Biochemistry and Cell Biology最新文献_第6页

Microgravity-induced immune dysregulation: phase-specific profiles of differential gene expression. 微重力诱导的免疫失调：差异基因表达的阶段特异性谱。

IF 2.1 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2025-0136

Martin Pelchat, Guy Trudel, Lynda Rocheleau, Daniel Stratis, Odette Laneuville

{"title":"Microgravity-induced immune dysregulation: phase-specific profiles of differential gene expression.","authors":"Martin Pelchat, Guy Trudel, Lynda Rocheleau, Daniel Stratis, Odette Laneuville","doi":"10.1139/bcb-2025-0136","DOIUrl":"https://doi.org/10.1139/bcb-2025-0136","url":null,"abstract":"Astronauts experience the reactivation of latent viruses in spaceflight, an indicator of reduced immunity. It is unclear how the immune system responds to pathogens in a microgravity environment. A longitudinal profile of leukocytes' transcriptome changes from participants to an Earth model of microgravity and from astronauts sojourning aboard the International Space Station revealed a reduced expression of immune-related genes while in microgravity. In the current study, we identified transcriptomic changes specific to the transition to and from bed/space, as well as the adaptation, and the recovery from microgravity/space exposure. The expression of immune-related gene shifted in opposite direction at phase transition compared to within the bed rest and reambulation phases. Differential expression of cytokine genes supported a reduced immune-response during the head down tilt bed rest phase and return to baseline levels at reambulation. Immunoglobulin gene expression increased after participants left the facility. The enrichment analysis of the differentially expressed genes identified the gene ontology terms virus/viral and genes previously involved in the modulation of the response to latent reactivation, including IFNL1, TNFSF14, IL10, and ISG15. Leukocytes' transcriptomic analysis revealed dynamic changes of immune-related gene expression timed with phases of spaceflight. The current analysis combined with previous evidence of herpesvirus reactivation during space mission represent a valuable model for the study of viral latency in vivo.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":"103 ","pages":"1-12"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145237838","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

Subacute exposure to aluminium chloride induces cytotoxicity and oxidative stress in rat erythrocytes: a dose-dependent study. 亚急性暴露于氯化铝诱导大鼠红细胞细胞毒性和氧化应激：剂量依赖性研究。

IF 2.1 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2024-0236

Farha Shahabuddin, Samina Naseem, Farah Khan

{"title":"Subacute exposure to aluminium chloride induces cytotoxicity and oxidative stress in rat erythrocytes: a dose-dependent study.","authors":"Farha Shahabuddin, Samina Naseem, Farah Khan","doi":"10.1139/bcb-2024-0236","DOIUrl":"10.1139/bcb-2024-0236","url":null,"abstract":"Aluminium (Al) toxicity has attracted considerable interest due to its bioavailability, environmental persistence, and adverse health effects. The present study investigates the effect of Al on rat erythrocytes under in vivo conditions. Rats were administered 0 (control), 25 (Al 1), 35 (Al 2), 45 (Al 3), and 55 (Al 4) mg/kg b.wt. of AlCl3 orally for 30 days. Hemolysates were prepared from different experimental groups and assayed for various biochemical parameters. AlCl3 administration significantly increased protein oxidation and lipid peroxidation, while decreasing total sulfhydryl and glutathione levels in rat erythrocytes. Methemoglobin level was increased and methemoglobin reductase activity was decreased upon AlCl3 treatment. Prolonged AlCl3 exposure inhibited the activities of antioxidant enzymes, and lowered the cells' antioxidant power. It also caused an increase in H2O2 and NO levels showing generation of oxidative and nitrosative stress. AlCl3 intoxication adversely affected the membrane-bound and metabolic enzyme activities. Alterations in all the biochemical parameters were found in an AlCl3 dose-dependent manner. Scanning electron microscopy showed gross morphological changes in erythrocytes from discocytes to acanthocytes and echinocytes, further supporting the damaging effect of aluminium. The aluminium-induced oxidative stress seems to be the key mechanism of damage to the cellular components that could lead to red cell senescence.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-14"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144186429","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

