响:有丝分裂持续时间在细胞命运决定中的作用。
IF 2.7 3区 生物学
BioEssays Pub Date : 2025-08-30 DOI: 10.1002/bies.70061
Cornelia Sala, Elmar Schiebel
{"title":"When the Clock Is Ticking: The Role of Mitotic Duration in Cell Fate Determination.","authors":"Cornelia Sala, Elmar Schiebel","doi":"10.1002/bies.70061","DOIUrl":"https://doi.org/10.1002/bies.70061","url":null,"abstract":"<p><p>Mitosis is a crucial phase of the cell cycle, during which several mechanisms work together to ensure accurate chromosome segregation and to eliminate defective cells if errors occur. One key mechanism is the spindle assembly checkpoint (SAC), which upon mitotic errors-such as those induced by genetic mutations, drug treatments, or environmental stresses-arrest cells in mitosis. Arrested cells may undergo apoptosis during mitosis or eventually exit mitosis even if the damage remains unrepaired. Mitotic exit is driven by a reduction in cyclin B1 levels, regulated during mitosis by multiple mechanisms affecting both its synthesis and degradation. Strikingly, cells harboring the tumor suppressor p53 can monitor the duration of mitosis and encode this information as a form of \"mitotic memory\". This memory influences the fate of daughter cells after mitotic exit by inducing G1 arrest through p53-dependent expression of the cyclin-dependent kinase (CDK) inhibitor p21. Recent studies have proposed mechanisms by which cyclin B1 levels are regulated during mitotic arrest and how p53 promotes mitotic-arrest-dependent transcription of p21 in G1. These findings indicate that both the expression of regulators that control mitotic duration and the activity of proteins that monitor the duration of mitosis and halt proliferation work together to determine cell fate following mitotic errors. Understanding these mechanisms offers valuable insights for cancer therapy, particularly regarding the strategic application of antimitotic agents.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":" ","pages":"e70061"},"PeriodicalIF":2.7,"publicationDate":"2025-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144943707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
BioEssays 9/2025 BioEssays 9/2025
IF 2.7 3区 生物学
BioEssays Pub Date : 2025-08-25 DOI: 10.1002/bies.70053
{"title":"BioEssays 9/2025","authors":"","doi":"10.1002/bies.70053","DOIUrl":"https://doi.org/10.1002/bies.70053","url":null,"abstract":"<p>In article 70044 Lana Kostic and Nick Barker review the evolving understanding of stem cell dynamics in the esophagus, with a focus on their roles in tissue homeostasis and cancer development. Challenging earlier models that proposed a uniform basal progenitor layer, recent findings suggest a heterogeneous pool of stem and progenitor cells with distinct phenotypic and functional traits. This cellular diversity may influence individual susceptibility to esophageal cancer, which can arise from random mutations or cancer stem cell activity. The authors highlight how advances in single-cell technologies and organoid models are reshaping perspectives on esophageal biology and offer promising avenues for therapeutic innovation. By re-evaluating stem cell identity and behavior, the article underscores the complexity of epithelial maintenance and the multifactorial nature of cancer initiation in the esophagus.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"47 9","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/bies.70053","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144894277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Issue Information: BioEssays 9/2025 期刊信息:BioEssays 9/2025
IF 2.7 3区 生物学
BioEssays Pub Date : 2025-08-25 DOI: 10.1002/bies.70052
{"title":"Issue Information: BioEssays 9/2025","authors":"","doi":"10.1002/bies.70052","DOIUrl":"https://doi.org/10.1002/bies.70052","url":null,"abstract":"","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"47 9","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/bies.70052","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144894407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Why Reinvent the Wheel? An Idea to Watch Extending Growth Cones to Migrating Neurons 为什么要重新发明轮子?观察生长锥向迁移神经元延伸的想法。
IF 2.7 3区 生物学
BioEssays Pub Date : 2025-08-22 DOI: 10.1002/bies.70059
Naomi Shvedov, Shawn Sorrells
{"title":"Why Reinvent the Wheel? An Idea to Watch Extending Growth Cones to Migrating Neurons","authors":"Naomi Shvedov,&nbsp;Shawn Sorrells","doi":"10.1002/bies.70059","DOIUrl":"10.1002/bies.70059","url":null,"abstract":"","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"47 10","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144943770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信