RNA Biology最新文献_第3页

Stress granules at the crossroads of the proteostasis network. 在蛋白质静止网络的十字路口的应力颗粒。

IF 4.1 3区生物学

RNA Biology Pub Date : 2026-12-01 Epub Date: 2026-10-12 DOI: 10.1080/15476286.2026.2731904

Rachel Kim, Erika N Calle Urgiles, Stephanie L Moon

{"title":"Stress granules at the crossroads of the proteostasis network.","authors":"Rachel Kim, Erika N Calle Urgiles, Stephanie L Moon","doi":"10.1080/15476286.2026.2731904","DOIUrl":"10.1080/15476286.2026.2731904","url":null,"abstract":"The proteostasis network maintains cell function by safeguarding the proteome through the coordinated actions of protein synthesis, quality control, and degradation machinery including chaperones and the ubiquitin-proteasome system. Proteostasis collapse and activation of the integrated stress response (ISR) occur in ageing and neurodegeneration. Upon proteotoxic stress, translation suppression during the ISR drives the assembly of non-translating mRNAs into biomolecular condensates called stress granules. Stress granules act as a double-edged sword in the proteostasis network, serving beneficial or detrimental roles through their effects on translation, protein quality control, and protein aggregation. In this review, we discuss how protein synthesis, quality control, and degradation factors regulate stress granule dynamics, and conversely how stress granules impact proteostasis. While stress granules may initially protect cells by sequestering misfolded, aggregation-prone proteins and regulating translation, they may evolve into sites of pathological aggregation. Clarifying these intersections may reveal therapeutic strategies for neurodegeneration and other disease processes.","PeriodicalId":21351,"journal":{"name":"RNA Biology","volume":"23 1","pages":"1-22"},"PeriodicalIF":4.1,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13671433/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149166338","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

RNA base-modification and A-to-I editing landscapes of oxidatively stressed human retinal pigment epithelium under Quantum Molecular Resonance electrotherapy and blood-derived secretome. 在量子分子共振电疗和血源性分泌组下氧化应激人视网膜色素上皮的RNA碱基修饰和A-to-I编辑景观。

IF 4.1 3区生物学

RNA Biology Pub Date : 2026-12-01 Epub Date: 2026-10-15 DOI: 10.1080/15476286.2026.2731889

Domenico Mordà, Simona Alibrandi, Concetta Scimone, Angela D'ascola, Federica Aliquò, Giorgia Abate, Gianantonio Pozzato, Sergio Zaccaria Scalinci, Rosalia D'angelo, Antonina Sidoti, Luigi Donato

{"title":"RNA base-modification and A-to-I editing landscapes of oxidatively stressed human retinal pigment epithelium under Quantum Molecular Resonance electrotherapy and blood-derived secretome.","authors":"Domenico Mordà, Simona Alibrandi, Concetta Scimone, Angela D'ascola, Federica Aliquò, Giorgia Abate, Gianantonio Pozzato, Sergio Zaccaria Scalinci, Rosalia D'angelo, Antonina Sidoti, Luigi Donato","doi":"10.1080/15476286.2026.2731889","DOIUrl":"10.1080/15476286.2026.2731889","url":null,"abstract":"Chemical modifications of RNA bases and adenosine-to-inosine (A-to-I) editing are regulatory layers essentially unexplored in the retinal pigment epithelium (RPE), whose oxidative dysfunction underlies age-related macular degeneration. We mapped both layers in ARPE-19 cells exposed to tert-butyl hydroperoxide under two non-pharmacological interventions, Quantum Molecular Resonance (QMR) electrotherapy and a patient blood-derived secretome, across 56 libraries spanning four arms, three time points and matched stressed and stress-free conditions (GEO: GSE328981). Base modifications were called with HARMLNC and A-to-I editing screened with a transition-signal caller, then re-analysed with REDItools3, JACUSA2 and LoDEI. The high-confidence set comprised 241 calls at 15 sites, all of classes canonical to tRNA and rRNA. The most prevalent was an adenosine modification at chrM:2617 in mitochondrial 16S rRNA (MT-RNR2), detected in 51 of 56 libraries and in every arm. Two positions 1 bp apart lie in an EZR/SYTL3 overlap region, whereas a third chromosome 6 site maps to HLA-C, 127.5 Mb away. No position of either layer differed between treatment arms: 7 testable modification sites (minimum p = 0.19) and, at single-nucleotide resolution under dedicated callers agreeing to r = 0.975-0.992, 15 curated editing positions (minimum q = 0.169). Two one-sided tests bound any change in substitution composition within 1.4% and in mean editing frequency within 10% for secretome and combination and 20% for QMR. Against a stress-free baseline internal to the cohort, only chrM:13710 (MT-ND5) changed detectably (q = 0.03). These layers are therefore small, largely constitutive and quantifiably undisturbed by either intervention at the resolution available.","PeriodicalId":21351,"journal":{"name":"RNA Biology","volume":"23 1","pages":"1-27"},"PeriodicalIF":4.1,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13679316/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183743","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

