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Chromosome hitchhiking: a potential strategy adopted by the selfish yeast plasmids to ensure symmetric inheritance during cell division. 染色体搭便车:自私酵母质粒在细胞分裂过程中确保对称遗传的一种潜在策略。
IF 3.8 3区 生物学
Biochemical Society transactions Pub Date : 2024-12-19 DOI: 10.1042/BST20231555
Deepanshu Kumar, Santanu Kumar Ghosh
{"title":"Chromosome hitchhiking: a potential strategy adopted by the selfish yeast plasmids to ensure symmetric inheritance during cell division.","authors":"Deepanshu Kumar, Santanu Kumar Ghosh","doi":"10.1042/BST20231555","DOIUrl":"10.1042/BST20231555","url":null,"abstract":"<p><p>The 2-micron plasmid residing within the host budding yeast Saccharomyces cerevisiae nucleus serves as a model system for understanding the mechanism of segregation and stable maintenance of circular endogenously present extrachromosomal DNA in eukaryotic cells. The plasmid is maintained at a high average copy number (40-60 copies per yeast cell) through generations despite there is no apparent benefit to the host. Notably, the segregation mechanism of 2-micron plasmid shares significant similarities with those of bacterial low-copy-number plasmids and episomal forms of viral genomes in mammalian cells. These similarities include formation of a complex where the plasmid- or viral encoded proteins bind to a plasmid- or viral genome-borne locus, respectively and interaction of the complex with the host proteins. These together form a partitioning system that ensures stable symmetric inheritance of both these genomes from mother to daughter cells. Recent studies with substantial evidence showed that the 2-micron plasmid, like episomes of viruses such as Epstein-Barr virus, relies on tethering itself to the host chromosomes in a non-random fashion for equal segregation. This review delves into the probable chromosome hitchhiking mechanisms of 2-micron plasmid during its segregation, highlighting the roles of specific plasmid-encoded proteins and their interactions with host proteins and the chromosomes. Understanding these mechanisms provides broader insights into the genetic stability and inheritance of extrachromosomal genetic elements across diverse biological systems.</p>","PeriodicalId":8841,"journal":{"name":"Biochemical Society transactions","volume":" ","pages":"2359-2372"},"PeriodicalIF":3.8,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817015","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
The integrin adhesome and control of anti-tumour immunity. 整合素黏附体与抗肿瘤免疫的调控。
IF 3.8 3区 生物学
Biochemical Society transactions Pub Date : 2024-12-19 DOI: 10.1042/BST20240386
Emily R Webb, Annabel Black, Nicole D Barth, Stefan N Symeonides, Valerie G Brunton
{"title":"The integrin adhesome and control of anti-tumour immunity.","authors":"Emily R Webb, Annabel Black, Nicole D Barth, Stefan N Symeonides, Valerie G Brunton","doi":"10.1042/BST20240386","DOIUrl":"10.1042/BST20240386","url":null,"abstract":"<p><p>It is widely regarded that the anti-tumour immune response drives clearance of tumours and leads to prolonged survival in patients. However, tumours are adept at reprogramming the surrounding microenvironment to an immunosuppressive milieu to prevent successful immune directed killing. Adhesion of cells to the extracellular matrix is essential for regulating cellular processes such as survival, proliferation and migration. This adhesion is largely conducted via integrins and their related intracellular signalling networks. Adhesion proteins such as focal adhesion kinase (FAK) are expressed in both tumour cells and cells of the surrounding microenvironment, and are often dysregulated in cancers. Recent work has demonstrated that adhesion proteins are contributing to regulation of the immunosuppressive microenvironment within tumours, and could provide a new avenue to target in combination with immunotherapies. Here, we provide an overview of the effort being made to elucidate the roles adhesion proteins play in modulating anti-tumour responses within a variety of cancer settings. In particular we focus on the multifaceted role of FAK within the tumour immune microenvironment. Finally, we summarise the data in clinical trials, where targeting FAK is being exploited to prime the tumour microenvironment and create potent responses when combined with immunotherapies.</p>","PeriodicalId":8841,"journal":{"name":"Biochemical Society transactions","volume":" ","pages":"2455-2468"},"PeriodicalIF":3.8,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11777417/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142783966","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
The AICD interactome: implications in neurodevelopment and neurodegeneration. AICD相互作用组:在神经发育和神经退行性变中的意义。
IF 3.8 3区 生物学
Biochemical Society transactions Pub Date : 2024-12-19 DOI: 10.1042/BST20241510
Laura Lok-Haang Ng, Jessica Chow, Kwok-Fai Lau
