BIOCHEMICAL SOCIETY TRANSACTIONS生物化学学会会刊

BIOCHEMICAL SOCIETY TRANSACTIONS(英文缩写 BIOCHEM SOC T),ISSN 0300-5127,eISSN 1470-8752,中文译名:生物化学学会会刊 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。

2026 年数据 · 影响因子
4.400
JCR 分区
Q2
CAS 分区
B2
近一年发文量
129
本站 PubMed 收录统计

发文量统计区间:2025-09-27 至 2026-09-27,按本站收录文献的发表日期统计。

ISSN: 0300-5127 · eISSN: 1470-8752 · 缩写: BIOCHEM SOC T ·中文: 生物化学学会会刊

期刊介绍

选择期刊介绍栏目

期刊简介

《Biochemical Society Transactions》是英国生物化学学会旗下的综述与评论型期刊,聚焦生物化学、分子生物学及细胞生物学的前沿进展。它主要发表由领域专家撰写的短篇综述、观点文章和会议报告,帮助读者快速把握快速演进的学科方向。读者群包括从事基础与转化研究的科研人员、研究生及教学人员,尤其适合需要跨子学科视野的读者。

研究方向

期刊覆盖生物化学与分子生物学的广泛主题,包括蛋白质结构与功能、酶学、代谢调控、信号转导、基因表达、膜生物学及疾病分子机制等。论文类型以邀请或投稿的短篇综述、观点与评论为主,也收录学术会议专题总结,强调对近期重要进展的整合与评述,而非原始实验数据。

期刊特色

该刊以短小精悍的综述见长,文章通常由活跃在一线的学者撰写,注重概念梳理与争议点评,而非穷尽文献。其内容适合希望快速了解某一子领域现状与趋势的读者,也适合作为研究生教学和课题选题的参考。对作者而言,写作需突出综合性与批判性,避免简单罗列文献。

投稿难度

投稿难度中等偏上,但并非仅由分区决定。期刊重视选题的前沿性、综述的整合深度和作者在该领域的信誉。建议在受邀或与编辑沟通后投稿,写作时明确核心问题、平衡不同观点,并控制篇幅与引用密度。若为自由投稿,需先确认主题是否在近期收录范围内。

历年影响因子趋势

JCR 数据年份影响因子JCR 分区
20214.919Q2
20223.900Q2
20233.800Q2
20244.300Q2
20254.400Q2

BIOCHEMICAL SOCIETY TRANSACTIONS 最新收录文献

  1. JCR分区: Q2 CAS分区: B2 影响因子: 4.4

    1. Nuclear envelope rupture and resealing: mechanisms, consequences, and disease implications.

    作者:
    Atsuki En, Kohta Ikegami
    日期:
    2026-10-28

    The nuclear envelope (NE) establishes an essential physical separation between the nucleoplasm and cytoplasm in eukaryotic cells. Its structural integrity ensures selective molecular exchange through nuclear pores, a fundamental feature of eukaryotic cells. For this reason, it has long been assumed that the NE remains intact. However, recent studies revealed localized rupture of the NE in diverse physiological and pathological contexts. These ruptures can be resealed by endogenous mechanisms, suggesting that rupture-resealing dynamics contribute to homeostasis and are altered in disease. In the present review, we summarize physiological and pathological contexts in which NE rupture has been observed. We evaluate major hypotheses regarding its causes and consequences and discuss current understanding of the mechanisms and regulation of NE resealing. We conclude by highlighting key knowledge gaps in the pathophysiological roles of NE rupture and resealing.

