Cellular and Molecular Life Sciences最新文献_第9页

Syndecan-3 positively regulates the pro-inflammatory function of macrophages. Syndecan-3正调控巨噬细胞的促炎功能。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-04-07 DOI: 10.1007/s00018-025-05649-1

So Young Lee, Endika Prieto-Fernández, Leire Egia-Mendikute, Asier Antoñana-Vildosola, Paloma Velasco-Beltrán, Alexandre Bosch, Borja Jimenez-Lasheras, Ander de Blas, Jone Etxaniz-Diaz de Durana, Eunate Valdaliso-Díez, Laura Bozal-Basterra, Amaia Ercilla, José Ezequiel Martin, Arkaitz Carracedo, Alena Gros, Ana M Aransay, Asís Palazón, Lorena Pérez-Gutiérrez

{"title":"Syndecan-3 positively regulates the pro-inflammatory function of macrophages.","authors":"So Young Lee, Endika Prieto-Fernández, Leire Egia-Mendikute, Asier Antoñana-Vildosola, Paloma Velasco-Beltrán, Alexandre Bosch, Borja Jimenez-Lasheras, Ander de Blas, Jone Etxaniz-Diaz de Durana, Eunate Valdaliso-Díez, Laura Bozal-Basterra, Amaia Ercilla, José Ezequiel Martin, Arkaitz Carracedo, Alena Gros, Ana M Aransay, Asís Palazón, Lorena Pérez-Gutiérrez","doi":"10.1007/s00018-025-05649-1","DOIUrl":"10.1007/s00018-025-05649-1","url":null,"abstract":"The tumour microenvironment (TME) is a highly structured ecosystem that surrounds a tumour and plays a crucial role in tumorigenesis. As one of the most abundant cell types in the TME, tumour-associated-macrophages (TAMs) can promote disease progression and resistance to therapy. Syndecan-3 (SDC3) is a cell-surface heparan sulphate proteoglycan expressed by TAMs, although its functional relevance in these cells remains unknown. Here, we demonstrated that pro-inflammatory cytokines drive the expression of SDC3 on the cell surface of macrophages. Genetic ablation of SDC3 in macrophages led to aberrant proliferation, adhesion and expression of CD40 and CD86 surface markers. Moreover, SDC3 defective macrophages exhibited distinctive gene expression patterns, leading to impaired tumour cell phagocytosis and increased tumour cell proliferation. Mechanistically, a decrease in the secretion of pro-inflammatory cytokines was observed in SDC3 KO macrophages, concomitant with impaired T cell effector functions. Additionally, a higher angiogenic capacity was observed in endothelial cells when co-cultured with macrophages deficient for SDC3, possibly mediated through an increased release of VEGFA, PECAM-1 and IL-8 by SDC3 KO cells. Collectively, we have identified SDC3 as a modulator of macrophage functions aiming at supporting a pro-inflammatory and anti-tumour phenotype in these cells.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"145"},"PeriodicalIF":6.2,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11977058/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

An update on mammalian and non-mammalian animal models for biomarker development in neurodegenerative disorders. 神经退行性疾病中生物标志物发育的哺乳动物和非哺乳动物模型的最新进展。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-04-07 DOI: 10.1007/s00018-025-05668-y

Ribhav Mishra, Arun Upadhyay

{"title":"An update on mammalian and non-mammalian animal models for biomarker development in neurodegenerative disorders.","authors":"Ribhav Mishra, Arun Upadhyay","doi":"10.1007/s00018-025-05668-y","DOIUrl":"10.1007/s00018-025-05668-y","url":null,"abstract":"Neurodegeneration is one of the leading factor for death globally, affecting millions of people. Developing animal models are critical to understand biological processes and comprehend pathological hallmarks of neurodegenerative diseases. For decades, many animal models have served as excellent tools to determine the disease progression, develop diagnostic methods and design novel therapies against distinct pathologies. Here, we provide a comprehensive overview of both, mammalian and non-mammalian animal models, with a focus on three most common and aggressive neurodegenerative disorders: Alzheimer's disease, Parkinson's disease and Spinocerebellar ataxia-1. We highlight various approaches including transgene, gene transfer, and chemically-induced methods used to develop disease models. In particular, we discuss applications of both non-mammalian and mammalian contributions in research on neurodegeneration. It is exciting to learn the roles of animal models in disease pathomechanisms, identifying biomarkers and hence devising novel interventions to treat neuropathological conditions.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"147"},"PeriodicalIF":6.2,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11977071/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Mosquito immune responses to Plasmodium parasites that limit malaria transmission. 蚊子对疟原虫的免疫反应限制疟疾的传播。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-04-07 DOI: 10.1007/s00018-025-05667-z