Conversations at the crossroads of the Human RNome Project: a collaborative reflection by the RNome Early Career Researchers. 人类染色体工程十字路口的对话：染色体早期职业研究者（ECR）的合作反思。

IF 3.4 3区生物学

RNA Biology Pub Date : 2026-12-01 Epub Date: 2026-01-29 DOI: 10.1080/15476286.2026.2613884

Bennett Henzeler, Rebekah Penrice-Randal, Rami Bechara, Özge Simsir, Shanice Jessica Hermon

引用次数: 0

RNA G-quadruplex-protein interactions: from nuclear RNA processing to cytoplasmic stress response and neurodegeneration. RNA g -四重体蛋白相互作用：从核RNA加工到细胞质应激反应和神经变性。

IF 4.1 3区生物学

RNA Biology Pub Date : 2026-12-01 Epub Date: 2026-04-15 DOI: 10.1080/15476286.2026.2658922

Dimitrios G Anastasakis, Markus Hafner

{"title":"RNA G-quadruplex-protein interactions: from nuclear RNA processing to cytoplasmic stress response and neurodegeneration.","authors":"Dimitrios G Anastasakis, Markus Hafner","doi":"10.1080/15476286.2026.2658922","DOIUrl":"10.1080/15476286.2026.2658922","url":null,"abstract":"RNA G-quadruplexes (rG4s) are stable secondary structures formed by non-canonical Hoogsteen base-pairing of guanine-rich sequences in precursor and mature messenger and non-coding RNAs. We review evidence that rG4s exist in two functionally distinct worlds. In the nucleus, rG4s fold co-transcriptionally to regulate gene expression and RNA processing and organizing membraneless organelles through liquid-liquid phase separation. Splicing regulation by rG4s is restricted to vertebrates and co-evolved with transcriptome complexity. In the cytoplasm, rG4s are actively maintained in an unfolded state by dedicated helicases and RNA-binding proteins, but fold upon stress to nucleate stress granules, that sequester mRNAs and sustain cell survival. When compartmentalization of rG4-protein interactions fails, cells lose both nuclear RNA processing control and cytoplasmic translational regulation and proper stress response. The same biophysical properties that make rG4s effective scaffolds for reversible phase separation in RNA processing, proteostasis, and acute stress become liabilities under chronic conditions: in ageing neurons, failure of rG4-protein homoeostasis transforms protective condensates into irreversible aggregates associated with α-synuclein, tau, TDP-43, and FUS pathology. We discuss the implications of a dynamic equilibrium of folded and unfolded rG4s in health and disease, with particular focus on their emerging roles in neurodegeneration.","PeriodicalId":21351,"journal":{"name":"RNA Biology","volume":" ","pages":"1-16"},"PeriodicalIF":4.1,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13085946/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147654873","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

Discovery of a mutation-containing circRNA in polyglutamine disease through systematic analysis of RNAs with CAG repeats. 通过对带有CAG重复序列的rna的系统分析，在多谷氨酰胺病中发现含有突变的环状rna。

IF 4.1 3区生物学

RNA Biology Pub Date : 2026-12-01 Epub Date: 2026-06-24 DOI: 10.1080/15476286.2026.2684791

Weronika Pawlik, Magdalena Woźna-Wysocka, Magdalena Jazurek-Ciesiołka, Jarosław Dulski, Tomasz M Witkoś, Agata Ciołak, Emilia Kozłowska, Edyta Kościańska, Luke C Bartelt, Julien Philippe, Jarosław Sławek, Paweł M Świtoński, Albert R La Spada, Agnieszka Fiszer

引用次数: 0

RNA polymerase II phosphorylation dynamics: from molecular mechanisms to human disease. RNA聚合酶II磷酸化动力学：从分子机制到人类疾病。

IF 4.1 3区生物学

RNA Biology Pub Date : 2026-12-01 Epub Date: 2026-07-02 DOI: 10.1080/15476286.2026.2695549