  2. JCR分区: Q2 CAS分区: B2 影响因子: 4.4

    2. Unmasking programmed cell death in rhinovirus-driven asthma pathology.

    作者:
    Wayne Cawthorne, Youming Zhang, Nicole Val, Michelle Nelson, Anna Raevski, Kazuhiro Ito, Reena Ghildyal
    日期:
    2026-10-28

    Rhinovirus (RV) infection is responsible for the majority of cases of viral exacerbations of asthma. Understanding the cellular and molecular mechanisms that cause asthma exacerbations is an absolute requirement for the development of effective treatments. Emerging literature suggests that cell death may have an important role in RV-induced exacerbations. Several types of programmed cell death (PCD) have been implicated in asthma, including apoptosis, necroptosis, pyroptosis, and ferroptosis. Increased presence of apoptotic airway epithelial cells in the sputum of adult and paediatric asthma patients is suggestive of defects in apoptosis. Elevated levels of phosphorylated mixed lineage kinase domain-like protein and receptor-interacting serine/threonine-protein kinase 3, markers of active necroptosis, have been found in the serum of asthmatic patients. Gasdermin B, a member of the gasdermin family of pyroptosis executioner proteins, has a strong genetic linkage to severe asthma. Expression level of GSDMB correlated with asthma exacerbations and antiviral pathways. Lipid peroxidation and increased airway iron levels, both suggestive of ferroptosis, have been observed in asthma patients. RV infection of epithelial cells triggers an inflammatory response, which can provide the necessary pro-inflammatory chemokines and cytokines to initiate PCD, such as tumour necrosis factor-α. RV exploits PCD such as apoptosis, necroptosis, pyroptosis, and ferroptosis to aid its replication and release, while modulating them probably to limit immune response. In the present review, we investigate the concept that pro-inflammatory PCD pathways modulated by RV infection in the context of asthma lead to prolonged inflammatory and immune responses that are key to asthma exacerbations.

  3. JCR分区: Q2 CAS分区: B2 影响因子: 4.4

    3. Exploring the antifungal activity of the wheat microbiome.

    作者:
    Louise F Thatcher, Simon R Law, Lachlan Dow, Lygie Esquirol
    日期:
    2026-10-28

    Wheat (Triticum aestivum) is a cornerstone of global food security, yet its productivity is threatened by fungal pathogens such as Fusarium graminearum, Zymoseptoria tritici, and Rhizoctonia solani. These pathogens not only reduce yield but can also compromise grain quality and food safety through the production of mycotoxins. Traditional control strategies, primarily reliant on chemical fungicides and resistant cultivars, face limitations due to evolving pathogen resistance, environmental concerns, and regulatory restrictions. In recent years, the plant microbiome has emerged as a promising frontier in sustainable crop protection. The wheat microbiome, encompassing microbial communities in the rhizosphere, endosphere (root and leaf), and phyllosphere, plays a pivotal role in plant health and resilience. These microbes can suppress fungal pathogens through diverse mechanisms, both directly and indirectly. This mini-review explores the antifungal potential of the wheat microbiome, highlighting key microbial taxa, mechanisms of action with a focus on the underlying biochemistry and molecular processes, and recent advances in omics and microbiome-based biocontrol strategies. This extends to a case study on our own endophyte biocontrol and biochemistry discovery pipeline. We detail the impacts of fungal pathogen exposure and farming practices on wheat microbiome composition and phytopathogen-suppressive traits and highlight pathways for harnessing microbial communities to enhance wheat resistance.

  4. JCR分区: Q2 CAS分区: B2 影响因子: 4.4

    4. The role of IRF5 as an immune regulator.

    作者:
    Laura Menocal, Amanda Y Y Huang, Anjali Rachelkar, Betsy J Barnes
    日期:
    2026-10-28

    Interferon regulatory factor 5 (IRF5) is a transcription factor at the nexus of immune regulation, inflammation, and autoimmune disease. Studies have shown that dysregulation of IRF5 is strongly implicated in the pathogenesis of autoimmune diseases including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and inflammatory bowel disease. While originally described as a regulator downstream of Toll-like receptor (TLR)-MyD88 signaling in myeloid cells, further studies demonstrate a more complex role for IRF5 in mediating adaptive immune responses as well. In this review, we provide a summary of the role of IRF5 across the major immune cell populations in which it is expressed. We discuss the mechanistic basis of IRF5 function in each population, highlight shared themes, and examine the evidence supporting IRF5 as a promising therapeutic target whose inhibition may selectively dampen pathological inflammation while preserving protective immunity. We thus provide an overview of how IRF5 bridges both innate and adaptive immune responses.

