Biochemical Society transactions最新文献

Histone H3 mutations and their impact on genome stability maintenance. 组蛋白 H3 突变及其对维持基因组稳定性的影响。

IF 3.8 3区生物学

Biochemical Society transactions Pub Date : 2024-09-09 DOI: 10.1042/BST20240177

Lucas D Caeiro, Ramiro E Verdun, Lluis Morey

引用次数: 0

How does CHD4 slide nucleosomes? CHD4 如何滑动核糖体？

IF 3.8 3区生物学

Biochemical Society transactions Pub Date : 2024-09-02 DOI: 10.1042/BST20230070

Xavier J Reid, Yichen Zhong, Joel P Mackay

{"title":"How does CHD4 slide nucleosomes?","authors":"Xavier J Reid, Yichen Zhong, Joel P Mackay","doi":"10.1042/BST20230070","DOIUrl":"https://doi.org/10.1042/BST20230070","url":null,"abstract":"Chromatin remodelling enzymes reposition nucleosomes throughout the genome to regulate the rate of transcription and other processes. These enzymes have been studied intensively since the 1990s, and yet the mechanism by which they operate has only very recently come into focus, following advances in cryoelectron microscopy and single-molecule biophysics. CHD4 is an essential and ubiquitous chromatin remodelling enzyme that until recently has received less attention than remodellers such as Snf2 and CHD1. Here we review what recent work in the field has taught us about how CHD4 reshapes the genome. Cryoelectron microscopy and single-molecule studies demonstrate that CHD4 shares a central remodelling mechanism with most other chromatin remodellers. At the same time, differences between CHD4 and other chromatin remodellers result from the actions of auxiliary domains that regulate remodeller activity by for example: (1) making differential interactions with nucleosomal epitopes such as the acidic patch and the N-terminal tail of histone H4, and (2) inducing the formation of distinct multi-protein remodelling complexes (e.g. NuRD vs ChAHP). Thus, although we have learned much about remodeller activity, there is still clearly much more waiting to be revealed.","PeriodicalId":8841,"journal":{"name":"Biochemical Society transactions","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142103968","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

Human E3 ubiquitin ligases: accelerators and brakes for SARS-CoV-2 infection. 人类 E3 泛素连接酶：SARS-CoV-2 感染的加速器和制动器。

IF 3.8 3区生物学

Biochemical Society transactions Pub Date : 2024-09-02 DOI: 10.1042/BST20230324

Jesse Pellman, Anna Goldstein, Mikołaj Słabicki

引用次数: 0

Progress towards understanding risk factor mechanisms in the development of autism spectrum disorders. 在了解自闭症谱系障碍发病的风险因素机制方面取得进展。

IF 3.8 3区生物学

Biochemical Society transactions Pub Date : 2024-09-02 DOI: 10.1042/BST20231004

Amelia Bryers, Cheryl A Hawkes, Edward Parkin, Neil Dawson

{"title":"Progress towards understanding risk factor mechanisms in the development of autism spectrum disorders.","authors":"Amelia Bryers, Cheryl A Hawkes, Edward Parkin, Neil Dawson","doi":"10.1042/BST20231004","DOIUrl":"https://doi.org/10.1042/BST20231004","url":null,"abstract":"Autism spectrum disorders (ASD) are a heterogenous set of syndromes characterised by social impairment and cognitive symptoms. Currently, there are limited treatment options available to help people with ASD manage their symptoms. Understanding the biological mechanisms that result in ASD diagnosis and symptomatology is an essential step in developing new interventional strategies. Human genetic studies have identified common gene variants of small effect and rare risk genes and copy number variants (CNVs) that substantially increase the risk of developing ASD. Reverse translational studies using rodent models based on these genetic variants provide new insight into the biological basis of ASD. Here we review recent findings from three ASD associated CNV mouse models (16p11.2, 2p16.3 and 22q11.2 deletion) that show behavioural and cognitive phenotypes relevant to ASD. These models have identified disturbed excitation-inhibition neurotransmitter balance, evidenced by dysfunctional glutamate and GABA signalling, as a key aetiological mechanism. These models also provide emerging evidence for serotoninergic neurotransmitter system dysfunction, although more work is needed to clarify the nature of this. At the brain network level, prefrontal cortex (PFC) dysfunctional connectivity is also evident across these models, supporting disturbed PFC function as a key nexus in ASD aetiology. Overall, published data highlight the utility and valuable insight gained into ASD aetiology from preclinical CNV mouse models. These have identified key aetiological mechanisms that represent putative novel therapeutic targets for the treatment of ASD symptoms, making them useful translational models for future drug discovery, development and validation.","PeriodicalId":8841,"journal":{"name":"Biochemical Society transactions","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142103969","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