{"title":"The AICD interactome: implications in neurodevelopment and neurodegeneration.","authors":"Laura Lok-Haang Ng, Jessica Chow, Kwok-Fai Lau","doi":"10.1042/BST20241510","DOIUrl":"10.1042/BST20241510","url":null,"abstract":"<p><p>The pathophysiological mechanism involving the proteolytic processing of amyloid precursor protein (APP) and the generation of amyloid plaques is of significant interest in research on Alzheimer's disease (AD). The increasing significance of the downstream AD-related pathophysiological mechanisms has sparked research interest in other products of the APP processing cascades, including the APP intracellular domain (AICD). The potential importance of AICD in various cellular processes in the central nervous system has been established through the identification of its interactors. The interaction between AICD and its physiological binding partners is implicated in cellular events including regulation of transcriptional activity, cytoskeletal dynamics, neuronal growth, APP processing and cellular apoptosis. On the contrary, AICD is also implicated in neurodegeneration, which is a potential outcome of the functional fluctuation of AICD-mediated neuronal processes within the neuronal network. In this review, we summarize the neuronal functions and pathological manifestations of the dynamic AICD interaction network.</p>","PeriodicalId":8841,"journal":{"name":"Biochemical Society transactions","volume":" ","pages":"2539-2556"},"PeriodicalIF":3.8,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11668293/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817018","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
Molecular regulators of chemotaxis in human hematopoietic stem cells. 人类造血干细胞趋化的分子调控因子
IF 3.8 3区 生物学
Biochemical Society transactions Pub Date : 2024-12-19 DOI: 10.1042/BST20240288
Yining Liu, Nanxi Geng, Xinxin Huang
{"title":"Molecular regulators of chemotaxis in human hematopoietic stem cells.","authors":"Yining Liu, Nanxi Geng, Xinxin Huang","doi":"10.1042/BST20240288","DOIUrl":"10.1042/BST20240288","url":null,"abstract":"<p><p>Hematopoietic stem cells (HSCs), essential for lifelong blood cell regeneration, are clinically utilized to treat various hematological disorders. These cells originate in the aorta-gonad-mesonephros region, expand in the fetal liver, and mature in the bone marrow. Chemotaxis, involving gradient sensing, polarization, and migration, directs HSCs and is crucial for their homing and mobilization. The molecular regulation of HSC chemotaxis involves chemokines, chemokine receptors, signaling pathways, and cytoskeletal proteins. Recent advances in understanding these regulatory mechanisms have deepened insights into HSC development and hematopoiesis, offering new avenues for therapeutic innovations. Strategies including glucocorticoid receptor activation, modulation of histone acetylation, stimulation of nitric oxide signaling, and interference with m6A RNA modification have shown potential in enhancing CXCR4 expression, thereby improving the chemotactic response and homing capabilities of human HSCs. This review synthesizes current knowledge on the molecular regulation of human HSC chemotaxis and its implications for health and disease.</p>","PeriodicalId":8841,"journal":{"name":"Biochemical Society transactions","volume":" ","pages":"2427-2437"},"PeriodicalIF":3.8,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142709206","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
Cellular mechanisms underlying pituitary adenylate cyclase activating polypeptide-stimulated secretion in the adrenal medulla. 垂体腺苷酸环化酶激活肾上腺髓质多肽刺激分泌的细胞机制。
IF 3.8 3区 生物学
Biochemical Society transactions Pub Date : 2024-12-19 DOI: 10.1042/BST20231326
Nicole A Bell, Xiaohuan Chen, David R Giovannucci, Arun Anantharam
{"title":"Cellular mechanisms underlying pituitary adenylate cyclase activating polypeptide-stimulated secretion in the adrenal medulla.","authors":"Nicole A Bell, Xiaohuan Chen, David R Giovannucci, Arun Anantharam","doi":"10.1042/BST20231326","DOIUrl":"10.1042/BST20231326","url":null,"abstract":"<p><p>The adrenal medulla is a key effector of the sympathetic nervous system in the periphery. Its primary function is to translate variations in sympathetic activity into hormone outputs that modify end organ function throughout the body. These hormones include epinephrine, norepinephrine, and a variety of vasoactive peptides. Hormone secretion occurs when neurotransmitters, delivered by sympathetic nerves, bind to, and activate receptors on adrenomedullary chromaffin cells. In this context, two neurotransmitters of particular importance are acetylcholine (ACh) and pituitary adenylate cyclase activating polypeptide (PACAP). PACAP, discovered initially as a secretagogue in the hypothalamus, is now appreciated to provoke a strong secretory response from chromaffin cells in vitro and in situ. However, the cellular mechanisms underlying PACAP-stimulated secretion are still poorly understood. In the sections below, we will summarize what is known about the actions of PACAP in the adrenal medulla, discuss recent advances that pertain to the PACAP signaling pathway, and highlight areas for future investigation.</p>","PeriodicalId":8841,"journal":{"name":"Biochemical Society transactions","volume":" ","pages":"2373-2383"},"PeriodicalIF":3.8,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11668280/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799401","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