Araceli González-Jiménez, Ithaisa Medina, Manuel J Alfonso, Carlos R Vázquez de Aldana, Olga Calvo

{"title":"RNA polymerase II phosphorylation dynamics: from molecular mechanisms to human disease.","authors":"Araceli González-Jiménez, Ithaisa Medina, Manuel J Alfonso, Carlos R Vázquez de Aldana, Olga Calvo","doi":"10.1080/15476286.2026.2695549","DOIUrl":"10.1080/15476286.2026.2695549","url":null,"abstract":"Accurate RNA polymerase II (RNAPII)-dependent gene expression requires dynamic phosphorylation of the carboxy-terminal domain (CTD) of its largest subunit, Rpb1, whose heptapeptide repeats form a regulatory platform known as the CTD code. Transcription-associated cyclin-dependent kinases (tCDKs) and CTD phosphatases coordinate the phosphorylation - dephosphorylation cycle of RNAPII throughout transcription, coupling RNA synthesis to co-transcriptional processing and chromatin regulation. By controlling stage-specific modification of the CTD, these enzymes integrate RNAPII activity into broader regulatory networks. Disruption of the delicate kinase - phosphatase balance impairs transcriptional fidelity, RNA maturation, and genome stability, either directly through altered CTD phosphorylation or indirectly through associated pathways. Such alterations are increasingly associated with developmental disorders, neurodegeneration, and cancer. Here, we synthesize current knowledge of RNAPII phosphorylation dynamics, highlighting key mechanistic principles, links to human disease, and emerging therapeutic strategies targeting this central phosphorylation-dependent regulatory system.","PeriodicalId":21351,"journal":{"name":"RNA Biology","volume":" ","pages":"1-20"},"PeriodicalIF":4.1,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13336285/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148346237","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

FTO-mediated m⁶A demethylation of BCL6 promotes gastric cancer progression by suppressing ferroptosis. fto介导的m26 BCL6去甲基化通过抑制铁下垂促进胃癌进展。

IF 4.1 3区生物学

RNA Biology Pub Date : 2026-12-01 Epub Date: 2026-06-10 DOI: 10.1080/15476286.2026.2684406

Yan Wang, Fangfang Fan, Zhongmin Zhan, Chenxu Yu, Shengchi Chen

{"title":"FTO-mediated m6A demethylation of BCL6 promotes gastric cancer progression by suppressing ferroptosis.","authors":"Yan Wang, Fangfang Fan, Zhongmin Zhan, Chenxu Yu, Shengchi Chen","doi":"10.1080/15476286.2026.2684406","DOIUrl":"10.1080/15476286.2026.2684406","url":null,"abstract":"B-cell lymphoma 6 (BCL6) functions in various cancers, but its role and regulation in gastric cancer (GC) remain unclear. N6-methyladenosine (m6A) modification is critical for tumorigenesis, and the demethylase FTO (highly expressed in GC) may regulate target gene stability via m6A. This study explored FTO's regulation of BCL6 m6A modification and its impact on GC progression through ferroptosis. qPCR assessed BCL6 expression in GC cells. BCL6 overexpression models were used to evaluate cell viability, apoptosis, and ferroptosis (via ROS, Fe2+, MDA, LDH, and ferroptosis-related proteins). RIP-PCR, MeRIP-qPCR, and mRNA stability assays examined FTO-BCL6 mRNA interaction and m6A effects. YTHDF2 knockdown validated its role, and co-silencing FTO/BCL6 clarified the axis's function. BCL6 was downregulated in GC cells. Its overexpression inhibited cell viability, promoted apoptosis, and induced ferroptosis. FTO bound BCL6 mRNA, removed m6A, and reduced its stability. YTHDF2 mediated FTO's negative regulation of BCL6. FTO knockdown enhanced ferroptosis and impaired GC cell function, partially reversed by BCL6 silencing. FTO suppresses BCL6 via m6A demethylation, inhibiting ferroptosis to promote GC progression. The FTO/BCL6 axis is a potential therapeutic target for GC.","PeriodicalId":21351,"journal":{"name":"RNA Biology","volume":" ","pages":"1-14"},"PeriodicalIF":4.1,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13271351/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148205869","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 architectural and functional landscape of transposon-derived chimeric RNAs. 转座子衍生的嵌合rna的结构和功能景观。

IF 4.1 3区生物学

RNA Biology Pub Date : 2026-12-01 Epub Date: 2026-10-20 DOI: 10.1080/15476286.2026.2743461