Suppression of double-stranded RNA sensing in cancer: molecular mechanisms and therapeutic potential. 抑制癌症中的双链 RNA 感知：分子机制和治疗潜力。

IF 3.8 3区生物学

Biochemical Society transactions Pub Date : 2024-09-02 DOI: 10.1042/BST20230727

Addison A Young, Holly E Bohlin, Jackson R Pierce, Kyle A Cottrell

{"title":"Suppression of double-stranded RNA sensing in cancer: molecular mechanisms and therapeutic potential.","authors":"Addison A Young, Holly E Bohlin, Jackson R Pierce, Kyle A Cottrell","doi":"10.1042/BST20230727","DOIUrl":"https://doi.org/10.1042/BST20230727","url":null,"abstract":"Immunotherapy has emerged as a therapeutic option for many cancers. For some tumors, immune checkpoint inhibitors show great efficacy in promoting anti-tumor immunity. However, not all tumors respond to immunotherapies. These tumors often exhibit reduced inflammation and are resistant to checkpoint inhibitors. Therapies that turn these 'cold' tumors 'hot' could improve the efficacy and applicability of checkpoint inhibitors, and in some cases may be sufficient on their own to promote anti-tumor immunity. One strategy to accomplish this goal is to activate innate immunity pathways within the tumor. Here we describe how this can be accomplished by activating double-stranded RNA (dsRNA) sensors. These sensors evolved to detect and respond to dsRNAs arising from viral infection but can also be activated by endogenous dsRNAs. A set of proteins, referred to as suppressors of dsRNA sensing, are responsible for preventing sensing 'self' dsRNA and activating innate immunity pathways. The mechanism of action of these suppressors falls into three categories: (1) Suppressors that affect mature RNAs through editing, degradation, restructuring, or binding. (2) Suppressors that affect RNA processing. (3) Suppressors that affect RNA expression. In this review we highlight suppressors that function through each mechanism, provide examples of the effects of disrupting those suppressors in cancer cell lines and tumors, and discuss the therapeutic potential of targeting these proteins and pathways.","PeriodicalId":8841,"journal":{"name":"Biochemical Society transactions","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142103970","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

Do tunneling nanotubes drive chemoresistance in solid tumors and other malignancies? 隧道纳米管是否会驱动实体瘤和其他恶性肿瘤的化疗抗药性？