Age-dependent regenerative mechanisms in the brain. 大脑中与年龄有关的再生机制。
IF 3.8 3区 生物学
Biochemical Society transactions Pub Date : 2024-12-19 DOI: 10.1042/BST20230547
Giada Vanacore, Jens Bager Christensen, N Sumru Bayin
{"title":"Age-dependent regenerative mechanisms in the brain.","authors":"Giada Vanacore, Jens Bager Christensen, N Sumru Bayin","doi":"10.1042/BST20230547","DOIUrl":"10.1042/BST20230547","url":null,"abstract":"<p><p>Repairing the adult mammalian brain represents one of the greatest clinical challenges in medicine. Injury to the adult brain often results in substantial loss of neural tissue and permanent functional impairment. In contrast with the adult, during development, the mammalian brain exhibits a remarkable capacity to replace lost cells. A plethora of cell-intrinsic and extrinsic factors regulate the age-dependent loss of regenerative potential in the brain. As the developmental window closes, neural stem cells undergo epigenetic changes, limiting their proliferation and differentiation capacities, whereas, changes in the brain microenvironment pose additional challenges opposing regeneration, including inflammation and gliosis. Therefore, studying the regenerative mechanisms during development and identifying what impairs them with age may provide key insights into how to stimulate regeneration in the brain. Here, we will discuss how the mammalian brain engages regenerative mechanisms upon injury or neuron loss. Moreover, we will describe the age-dependent changes that affect these processes. We will conclude by discussing potential therapeutic approaches to overcome the age-dependent regenerative decline and stimulate regeneration.</p>","PeriodicalId":8841,"journal":{"name":"Biochemical Society transactions","volume":" ","pages":"2243-2252"},"PeriodicalIF":3.8,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11668278/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142709187","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
The role of protein O-GlcNAcylation in diabetic cardiomyopathy. 蛋白质 O-GlcNAcylation 在糖尿病心肌病中的作用。
IF 3.8 3区 生物学
Biochemical Society transactions Pub Date : 2024-12-19 DOI: 10.1042/BST20240262
John C Chatham, Adam R Wende
{"title":"The role of protein O-GlcNAcylation in diabetic cardiomyopathy.","authors":"John C Chatham, Adam R Wende","doi":"10.1042/BST20240262","DOIUrl":"10.1042/BST20240262","url":null,"abstract":"<p><p>It is well established that diabetes markedly increases the risk of multiple types of heart disease including heart failure. However, despite substantial improvements in the treatment of heart failure in recent decades the relative increased risk associated with diabetes remains unchanged. There is increasing appreciation of the importance of the post translational modification by O-linked-N-acetylglucosamine (O-GlcNAc) of serine and threonine residues on proteins in regulating cardiomyocyte function and mediating stress responses. In response to diabetes there is a sustained increase in cardiac O-GlcNAc levels, which has been attributed to many of the adverse effects of diabetes on the heart. Here we provide an overview of potential mechanisms by which increased cardiac O-GlcNAcylation contributes to the adverse effects on the heart and highlight some of the key gaps in our knowledge.</p>","PeriodicalId":8841,"journal":{"name":"Biochemical Society transactions","volume":" ","pages":"2343-2358"},"PeriodicalIF":3.8,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142724382","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
Tools and techniques for quantitative glycoproteomic analysis. 定量糖蛋白组学分析的工具和技术。
IF 3.8 3区 生物学
Biochemical Society transactions Pub Date : 2024-12-19 DOI: 10.1042/BST20240257
Siyuan Kong, Wei Zhang, Weiqian Cao
{"title":"Tools and techniques for quantitative glycoproteomic analysis.","authors":"Siyuan Kong, Wei Zhang, Weiqian Cao","doi":"10.1042/BST20240257","DOIUrl":"10.1042/BST20240257","url":null,"abstract":"<p><p>Recent advances in mass spectrometry (MS)-based methods have significantly expanded the capabilities for quantitative glycoproteomics, enabling highly sensitive and accurate quantitation of glycosylation at intact glycopeptide level. These developments have provided valuable insights into the roles of glycoproteins in various biological processes and diseases. In this short review, we summarize pertinent studies on quantitative techniques and tools for site-specific glycoproteomic analysis published over the past decade. We also highlight state-of-the-art MS-based software that facilitate multi-dimension quantification of the glycoproteome, targeted quantification of specific glycopeptides, and the analysis of glycopeptide isomers. Additionally, we discuss the potential applications of these technologies in clinical biomarker discovery and the functional characterization of glycoproteins in health and disease. The review concludes with a discussion of current challenges and future perspectives in the field, emphasizing the need for more precise, high-throughput and efficient methods to further advance quantitative glycoproteomics and its applications.</p>","PeriodicalId":8841,"journal":{"name":"Biochemical Society transactions","volume":" ","pages":"2439-2453"},"PeriodicalIF":3.8,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799466","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