Ana Beatriz F Barletta, Carolina Barillas-Mury, Alvaro Molina-Cruz

引用次数: 0

Single-cell transcriptomics reveals liver developmental trajectory during lineage reprogramming of human induced hepatocyte-like cells. 单细胞转录组学揭示了人类诱导的肝细胞样细胞谱系重编程过程中的肝脏发育轨迹。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-04-06 DOI: 10.1007/s00018-025-05677-x

Nan Jiang, Guangya Li, Sen Luo, Xi Kong, Shigang Yin, Jianhua Peng, Yong Jiang, Wei Tao, Cheng Li, Huangfan Xie, Hongkui Deng, Bingqing Xie

{"title":"Single-cell transcriptomics reveals liver developmental trajectory during lineage reprogramming of human induced hepatocyte-like cells.","authors":"Nan Jiang, Guangya Li, Sen Luo, Xi Kong, Shigang Yin, Jianhua Peng, Yong Jiang, Wei Tao, Cheng Li, Huangfan Xie, Hongkui Deng, Bingqing Xie","doi":"10.1007/s00018-025-05677-x","DOIUrl":"10.1007/s00018-025-05677-x","url":null,"abstract":"Hepatocytes are crucial for drug screening, disease modeling, and clinical transplantation, yet generating functional hepatocytes in vitro is challenging due to the difficulty of establishing their authentic gene regulatory networks (GRNs). We have previously developed a two-step lineage reprogramming strategy to generate functionally competent human induced hepatocytes (hiHeps), providing an effective model for studying the establishment of hepatocyte-specific GRNs. In this study, we utilized high-throughput single-cell RNA sequencing (scRNA-seq) to explore the cell-fate transition and the establishment of hepatocyte-specific GRNs involved in the two-step reprogramming process. Our findings revealed that the late stage of the reprogramming process mimics the natural trajectory of liver development, exhibiting similar transcriptional waves of developmental genes. CD24 and DLK1 were identified as surface markers enriching two distinct hepatic progenitor populations respectively. Lipid metabolism emerged as a key enhancer of hiHeps maturation. Furthermore, transcription factors HNF4A and HHEX were identified as pivotal gatekeepers directing cell fate decisions between hepatocytes and intestinal cells. Collectively, this study provides valuable insights into the establishment of hepatocyte-specific GRNs during hiHeps induction at single-cell resolution, facilitating more efficient production of functional hepatocytes for therapeutic applications.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"139"},"PeriodicalIF":6.2,"publicationDate":"2025-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11973031/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Metabolic flux analysis in hiPSC-CMs reveals insights into cardiac dysfunction in propionic acidemia. hiPSC-CMs的代谢通量分析揭示了丙酸血症心功能障碍的见解。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-04-02 DOI: 10.1007/s00018-025-05661-5

Eva Richard, Hannah Marchuk, Mar Álvarez, Wentao He, Xiaoxin Chen, Lourdes R Desviat, Guo-Fang Zhang

