Biochemistry and Cell Biology最新文献_第2页

SOX2 transcriptional regulation by enhancer elements: a comprehensive review with a unified enhancer nomenclature. Sox2转录调控的增强子元件：一个全面的审查与统一的增强子命名。

IF 2.2 3区生物学

Biochemistry and Cell Biology Pub Date : 2026-01-01 DOI: 10.1139/bcb-2025-0375

Mariia Cherednychenko, Natalia A Gajewska, Jennifer A Mitchell

{"title":"SOX2 transcriptional regulation by enhancer elements: a comprehensive review with a unified enhancer nomenclature.","authors":"Mariia Cherednychenko, Natalia A Gajewska, Jennifer A Mitchell","doi":"10.1139/bcb-2025-0375","DOIUrl":"10.1139/bcb-2025-0375","url":null,"abstract":"Transcription factor SOX2 is essential for a number of biological processes, including mammalian nervous system development and adult brain stem cell maintenance. Expression of this gene requires precise control by a complex network of regulatory elements, which still remains poorly understood. Years of research by different groups have generated a large amount of data on multiple SOX2 enhancers, with varying levels of evidence for their activity across species and tissues. However, the volume of information in the field and inconsistent nomenclature, with the same enhancer referred to by different study-specific names, make understanding progress in SOX2 enhancer regulation challenging. In this review, we brought together current knowledge on predicted and experimentally validated SOX2 enhancers, highlighting links between conserved elements studied in different species. We also propose a unified enhancer naming system based on the distance from the SOX2 transcription start site in the genome of interest, aiming to improve consistency and make communication in the field more straightforward.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-15"},"PeriodicalIF":2.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146096757","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

Structural determinants for the monomeric and phospholipid-transport P4B-ATPase via comprehensive in silico analysis of P4-ATPase structures. 通过对p4 - atp酶结构的全面硅分析，单体和磷脂转运p4b - atp酶的结构决定因素。

IF 2.2 3区生物学

Biochemistry and Cell Biology Pub Date : 2026-01-01 DOI: 10.1139/bcb-2025-0324

Kadambari Vijay Sai, Danny Farhat, Sai Anvithaa Sundar Rajan, Jyh-Yeuan Lee

{"title":"Structural determinants for the monomeric and phospholipid-transport P4B-ATPase via comprehensive in silico analysis of P4-ATPase structures.","authors":"Kadambari Vijay Sai, Danny Farhat, Sai Anvithaa Sundar Rajan, Jyh-Yeuan Lee","doi":"10.1139/bcb-2025-0324","DOIUrl":"10.1139/bcb-2025-0324","url":null,"abstract":"The P4-ATPase family of phospholipid flippases plays a critical role in maintenance of membrane asymmetry and cellular protein traffic and eukaryotic homeostasis. Several structures of these phospholipid flippases have been resolved, along with extensive biochemical characterization of the substrate transport properties. However, an essential subfamily of monomeric phospholipid flippases, the P4B-ATPases, remains to be characterized in depth. While P4B-ATPases appear to share similar lipid transport properties to their heterodimeric counterparts, the P4A-ATPases, the basis of their substrate translocation as monomers is currently unknown. In this study, we investigated the divergence of P4B-ATPases from other P-type ATPases using a structure-based analysis of sequence conservation. Our results showed conservative and nonconservative pockets and pathways in the P4B-ATPases near critical residues for the substrate transport pathway. P4B-ATPases also exhibit a unique interaction of an invariant proline near a conserved TM1-2 aromatic cluster, where dynamics simulation confirmed interactions with phospholipids and cholesterol by this conserved aromatic cluster. A critical TM6 residue was observed orienting into a conserved P4B-pathway whose function is currently unknown but a disease mutation hotspot, suggesting that P4B-ATPases exhibit novel transport and/or regulatory mechanisms. Our results provide a molecular framework for further studies on this essential subfamily of monomeric phospholipid flippases.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-11"},"PeriodicalIF":2.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147509533","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

NCOR1 alleviates myocardial infarction by improving lipid peroxidation through PPARG/PINK1-mediated mitophagy. NCOR1通过PPARG/ pink1介导的线粒体自噬改善脂质过氧化，从而减轻心肌梗死。