CD38 deficiency prevents diabetic nephropathy by inhibiting lipid accumulation and oxidative stress through activation of the SIRT3 pathway. CD38 缺乏症可通过激活 SIRT3 途径抑制脂质积累和氧化应激，从而预防糖尿病肾病。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 Epub Date: 2024-08-08 DOI: 10.1139/bcb-2024-0058

Ling-Fang Wang, Qian Li, Jia Le Zhao, Ke Wen, Ya-Ting Zhang, Qi-Hang Zhao, Qi Ding, Jia-Hui Li, Xiao-Hui Guan, Yun-Fei Xiao, Ke-Yu Deng, Hong-Bo Xin

{"title":"CD38 deficiency prevents diabetic nephropathy by inhibiting lipid accumulation and oxidative stress through activation of the SIRT3 pathway.","authors":"Ling-Fang Wang, Qian Li, Jia Le Zhao, Ke Wen, Ya-Ting Zhang, Qi-Hang Zhao, Qi Ding, Jia-Hui Li, Xiao-Hui Guan, Yun-Fei Xiao, Ke-Yu Deng, Hong-Bo Xin","doi":"10.1139/bcb-2024-0058","DOIUrl":"10.1139/bcb-2024-0058","url":null,"abstract":"Diabetic nephropathy (DN) is one of the most common complications of diabetes. Our previous study showed that CD38 knockout (CD38KO) mice had protective effects on many diseases. However, the roles and mechanisms of CD38 in DN remain unknown. Here, DN mice were generated by high-fat diet (HFD) feeding plus streptozotocin (STZ) injection in male CD38KO and CD38flox mice. Mesangial cells (SV40 MES 13 cells) were used to mimic the injury of DN with palPagination Donemitic acid (PA) treatment in vitro. Our results showed that CD38 expression was significantly increased in kidney of diabetic CD38flox mice and SV40 MES 13 cells treated with PA. CD38KO mice were significantly resistant to diabetes-induced renal injury. Moreover, CD38 deficiency markedly decreased HFD/STZ-induced lipid accumulation, fibrosis, and oxidative stress in kidney tissue. In contrast, overexpression of CD38 aggravated PA-induced lipid accumulation and oxidative stress. CD38 deficiency increased expression of SIRT3, while overexpression of CD38 decreased its expression. More importantly, 3-TYP, an inhibitor of SIRT3, significantly enhanced PA-induced lipid accumulation and oxidative stress in CD38 overexpressing cell lines. In conclusion, our results demonstrated that CD38 deficiency prevented DN by inhibiting lipid accumulation and oxidative stress through activation of the SIRT3 pathway.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-12"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141905787","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

A role for NFIB in SOX2 downregulation and epigenome accessibility changes due to long-term estrogen treatment of breast cancer epithelial cells. NFIB在乳腺癌上皮细胞长期雌激素治疗导致的SOX2下调和表观基因组可及性改变中的作用

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2024-0287

Luis E Abatti, Zoe E Gillespie, Patricia Lado-Fernández, Manuel Collado, Jennifer A Mitchell