{"title":"Metabolic flux analysis in hiPSC-CMs reveals insights into cardiac dysfunction in propionic acidemia.","authors":"Eva Richard, Hannah Marchuk, Mar Álvarez, Wentao He, Xiaoxin Chen, Lourdes R Desviat, Guo-Fang Zhang","doi":"10.1007/s00018-025-05661-5","DOIUrl":"10.1007/s00018-025-05661-5","url":null,"abstract":"Propionic acidemia is an inborn error of metabolism caused by mutations in either the PCCA or PCCB genes. Patients with propionic acidemia experience a range of complications, including life-threatening cardiac dysfunctions. However, the pathological mechanisms underlying propionic acidemia-associated cardiac diseases remain largely unknown. To gain insights into the metabolic alterations in propionic acidemia, we studied human induced pluripotent stem cell-derived cardiomyocytes generated from a patient with propionic acidemia with two pathogenic PCCA mutations (p.Cys616_Val633del and p.Gly477Glufs9*) and from a healthy individual. Using stable isotope-based metabolic flux analysis, we confirmed that the PCCA mutations lead to impaired propionyl-CoA carboxylase activity in human induced pluripotent stem cell-derived cardiomyocytes. In addition to being converted to propionylcarnitine, the accumulated propionyl-CoA can also be hydrolyzed to propionate and exported out of the cell, serving as a secondary \"pressure valve\" to regulate cellular propionyl-CoA levels. Interestingly, the deficiency of propionyl-CoA carboxylase was found to shift fuel metabolism from fatty acid oxidation to increased glucose metabolism human in induced pluripotent stem cell-derived cardiomyocytes from patients with propionic acidemia. This metabolic switch is less energy-efficient and may contribute to the development of chronic cardiac dysfunction in patients with propionic acidemia.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"137"},"PeriodicalIF":6.2,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11965053/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143763035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

PRDM16 suppresses pyroptosis to attenuate the progression of AKI caused by rhabdomyolysis via upregulation of USP10. PRDM16通过上调USP10抑制焦亡，减轻横纹肌溶解引起的AKI的进展。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-04-02 DOI: 10.1007/s00018-025-05666-0

Bocheng Han, Qiang Zheng, Huiling Li, Yongjun Wang, Dongshan Zhang

{"title":"PRDM16 suppresses pyroptosis to attenuate the progression of AKI caused by rhabdomyolysis via upregulation of USP10.","authors":"Bocheng Han, Qiang Zheng, Huiling Li, Yongjun Wang, Dongshan Zhang","doi":"10.1007/s00018-025-05666-0","DOIUrl":"10.1007/s00018-025-05666-0","url":null,"abstract":"Previous studies have indicated that PRDM16 suppresses apoptosis and ferroptosis, thereby mitigating the development of AKI triggered by ischemia, cisplatin, and sepsis. Nevertheless, the exact function and control mechanisms of PRDM16 in rhabdomyolysis-induced AKI are not fully understood. In this investigation, PRDM16 was found to inhibit ferrous myoglobin-induced pyroptosis in Boston University mouse proximal tubule (BUMPT) cells. At the molecular level, PRDM16 binds to the USP10 promoter, enhancing its expression and subsequently inhibiting the NLRP3-Caspase1-GSDMD and Caspase3-GSDME pathways. Rhabdomyolysis-induced AKI was alleviated in PRDM16 KI mice, whereas PRDM16 KO exacerbated the condition. Furthermore, PNPs-encapsulated formononetin significantly attenuated the progression of rhabdomyolysis-induced AKI. In conclusion, PRDM16 suppresses pyroptosis and ameliorates rhabdomyolysis-induced AKI by regulating the USP10/NLRP3-Caspase1-GSDMD and Caspase3-GSDME pathways. PNPs-encapsulated formononetin emerges as a promising therapeutic strategy.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"138"},"PeriodicalIF":6.2,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11965059/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Siglec-15 is a putative receptor for porcine epidemic diarrhea virus infection. siglece -15被认为是猪流行性腹泻病毒感染的受体。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-04-02 DOI: 10.1007/s00018-025-05672-2

Zhihua Feng, Yajuan Fu, Sheng Yang, Heng Zhao, Minhua Lin, Chuancheng Liu, Weili Huang, Xinyan He, Yao Chen, Jianxin Chen, Yangkun Shen, Zhaolong Li, Qi Chen