Yangquan Xiang, Hongqing Liang

{"title":"The architectural and functional landscape of transposon-derived chimeric RNAs.","authors":"Yangquan Xiang, Hongqing Liang","doi":"10.1080/15476286.2026.2743461","DOIUrl":"10.1080/15476286.2026.2743461","url":null,"abstract":"This review systematically examines the architectural and functional landscape of transposable element (TE)-derived chimeric RNAs, classifying them into three major categories: TE-coding gene chimeras, TE-lncRNA chimeras and TE-TE chimeras. We delineate four potential molecular mechanisms contributing to their biogenesis: transcriptional read-through coupled with cis-splicing, promoter hijacking by TE-derived regulatory elements, trans-splicing of independent transcripts and epigenetic regulation of TE genomic loci. Functionally, TE and their chimeric RNAs can coordinately participate in genomic regulation at different levels: they remodel native gene expression patterns via alternative promoters, introduce novel functional domains into proteins and lncRNAs, and form integrated transcriptional regulatory networks. These chimeric transcripts exert critical roles in early embryonic development, stem cell potency, differentiation or pathogenic condition. Looking forward, long-read sequencing and genomic targeting technologies hold great promise to unravel the functionality and therapeutic application of TE-derived chimeric RNAs. Collectively, this review establishes TE-derived chimeric RNAs as fundamental drivers of transcriptomic innovation, evolutionary adaptation and disease aetiology, bridging basic genome biology with physiology and clinical translation.","PeriodicalId":21351,"journal":{"name":"RNA Biology","volume":"23 1","pages":"1-18"},"PeriodicalIF":4.1,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13690279/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228769","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

Essential role of hsa-miR-203a-3p in type I interferons immune homeostasis during influenza and NDV infection. hsa-miR-203a-3p在流感和NDV感染期间I型干扰素免疫稳态中的重要作用

IF 4.1 3区生物学

RNA Biology Pub Date : 2026-12-01 Epub Date: 2026-03-05 DOI: 10.1080/15476286.2026.2640211

Pramod Kumar, Ashish Kumar, Akhilesh Kumar, Himanshu Kumar

{"title":"Essential role of hsa-miR-203a-3p in type I interferons immune homeostasis during influenza and NDV infection.","authors":"Pramod Kumar, Ashish Kumar, Akhilesh Kumar, Himanshu Kumar","doi":"10.1080/15476286.2026.2640211","DOIUrl":"10.1080/15476286.2026.2640211","url":null,"abstract":"MicroRNAs (miRNAs) are small, non-coding RNA molecules that act as essential post-transcriptional regulators in various biological processes. Many studies suggest that miRNAs may modulate the host's immune response or even viral replication during infection. We have identified hsa-miR-203a-3p as a key regulatory candidate influencing innate immune responses, based on a comprehensive analysis of publicly available transcriptomic datasets involving H7N9, HCV, or DENV2 infection. Pathway enrichment analysis of microRNA-targeted genes reveals that hsa-miR-203a-3p targets several components of type I interferon signalling and JAK-STAT pathway. In this study, we report a novel role of hsa-miR-203a-3p as it is elevated in response to polyinosinic-polycytidylic acid [poly(I:C)] transfection and infection with RNA viruses Newcastle Disease Virus (NDV) and A/PR8/H1N1 influenza virus. We found that hsa-miR-203a-3p promotes the A/PR8/H1N1 virus replication by suppressing the host's type-I interferons and interferon-stimulated genes. Our investigation demonstrated that overexpression of hsa-miR-203a-3p led to reduced expression of interferon stimulated genes (ISGs). This regulation is likely mediated through the direct binding of hsa-miR-203a-3p to the 3' UTRs of Janus-activated kinase 1 (JAK1), STAT1 and several IFN-α transcripts. Collectively, these findings highlight the pivotal role of hsa-miR-203a-3p in immune homoeostasis; it regulates type I IFN signalling and downstream antiviral responses, thereby facilitating A/PR8/H1N1 and NDV infection.","PeriodicalId":21351,"journal":{"name":"RNA Biology","volume":"23 1","pages":"1-16"},"PeriodicalIF":4.1,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12969740/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147356313","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

lncRNAs: key player in Aβ deposition. lncRNAs: Aβ沉积的关键角色。

IF 4.1 3区生物学

RNA Biology Pub Date : 2026-12-01 Epub Date: 2026-03-05 DOI: 10.1080/15476286.2026.2639017

Ruo-Mei Wang, Zi-Qiang Wang

引用次数: 0