IF 2.2 3区生物学

Biochemistry and Cell Biology Pub Date : 2026-01-01 DOI: 10.1139/bcb-2025-0075

Zhenzhen Liu, Yanru He, Wenjing Zhu

{"title":"NCOR1 alleviates myocardial infarction by improving lipid peroxidation through PPARG/PINK1-mediated mitophagy.","authors":"Zhenzhen Liu, Yanru He, Wenjing Zhu","doi":"10.1139/bcb-2025-0075","DOIUrl":"10.1139/bcb-2025-0075","url":null,"abstract":"Abnormal lipid accumulation following myocardial infarction (MI) serves as a critical pathological factor contributing to cardiomyocyte injury. The nuclear receptor corepressor 1 (NCOR1) is famous as a key regulator in atherosclerosis, fatty liver, and other metabolic diseases, and recent evidence suggested that NCOR1 exerted a protective action in damaged heart cells. In this study, in a murine MI model induced by left anterior descending coronary artery ligation, we observed a significant downregulation of NCOR1 in myocardial tissues. NCOR1 was also downregulated in oxygen-glucose deprivation (OGD)-treated H9C2 cells, in which NCOR1 overexpression improved lipid metabolic dysregulation and peroxidation. Mechanistically, NCOR1 interacted with peroxisome proliferator activated receptor gamma (PPARγ) protein, which transcriptionally activated the expression of the mitophagy marker gene PINK1. Either knockdown of PPARγ or PINK1 was able to reverse the improvement of NCOR1 overexpression on OGD-induced dysregulation of mitophagy, lipid peroxidation, and cardiomyocyte damage. Finally, we demonstrated that NCOR overexpression (mediated by lentiviral vector) reduced infarct size, attenuated myocardial damage, and significantly improved cardiac function in MI mice. These findings not only identify NCOR1 as a novel protector in hypoxic-ischemic myocardium but also delineate the \"NCOR1-PPARγ-PINK1\" axis as a novel mechanism for improving mitochondrial function and lipid peroxidation, offering a promising therapeutic target for MI treatment.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":"104 ","pages":"1-15"},"PeriodicalIF":2.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146059177","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

Extracellular vesicle-derived heat shock proteins as biotargets in cancer. 细胞外囊泡衍生的热休克蛋白作为癌症的生物靶点。

IF 2.2 3区生物学

Biochemistry and Cell Biology Pub Date : 2026-01-01 DOI: 10.1139/bcb-2025-0148

C L Lim, J J W Low, M Z M Zulkifli, N S Ab Mutalib, S F Masre, N A Abdul Murad, N Abu

引用次数: 0

An optimized protocol for identifying S-acylated proteins in Dictyostelium discoideum. 一种鉴定盘状盘齿龙s -酰化蛋白的优化方案。

IF 2.2 3区生物学

Biochemistry and Cell Biology Pub Date : 2026-01-01 DOI: 10.1139/bcb-2026-0052

Samer A Owiar, William D Kim, Robert J Huber

引用次数: 0

Does the beta subunit of mitochondrial trifunctional protein modulate monolysocardiolipin acylation to cardiolipin? 线粒体三功能蛋白的β亚基是否调节单多心磷脂酰化为心磷脂？