IF 3.8 3区生物学

Biochemical Society transactions Pub Date : 2024-08-28 DOI: 10.1042/BST20231364

Akshat Sarkari, Emil Lou

{"title":"Do tunneling nanotubes drive chemoresistance in solid tumors and other malignancies?","authors":"Akshat Sarkari, Emil Lou","doi":"10.1042/BST20231364","DOIUrl":"10.1042/BST20231364","url":null,"abstract":"Intercellular communication within the tumor microenvironment (TME) is essential for establishing, mediating, and synchronizing cancer cell invasion and metastasis. Cancer cells, individually and collectively, react at the cellular and molecular levels to insults from standard-of-care treatments used to treat patients with cancer. One form of cell communication that serves as a prime example of cellular phenotypic stress response is a type of cellular protrusion called tunneling nanotubes (TNTs). TNTs are ultrafine, actin-enriched contact-dependent forms of membrane protrusions that facilitate long distance cell communication through transfer of various cargo, including genetic materials, mitochondria, proteins, ions, and various other molecules. In the past 5-10 years, there has been a growing body of evidence that implicates TNTs as a novel mechanism of cell-cell communication in cancer that facilitates and propagates factors that drive or enhance chemotherapeutic resistance in a variety of cancer cell types. Notably, recent literature has highlighted the potential of TNTs to serve as cellular conduits and mediators of drug and nanoparticle delivery. Given that TNTs have also been shown to form in vivo in a variety of tumor types, disrupting TNT communication within the TME provides a novel strategy for enhancing the cytotoxic effect of existing chemotherapies while suppressing this form of cellular stress response. In this review, we examine current understanding of interplay between cancer cells occurring via TNTs, and even further, the implications of TNT-mediated tumor-stromal cross-talk and the potential to enhance chemoresistance. We then examine tumor microtubes, an analogous cell protrusion heavily implicated in mediating treatment resistance in glioblastoma multiforme, and end with a brief discussion of the effects of radiation and other emerging treatment modalities on TNT formation.","PeriodicalId":8841,"journal":{"name":"Biochemical Society transactions","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141733482","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

Satellite cell dynamics during skeletal muscle hypertrophy. 骨骼肌肥大过程中卫星细胞的动态变化

IF 3.8 3区生物学

Biochemical Society transactions Pub Date : 2024-08-28 DOI: 10.1042/BST20240201

Tolulope P Saliu, Jensen Goh, Gyumin Kang, Benjamin I Burke, Ahmed Ismaeel, John J McCarthy

引用次数: 0

Cytokinin and reproductive shoot architecture: bigger and better? 细胞分裂素和生殖芽结构：越大越好？

IF 3.8 3区生物学

Biochemical Society transactions Pub Date : 2024-08-28 DOI: 10.1042/BST20231565

Catriona H Walker, Tom Bennett

引用次数: 0

TDP-43 in nuclear condensates: where, how, and why. 核凝聚物中的 TDP-43：在哪里、如何以及为什么。

IF 3.8 3区生物学

Biochemical Society transactions Pub Date : 2024-08-28 DOI: 10.1042/BST20231447

Ruaridh Lang, Rachel E Hodgson, Tatyana A Shelkovnikova

引用次数: 0

Molecular aspects of Interleukin-36 cytokine activation and regulation. 白细胞介素-36 细胞因子激活和调节的分子方面。

IF 3.8 3区生物学

Biochemical Society transactions Pub Date : 2024-08-28 DOI: 10.1042/BST20230548

Jennifer Keller, James R O' Siorain, Thomas M Kündig, Mark Mellett

{"title":"Molecular aspects of Interleukin-36 cytokine activation and regulation.","authors":"Jennifer Keller, James R O' Siorain, Thomas M Kündig, Mark Mellett","doi":"10.1042/BST20230548","DOIUrl":"10.1042/BST20230548","url":null,"abstract":"Interleukin-36 (IL-36) cytokines are structurally similar to other Interleukin-1 superfamily members and are essential to convey inflammatory responses at epithelial barriers including the skin, lung, and gut. Due to their potent effects on immune cells, IL-36 cytokine activation is regulated on multiple levels, from expression and activation to receptor binding. Different IL-36 isoforms convey specific responses as a consequence of particular danger- or pathogen-associated molecular patterns. IL-36 expression and activation are regulated by exogenous pathogens, including fungi, viruses and bacteria but also by endogenous factors such as antimicrobial peptides or cytokines. Processing of IL-36 into potent bioactive forms is necessary for host protection but can elevate tissue damage. Indeed, exacerbated IL-36 signalling and hyperactivation are linked to the pathogenesis of diseases such as plaque and pustular psoriasis, emphasising the importance of understanding the molecular aspects regulating IL-36 activation. Here, we summarise facets of the electrochemical properties, regulation of extracellular cleavage by various proteases and receptor signalling of the pro-inflammatory and anti-inflammatory IL-36 family members. Additionally, this intriguing cytokine subfamily displays many characteristics that are unique from prototypical members of the IL-1 family and these key distinctions are outlined here.","PeriodicalId":8841,"journal":{"name":"Biochemical Society transactions","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141465973","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