{"title":"A role for NFIB in SOX2 downregulation and epigenome accessibility changes due to long-term estrogen treatment of breast cancer epithelial cells.","authors":"Luis E Abatti, Zoe E Gillespie, Patricia Lado-Fernández, Manuel Collado, Jennifer A Mitchell","doi":"10.1139/bcb-2024-0287","DOIUrl":"10.1139/bcb-2024-0287","url":null,"abstract":"Estrogen (E2) regulates the differentiation and proliferation of mammary progenitor cells by modulating the transcription of multiple genes. One of the genes that is downregulated by E2 is SOX2, a transcription factor associated with stem and progenitor cells that is overexpressed during breast tumourigenesis. To elucidate the mechanisms underlying E2-mediated SOX2 repression, we investigated epigenome and transcriptome changes following short- and long-term E2 exposure in breast cancer cells. We found that short-term E2 exposure reduces chromatin accessibility at the downstream SOX2 SRR134 enhancer, decreasing SOX2 expression. In contrast, long-term E2 exposure completely represses SOX2 transcription while maintaining accessibility at the SRR124-134 enhancer cluster, keeping it poised for reactivation. This repression was accompanied by widespread epigenome and transcriptome changes associated with commitment towards a more differentiated and less invasive luminal phenotype. Finally, we identified a role for the transcription factor NFIB in this process, suggesting it collaborates with the estrogen receptor to mediate SOX2 repression and genome-wide epigenome accessibility changes.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-14"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514410","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

Perturbation of calcium homeostasis invokes eryptosis-like cell death in enucleated bone marrow stem cells. 扰乱钙稳态会导致无核骨髓干细胞发生红细胞增多症样细胞死亡。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 Epub Date: 2024-11-18 DOI: 10.1139/bcb-2024-0106

Wei Yan, Ruolan Wu, Yingying Lee, Liqun Xu, Xiao Li, Junwei Li, Ronghao Deng, Xing Fan, Yilang Wu, Haibao Zhu, Aihua Mao, Jianxin Shen, Chi-Ju Wei

{"title":"Perturbation of calcium homeostasis invokes eryptosis-like cell death in enucleated bone marrow stem cells.","authors":"Wei Yan, Ruolan Wu, Yingying Lee, Liqun Xu, Xiao Li, Junwei Li, Ronghao Deng, Xing Fan, Yilang Wu, Haibao Zhu, Aihua Mao, Jianxin Shen, Chi-Ju Wei","doi":"10.1139/bcb-2024-0106","DOIUrl":"10.1139/bcb-2024-0106","url":null,"abstract":"Enucleated cells, also known as cytoplasts, are valuable tools with a wide range of applications. However, their potential for bio-engineering is greatly restricted by the short lifespan. We postulated that the enucleation process damages the integrity of the plasma membrane and thus activates a cell death program(s). The results showed that a tiny hole was generated transiently on the plasma membrane when the nucleus was spun off, while force-gated ion channels were activated in response to the pulling by the nucleus. Influx of extracellular calcium stimulated the opening of calcium channels and the release of calcium from endoplasmic reticulum and mitochondria. Long lasting calcium transient increased protein phosphorylation and activated caspase 9 and calpain proteinase activities. Subsequently, mitochondria membrane permeability and Reactive Oxygen Species (ROS) levels were significantly elevated, which eventually led to eryptosis-like cell death. When extracellular calcium was maintained at optimal concentration, the lifespan of enucleated cells was extended; however, huge amounts of vacuoles appeared in the cytoplasm, possibly derived from enlarged autophagosomes. Inhibition of vacuolation by inhibitors of autophagy or in co-culture with primary muscle cells did not rescue cells dying from the paraptosis-like pathway. These results offer valuable insights for further investigation into the intricate mechanisms underlying enucleated cell death.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-11"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142646832","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

WDR4 promotes colorectal cancer progression by activating the GSK3β/β-catenin pathway. WDR4通过激活GSK3β/β-catenin通路促进结直肠癌的进展。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2024-0168

Hongyu Wang, Liyang Liang, Yanfei Wang, Xuan Zhong, Chao Zhang, Zhipeng Liu, Jinzhong Liu, Wanning Hu