IF 2.2 3区生物学

Biochemistry and Cell Biology Pub Date : 2026-01-01 DOI: 10.1139/bcb-2026-0094

Grant M Hatch

{"title":"Does the beta subunit of mitochondrial trifunctional protein modulate monolysocardiolipin acylation to cardiolipin?","authors":"Grant M Hatch","doi":"10.1139/bcb-2026-0094","DOIUrl":"10.1139/bcb-2026-0094","url":null,"abstract":"The alpha subunit of mitochondrial trifunctional protein (αTFP) catalyzes the acylation of monolysocardiolipin (MLCL) to cardiolipin (CL). We determined whether the beta subunit of mitochondrial trifunctional protein (βTFP) impacted the ability of αTFP to promote CL resynthesis from MLCL. Purified recombinant αTFP, but not βTFP, exhibited acylation of MLCL to CL with [1-14C]linoleoyl-coenzyme A. Incubation of both αTFP and βTFP together did not alter the ability of αTFP to catalyze the acylation of MLCL to CL with [1-14C]linoleoyl-coenzyme A. HeLa cells were transfected with recombinant αTFP, βTFP, or both, then incubated with [1-14C]linoleate, and radioactivity incorporated into CL was determined. Expression of αTFP increased [1-14C]linoleate incorporation into CL 2-fold (p < 0.05), whereas expression of βTFP did not affect [1-14C]linoleate incorporation into CL. Expression of both αTFP and βTFP together increased [1-14C]linoleate incorporation into CL to an identical level to that achieved with αTFP alone. Barth syndrome (BTHS) patient lymphoblasts, which exhibit elevated MLCL and reduced CL, were incubated with βTFP inhibitory RNA, and CL mass was determined. Incubation of BTHS lymphoblasts with βTFP inhibitory RNA increased CL mass 1.5-2-fold (p < 0.05). We hypothesize that the βTFP may regulate CL resynthesis in BTHS lymphoblasts.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-5"},"PeriodicalIF":2.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148175110","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

Characterization of IFN-γ-mediated cellular responses in the HMC3 cell line. IFN-γ介导的HMC3细胞系细胞反应的表征。

IF 2.2 3区生物学

Biochemistry and Cell Biology Pub Date : 2026-01-01 DOI: 10.1139/bcb-2025-0283

Esmé S M Franck, Jasmyne A Storm, Jueqin Lu, Mon Francis M Obtial, Sanoji Wijenayake

{"title":"Characterization of IFN-γ-mediated cellular responses in the HMC3 cell line.","authors":"Esmé S M Franck, Jasmyne A Storm, Jueqin Lu, Mon Francis M Obtial, Sanoji Wijenayake","doi":"10.1139/bcb-2025-0283","DOIUrl":"10.1139/bcb-2025-0283","url":null,"abstract":"Microglia, the primary immune cells of the brain parenchyma, play critical roles in neurodevelopment and homeostasis. The human microglia clone 3 (HMC3) cell line has long been a staple in vitro tool for exploring microglia dynamics. However, recent evidence suggests that HMC3 cells behave less like natural microglia and more like pericytes and astrocytes. Until a large-scale shift in replacing HMC3 cells with alternative in vitro models occurs, it is important to standardize characterization techniques used to study HMC3 polarization dynamics to enhance repeatability of findings. Here, we characterized the morphological, cellular, and molecular responses of HMC3 cells in response to 10 and 50 ng/mL interferon-gamma (IFN-γ) treatment. We created an HMC3-specific morphology atlas, conducted manual and automated morphology assessments, quantified live and dead cell counts, and assessed mitochondrial output and the accumulation of reactive oxygen species. We also quantified transcript and protein abundance of candidate markers of chemokine secretion, cytokine signaling, endosomal processes, and cytoprotective responses. We presented detailed methodology on cell culturing, treatments, target selection, internal reference controls, primer design, validation, testing, and quantification to enhance the reproducibility of the data. Our study will increase the rigor of target selection and shed light on the unique polarization dynamics of HMC3 cells.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-25"},"PeriodicalIF":2.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147669564","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

AXIN1-dependent regulation of lung macrophage MHC-II expression shapes CD4⁺T cell responses during BCG infection. 卡介苗感染期间肺巨噬细胞MHC II表达的axin1依赖性调控影响CD4 + T细胞反应

IF 2.2 3区生物学

Biochemistry and Cell Biology Pub Date : 2026-01-01 DOI: 10.1139/bcb-2025-0382

Xiaoling Liang, Ruoying Chen, Yuerong Zeng, Haiyan Peng, Zhelong Feng, Haimei Zhou, Xiangru Kong, Jintao Qin, Limei Zhu, Guoli Li, Honghuan Song, Yan Li, Yajing Wang