  5. JCR分区: Q2 CAS分区: B2 影响因子: 4.4

    5. Overview of pathways and dynamic interactions of c-type cytochromes in Geobacter sulfurreducens.

    作者:
    Alexandre Almeida, Marta A Silva, Jorge M A Antunes, Mafalda V Fernandes, Leonor Morgado, Carlos A Salgueiro
    日期:
    2026-09-23

    Extracellular electron transfer (EET) is a central process in the respiratory metabolism of electrogenic bacteria, enabling cells to exchange electrons with extracellular acceptors and donors. This capability has opened opportunities to exploit these bacteria in diverse practical applications, many of which would benefit from a precise understanding of the electron transfer (ET) events occurring within their respiratory chains. These chains rely on highly populated networks of c-type cytochromes that mediate electron flow across cellular compartments toward terminal electron acceptors. Although genomic, proteomic, biochemical, and structural studies have identified many ET components, defining their physiological redox partners and the directionality of electron flow remains challenging. This difficulty arises from the similar spectroscopic properties of key cytochromes, their transient interactions, and the complex overlap of their redox potential windows. In the present review, we examine how recently developed NMR-based strategies have been used to identify redox complexes established between cytochromes located in the inner membrane, periplasm, outer membrane, and extracellular conductive structures in the bacterium Geobacter sulfurreducens. These strategies exploited the distinct redox-dependent NMR fingerprints of individual heme groups, allowing direct detection of electron exchange, redox equilibria, and transient protein-protein interactions. Collectively, these studies reveal that ET pathways are not organized as single linear chains, but rather as dynamic and highly interconnected redox networks characterized by weak transient redox complexes and extensive promiscuity. This organization provides bacterial electron-buffering capacity, functional flexibility, and adaptability to changing environmental redox conditions.

  6. JCR分区: Q2 CAS分区: B2 影响因子: 4.4

    6. Building peroxisomes: perspectives on plant peroxins.

    作者:
    Gabrielle C Buck, Bonnie Bartel
    日期:
    2026-09-23

    Peroxisomes are dynamic organelles with diverse metabolic functions that are essential for life in plants and mammals. In humans, peroxisomal defects underlie peroxisome biogenesis disorders, which are often fatal. In plants, peroxisomes contribute to photorespiration and phytohormone production during plant development and are the sole site of fatty acid β-oxidation, which is critical for fat mobilization during germination. Despite their functional diversity, much of the machinery involved in building and maintaining peroxisomes is conserved across most eukaryotes. The model plant Arabidopsis thaliana is ideal for peroxisome studies due to its large peroxisomes, whole-organism and molecular assays for peroxisome function, and facile genetics. New applications of microscopy, computational modeling, and biochemistry have advanced the understanding of peroxisome biogenesis across eukaryotic life. These advances have generated insights into the functions of the proteins involved in peroxisome biogenesis, known as peroxins. Here, we review knowledge of Arabidopsis thaliana peroxins and discuss how new perspectives on peroxin functions across kingdoms inform future research on plant peroxisomes.

  7. JCR分区: Q2 CAS分区: B2 影响因子: 4.4

    7. The diverse gating mechanisms of bacterial MscS-like ion channels.

    作者:
    Giorgos Hiotis, Yoshitaka Nakayama, Swati Yadav, Thomas Walz
    日期:
    2026-09-23

    Bacterial mechanosensitive (MS) channels protect cells against hypoosmotic shock by opening, in response to increased membrane tension, a transmembrane pore that allows rapid efflux of osmolytes. The MS channel of small conductance (MscS) in Escherichia coli has been extensively characterized both functionally and structurally, establishing its channel properties and revealing its architecture and the conformational changes that underlie channel gating. In particular, several lipids associated with MscS have been proposed to play a role in its mechanosensitivity. MscS is the founding member of the superfamily of MscS-like channels that share a structurally conserved core with MscS but feature additional structural elements that result in distinct functional properties. In addition to MscS, E. coli expresses five MscS-like channels. In the present review, we summarize recent advances in the structural characterization of E. coli MscS-like channels that revealed diverse gating mechanisms. Unlike the mechanosensation of MscS that appears to depend on its associated lipids, the mechanosensation of MscS-like channels seems to be the result of the deformation they cause on their surrounding membrane. Despite the diversity in observed gating mechanisms, we highlight unifying principles that dictate the properties of MscS-like channels and MS channels in general.