{"title":"WDR4 promotes colorectal cancer progression by activating the GSK3β/β-catenin pathway.","authors":"Hongyu Wang, Liyang Liang, Yanfei Wang, Xuan Zhong, Chao Zhang, Zhipeng Liu, Jinzhong Liu, Wanning Hu","doi":"10.1139/bcb-2024-0168","DOIUrl":"10.1139/bcb-2024-0168","url":null,"abstract":"WD repeat domain 4 (WDR4) has been reported to promote tumor metastasis in various cancers. However, its precise function in colorectal cancer (CRC) has not been reported yet. Herein, the expression pattern of WDR4 in CRC was determined by analyzing Gene Expression Omnibus datasets (GSE110225, GSE127069, GSE156355, and GSE184093) and GEPIA online dataset. In vitro and in vivo experiments, including CCK-8, colony formation, flow cytometry, wound healing, transwell assays, and xenograft mouse models, were used to investigate the role of WDR4 in CRC. Firstly, data from Kaplan-Meier database showed that high expression of WDR4 was associated with the poor prognosis of CRC patients. Then, upregulation of WDR4 was confirmed in clinical CRC tissues. In vitro functional experiments suggested that overexpression of WDR4 promoted cell proliferation, migration, and invasion, while knockdown of WDR4 has the opposite effects. Also, the oncogenic role of WDR4 was also verified in in vivo experiments. CO-IP-LC/MS analysis uncovered that glycogen synthase kinase 3β (GSK3β) is the central protein that binds to WDR4. Mechanistically, WDR4 activated the β-catenin pathway by promoting GSK3β phosphorylation. This study demonstrates that WDR4 promotes CRC progression through activating GSK3β/β-catenin pathway, indicating that WDR4 might be a potential therapeutic target for CRC treatment.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-12"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514501","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

Retraction: Long noncoding RNA HIF1A-AS2 facilitates cell survival and migration by sponging miR-33b-5p to modulate SIRT6 expression in osteosarcoma. 缩稿：长链非编码RNA HIF1A-AS2通过海绵miR-33b-5p调节SIRT6在骨肉瘤中的表达，促进细胞存活和迁移。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2025-0019

引用次数: 0

Omega-3 polyunsaturated fatty acids modify glucose metabolism in THP-1 monocytes. Omega-3多不饱和脂肪酸改变THP-1单核细胞的葡萄糖代谢。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2024-0202

Michael J Byun, Roni Armon, Tamiris F G Souza, Hope D Anderson, Ayesha Saleem, Samantha D Pauls

{"title":"Omega-3 polyunsaturated fatty acids modify glucose metabolism in THP-1 monocytes.","authors":"Michael J Byun, Roni Armon, Tamiris F G Souza, Hope D Anderson, Ayesha Saleem, Samantha D Pauls","doi":"10.1139/bcb-2024-0202","DOIUrl":"10.1139/bcb-2024-0202","url":null,"abstract":"Chronic inflammation is a driving factor in diseases like obesity and type 2 diabetes. Enhanced cellular glucose metabolism may contribute to heightened immune activation. A human supplementation trial showed that the n-3 PUFA α-linolenic acid (ALA) reduced oxidative phosphorylation in monocytes. Our objective here is to assess the direct effects of ALA and docosahexaenoic acid (DHA) on glucose metabolism in a cell culture model and to explore possible molecular mechanisms. THP-1 monocytes were treated with 10-40 µmol/L of ALA or DHA and compared with vehicle and oleic acid controls. The Seahorse XFe24 and Oroboros O2k Oxygraph systems were used to approximate catabolic rates in the presence of glucose. Both ALA and DHA reduced oxidative phosphorylation. We identified pyruvate dehydrogenase kinase 4 (PDK4) as a possible mechanistic candidate explaining the effect of DHA. Additionally, both n-3 PUFAs reduced lipopolysaccharides-induced IL-1β production, while only DHA increased reactive oxygen species to a small but significant extent. Our data suggest that ALA and DHA trigger a re-wiring of bioenergetic pathways in monocytes, possibly via the upregulation of PDK4. Given the close relationship between cell metabolism and immune cell activation, this may represent a novel mechanism by which n-3 fatty acids modulate immune function and inflammation.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-10"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143121857","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