{"title":"AXIN1-dependent regulation of lung macrophage MHC-II expression shapes CD4⁺T cell responses during BCG infection.","authors":"Xiaoling Liang, Ruoying Chen, Yuerong Zeng, Haiyan Peng, Zhelong Feng, Haimei Zhou, Xiangru Kong, Jintao Qin, Limei Zhu, Guoli Li, Honghuan Song, Yan Li, Yajing Wang","doi":"10.1139/bcb-2025-0382","DOIUrl":"10.1139/bcb-2025-0382","url":null,"abstract":"Tuberculosis (TB), caused by Mycobacterium tuberculosis (M. tb), continues to be the second leading cause of infectious disease-related mortality globally, surpassed only by COVID-19. The Wnt/β-catenin signaling pathway is involved in regulating TB pathogenesis, with AXIN1-a key negative regulator of this pathway-emerging as a potential target for modulating immune responses. Our study explored the function of AXIN1 in TB by examining its expression in peripheral blood mononuclear cells (PBMCs) from TB patients and its effects on macrophage and CD4+T cell functions. We found that AXIN1 expression was significantly downregulated the PBMCs of TB patients and in macrophages infected with Bacillus Calmette-Guérin (BCG). In Tcf/Lef-Gfp transgenic mice intratracheally infected with Mycobacterium bovis BCG, treatment with XAV939 to upregulate AXIN1 expression inhibited Wnt/β-catenin signaling, reduced the proportions of CD4+T cells and macrophages, and decreased the percentage of MHC-II-positive macrophages. Conversely, downregulating AXIN1 in macrophages enhanced CD4+T cell activation and MHC-II-dependent antigen presentation following BCG infection. The accumulated evidence indicates that AXIN1 plays a critical role in modulating macrophage phagocytosis and CD4+T cell reactions because of M. tb infection. Understanding the mechanisms underlying the regulation of the innate-to-adaptive immune transition by AXIN1 could provide new insights into TB pathogenesis and inform the development of novel therapeutic and vaccine strategies.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-12"},"PeriodicalIF":2.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147466343","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

Broad-stroke regulation by DNA sequence-specific transcription factors. DNA序列特异性转录因子调控脑卒中。

IF 2.2 3区生物学

Biochemistry and Cell Biology Pub Date : 2026-01-01 DOI: 10.1139/bcb-2026-0135

Zachary Bigelow, Sergei Nechaev

引用次数: 0

Suppression of CBP/p300 induces growth inhibition and autophagy of hepatocellular carcinoma cells through regulation of EPHA2 by its super-enhancer acetylation. 抑制CBP/p300通过调节EPHA2的超增强子乙酰化诱导肝癌细胞的生长抑制和自噬。

IF 2.2 3区生物学

Biochemistry and Cell Biology Pub Date : 2026-01-01 DOI: 10.1139/bcb-2025-0377

Lishan Xi, Bodi Zhang, Bei Lan

{"title":"Suppression of CBP/p300 induces growth inhibition and autophagy of hepatocellular carcinoma cells through regulation of EPHA2 by its super-enhancer acetylation.","authors":"Lishan Xi, Bodi Zhang, Bei Lan","doi":"10.1139/bcb-2025-0377","DOIUrl":"10.1139/bcb-2025-0377","url":null,"abstract":"CREB binding protein (CBP) and its homolog E1A binding protein p300 (p300) are crucial lysine acetyltransferases that have been shown to play key roles in various human malignancies. However, the precise functions and regulatory mechanisms of CBP/p300 in hepatocellular carcinoma (HCC) remain to be explored. Herein, we report that the expression levels of CBP and p300 are upregulated in HCC compared to normal tissues, and high CBP expression is associated with poor overall survival based on TCGA data. Combined knockdown of CBP and p300 or treatment with the CBP/p300 histone acetyltransferases (HAT) inhibitor A-485 reduces cell viability and promotes cell death in HCC cell lines. Additionally, inhibition of CBP/p300 activates autophagy, which mediates cell death in HCC cells. Mechanistically, the inhibition of CBP/p300 HAT activity attenuates H3K27ac at Ephrin type-A receptor 2 (EPHA2) super-enhancer and suppresses the expression of EPHA2. EPHA2 overexpression can partially rescue CBP/p300 HAT inhibition-mediated autophagy and loss of cell viability. These findings reveal a novel epigenetic mechanism of CBP/p300 in HCC and identify the CBP/p300 inhibitor A-485 as a promising therapeutic candidate for HCC.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-12"},"PeriodicalIF":2.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148026397","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