  8. JCR分区: Q2 CAS分区: B2 影响因子: 4.4

    8. NINJ1: implications for plasma membrane rupture and disease.

    作者:
    Elliott M Bernard, Ella Hartenian
    日期:
    2026-09-23

    Cell death pathways are ancient strategies that maintain homeostasis and protect organisms from infection and injury. Lytic cell death culminates in the rupture of the plasma membrane, which was recently revealed to be driven by Ninjurin-1 (NINJ1), a plasma membrane protein that oligomerizes during cell death. NINJ1 oligomerization creates lesions in the plasma membrane that facilitate the release of cytosolic contents. In the present review, we discuss what is currently known about NINJ1 biology, focusing on the most current research into potential mechanisms of activation. We then highlight how NINJ1 has been implicated in specific disease contexts and discuss potential ways NINJ1 may contribute to disease. We conclude with the remaining open questions relating to NINJ1 biology.

  9. JCR分区: Q2 CAS分区: B2 影响因子: 4.4

    9. Nitric oxide as a mechanistic link between metabolic dysfunction and cognitive decline in type 2 diabetes.

    作者:
    Ana L Marçal, João Laranjinha, Cátia F Lourenço
    日期:
    2026-09-23

    Type 2 diabetes mellitus (T2DM) is increasingly recognised as a driver of cerebrovascular dysfunction and cognitive decline, yet the molecular mechanisms underlying this association remain incompletely understood. Here, we review and support a key mechanistic role for nitric oxide (•NO), a pleiotropic diffusible messenger that integrates vascular, neuronal, and metabolic functions within the neurovascular unit (NVU). Under physiological conditions, •NO integrates vascular and metabolic responses by coupling blood supply to neuronal activity and fine-tuning cellular energy metabolism. In T2DM, chronic hyperglycemia and insulin resistance converge to reduce •NO bioavailability through multiple mechanisms: mitochondrial and NADPH oxidase-derived superoxide production, endothelial nitric oxide synthases (eNOS) uncoupling via BH4 oxidation, and impaired PI3K-Akt-dependent eNOS activation. The resulting redox imbalance shifts the cerebrovascular environment towards oxidant-mediated damage, compromising the functional and structural integrity of the NVU. This translates into impaired cerebral blood flow regulation and maladaptive remodelling of the cerebrovascular network, ultimately disrupting neurovascular coupling (NVC) and reducing regional cerebral perfusion. Together, impaired perfusion and disrupted NVC result in a sustained mismatch between energy supply and neuronal demand, particularly in metabolically vulnerable regions such as the hippocampus, ultimately leading to progressive cognitive impairment. In sum, the present review integrates current mechanistic evidence positioning •NO dysregulation as a central driver of neurovascular and metabolic dysfunction in T2DM, linking impaired cerebral perfusion, disrupted NVC, and structural vascular remodelling to cognitive decline.

  10. JCR分区: Q2 CAS分区: B2 影响因子: 4.4

    10. Ubiquitin E3 ligase activity in TRIpartite Motif (TRIM) family proteins.

    作者:
    Jane Dudley-Fraser, Katrin Rittinger
    日期:
    2026-09-23

    TRIpartite Motif (TRIM) family proteins are required for healthy development and homeostasis, while their dysregulation is observed in a wide range of diseases. Although diverse cellular roles are emerging for TRIMs, the majority function as ubiquitin E3 ligases by means of their RING (really interesting new gene) domain. Here, we delve into what is known about TRIM ubiquitin E3 ligase mechanisms, their ubiquitin chain specificities, and how they can be regulated through homo- and hetero-multimerisation and post-translational modifications.

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指标接近的期刊