Advances in the molecular understanding of GPCR-arrestin complexes. 对 GPCR-arrestin复合物的分子认识取得进展。
IF 3.8 3区 生物学
Biochemical Society transactions Pub Date : 2024-12-19 DOI: 10.1042/BST20240170
Ivana Petrovic, Stephan Grzesiek, Polina Isaikina
{"title":"Advances in the molecular understanding of GPCR-arrestin complexes.","authors":"Ivana Petrovic, Stephan Grzesiek, Polina Isaikina","doi":"10.1042/BST20240170","DOIUrl":"10.1042/BST20240170","url":null,"abstract":"<p><p>Arrestins are essential proteins for the regulation of G protein-coupled receptors (GPCRs). They mediate GPCR desensitization after the activated receptor has been phosphorylated by G protein receptor kinases (GRKs). In addition, GPCR-arrestin interactions may trigger signaling pathways that are distinct and independent from G proteins. The non-visual GPCRs encompass hundreds of receptors with varying phosphorylation patterns and amino acid sequences, which are regulated by only two human non-visual arrestin isoforms. This review describes recent findings on GPCR-arrestin complexes, obtained by structural techniques, biophysical, biochemical, and cellular assays. The solved structures of complete GPCR-arrestin complexes are of limited resolution ranging from 3.2 to 4.7 Å and reveal a high variability in the relative receptor-arrestin orientation. In contrast, biophysical and functional data indicate that arrestin recruitment, activation and GPCR-arrestin complex stability depend on the receptor phosphosite sequence patterns and density. At present, there is still a manifest lack of high-resolution structural and dynamical information on the interactions of native GPCRs with both GRKs and arrestins, which could provide a detailed molecular understanding of the genesis of receptor phosphorylation patterns and the specificity GPCR-arrestin interactions. Such insights seem crucial for progress in the rational design of advanced, arrestin-specific therapeutics.</p>","PeriodicalId":8841,"journal":{"name":"Biochemical Society transactions","volume":" ","pages":"2333-2342"},"PeriodicalIF":3.8,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142602729","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
Linking glycosphingolipid metabolism to disease-related changes in the plasma membrane proteome. 鞘糖脂代谢与质膜蛋白质组疾病相关变化的联系
IF 3.8 3区 生物学
Biochemical Society transactions Pub Date : 2024-12-19 DOI: 10.1042/BST20240315
Holly Monkhouse, Janet E Deane
{"title":"Linking glycosphingolipid metabolism to disease-related changes in the plasma membrane proteome.","authors":"Holly Monkhouse, Janet E Deane","doi":"10.1042/BST20240315","DOIUrl":"10.1042/BST20240315","url":null,"abstract":"<p><p>Glycosphingolipids (GSLs) are vital components of the plasma membrane (PM), where they play crucial roles in cell function. GSLs form specialised membrane microdomains that organise lipids and proteins into functional platforms for cell adhesion and signalling. GSLs can also influence the function of membrane proteins and receptors, via direct protein-lipid interactions thereby affecting cell differentiation, proliferation, and apoptosis. Research into GSL-related diseases has primarily focussed on lysosomal storage disorders, where defective enzymes lead to the accumulation of GSLs within lysosomes, causing cellular dysfunction and disease. However, recent studies are uncovering the broader cellular impact of GSL imbalances including on a range of organelles and cellular compartments such as the mitochondria, endoplasmic reticulum and PM. In this review we describe the mechanisms by which GSL imbalances can influence the PM protein composition and explore examples of the changes that have been observed in the PM proteome upon GSL metabolic disruption. Identifying and understanding these changes to the PM protein composition will enable a more complete understanding of lysosomal storage diseases and provide new insights into the pathogenesis of other GSL-related diseases, including cancer and neurodegenerative disorders.</p>","PeriodicalId":8841,"journal":{"name":"Biochemical Society transactions","volume":" ","pages":"2477-2486"},"PeriodicalIF":3.8,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11668283/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142783962","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
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