MCPIP1 deficiency alleviates abdominal aortic aneurysm formation by inhibiting MAPK signaling. MCPIP1缺失通过抑制MAPK信号通路减轻腹主动脉瘤的形成。

IF 2.1 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2024-0260

Ming Xue, Hailing Ding, Yongxin Han, Yuhua Wei, Xuming Wang, Xiaohan Wang, Xiangqian Kong

{"title":"MCPIP1 deficiency alleviates abdominal aortic aneurysm formation by inhibiting MAPK signaling.","authors":"Ming Xue, Hailing Ding, Yongxin Han, Yuhua Wei, Xuming Wang, Xiaohan Wang, Xiangqian Kong","doi":"10.1139/bcb-2024-0260","DOIUrl":"10.1139/bcb-2024-0260","url":null,"abstract":"Abdominal aortic aneurysm (AAA) is a chronic and severe aortic disease. Our previous studies have indicated that monocyte chemotactic protein-induced protein-1 (MCPIP1) is involved in AAA. However, the exact effect of MCPIP1 on angiotensin II (Ang II)-induced AAA formation is currently unknown. MCPIP1 deficiency reduced AAA formation in Ang II-induced mice. Less collagen and elastin degradation were observed in MCPIP1-deficient mice treated with Ang II. Ang II decreased αSMA and SM22α levels in aortas and vascular smooth muscle cells (VSMCs), whereas MCPIP1 deficiency reduced this decrease. MCPIP1 deficiency also attenuated Ang II-induced expression of MAPK signaling-associated proteins in aortas and VSMCs. Silencing MCPIP1 decreased proliferation and migration in Ang II-induced VSMCs. Furthermore, inactivation of ERK1/2 with PD98059 reduced Ang II-induced proliferation and migration of VSMCs. Dual luciferase and chromatin immunoprecipitation assay results confirmed that MCPIP1 was transcriptionally regulated by KLF4. KLF4 knockdown reversed the facilitating effect of Ang II on MCPIP1 expression. In conclusion, our findings suggest that MCPIP1 promotes Ang II-induced VSMCs phenotypic switching via the MAPK signaling pathway.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-12"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144246217","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 future of scientific research-centralized expertise and specialization through full-service core facilities. 未来的科研集中的专业知识和专业化通过全方位服务的核心设施。

IF 2.1 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2025-0244

James Jonkman, Troy Ketela, Nhu-An Pham, Nikolina Radulovich, Genevieve Gasmi-Seabrook, Aaron D Schimmer

{"title":"The future of scientific research-centralized expertise and specialization through full-service core facilities.","authors":"James Jonkman, Troy Ketela, Nhu-An Pham, Nikolina Radulovich, Genevieve Gasmi-Seabrook, Aaron D Schimmer","doi":"10.1139/bcb-2025-0244","DOIUrl":"10.1139/bcb-2025-0244","url":null,"abstract":"Research is undergoing a paradigm shift. High-impact discoveries frequently require multidisciplinary approaches and are increasing in technological complexity. The days in which a single trainee can master all of the knowledge and technical skills necessary to complete a project by themselves are passing. In this evolving landscape, scientific cores-centralized facilities that provide advanced technologies and expert guidance-are becoming indispensable to the research pipeline. In this editorial, we suggest how core facilities in academic centers can evolve to meet these changes in research expectations by acting as full-service facilities, or like academic contract research organizations. In this new model, full-service cores will offer comprehensive project support, including the execution of the experiment. This paradigm shift will speed discovery, but requires modifications to existing research culture, including changing lab and project management approaches, increased recognition of the role of core directors and revised training expectations. Investigators and trainees will be expected to master narrow analytical but broad conceptual domains, while scientific cores will provide the technical and multidisciplinary expertise required to generate complex datasets. Revising the existing model will also require significant financial investment from host institutions and funding agencies. While initially challenging to implement, we predict that early adopters of this new model will be at the forefront of scientific discovery.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":"103 ","pages":"1-4"},"PeriodicalIF":2.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145136273","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