{"title":"Siglec-15 is a putative receptor for porcine epidemic diarrhea virus infection.","authors":"Zhihua Feng, Yajuan Fu, Sheng Yang, Heng Zhao, Minhua Lin, Chuancheng Liu, Weili Huang, Xinyan He, Yao Chen, Jianxin Chen, Yangkun Shen, Zhaolong Li, Qi Chen","doi":"10.1007/s00018-025-05672-2","DOIUrl":"10.1007/s00018-025-05672-2","url":null,"abstract":"Porcine epidemic diarrhea virus (PEDV) has caused significant losses in the pork industry, but the mechanism of PEDV infection is still unclear. On the basis of our RNA-Seq data and due to the potential role of sialic acid as a coreceptor, we investigated the function of sialic acid-binding Ig-like lectin 15 (Siglec-15) to determine its role as a receptor in PEDV infection. We found that Siglec-15 enhances PEDV infection by promoting viral adsorption to host cells. Coimmunoprecipitation and immunofluorescence assays revealed that Siglec-15 binds to the S1 subunit and M protein of PEDV. PEDV infectivity was significantly reduced in Siglec-15 knockout mice. In addition, we developed a monoclonal antibody targeting Siglec-15 that can effectively inhibit PEDV infection both in vitro and in vivo. Overall, our study suggests that Siglec-15 may be a receptor for PEDV infection, which is important for related mechanistic studies and reveals a novel target for anti-PEDV therapeutic development.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"136"},"PeriodicalIF":6.2,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11965083/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143763038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Genome-wide profiling and functional characterization of circular RNAs in neural development and injury: insights from a rat model research. 环状rna在神经发育和损伤中的全基因组分析和功能表征：来自大鼠模型研究的见解。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-04-01 DOI: 10.1007/s00018-025-05665-1

Jian Yang, Nana Jin, Shuqiang Zhang, Ya Tan, Zhifeng Chen, Xiaoli Huang, Guicai Li, Bin Yu, Jianhua Shi, Xiaosong Gu, Zhiming Cui, Lian Xu

{"title":"Genome-wide profiling and functional characterization of circular RNAs in neural development and injury: insights from a rat model research.","authors":"Jian Yang, Nana Jin, Shuqiang Zhang, Ya Tan, Zhifeng Chen, Xiaoli Huang, Guicai Li, Bin Yu, Jianhua Shi, Xiaosong Gu, Zhiming Cui, Lian Xu","doi":"10.1007/s00018-025-05665-1","DOIUrl":"10.1007/s00018-025-05665-1","url":null,"abstract":"Circular RNAs (circRNAs) have re-emerged as promising gene regulators in various physiological and pathological conditions. However, the expression patterns of circRNAs in the developing spinal cord of mammals and the comprehensive distribution of circRNAs across different tissues remain poorly understood. In this study, rats were used as the model organism. We conducted a comprehensive analysis of 15 RNA-Seq datasets comprising 217 rat samples and developed a web-based resource, CiRNat, to facilitate access to these data. We identified 15,251 credible circRNAs and validated them through experimental approaches. Notably, we observed two significant time points for circRNA increase during spinal cord development, approximately at embryonic day 14 (E14d) and postnatal week 4 (P4w). Analysis of circRNA expression in various rat tissues revealed higher expression levels in central nervous system tissues compared to peripheral nervous system tissues and other tissues. Furthermore, some highly abundant circRNAs exhibited tissue- and species-specific expression patterns and differed from their cognate linear RNAs, such as those derived from Gigyf2. Integrating polysome profiling and bioinformatic predictions suggested potential functions of certain circRNAs as miRNA sponges and translational templates. Collectively, this study provides the first comprehensive landscape of circRNAs in the developing spinal cord, offering an important resource and new insights for future exploration of functional circRNAs in central nervous system development and related diseases.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"135"},"PeriodicalIF":6.2,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11961807/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143763032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Dysregulated cholesterol uptake and efflux of bone marrow-derived α-SMA⁺ macrophages contribute to atherosclerotic plaque formation. 骨髓源性α-SMA+巨噬细胞的胆固醇摄取和外排失调有助于动脉粥样硬化斑块的形成。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-03-30 DOI: 10.1007/s00018-025-05655-3

Menglu Li, Lili Wu, Yuxin Wen, Anni Wang, Xiao Zhou, Lijie Ren, Qiongyu Lu, Fengchan Li, Li Zhu, Chaojun Tang

{"title":"Dysregulated cholesterol uptake and efflux of bone marrow-derived α-SMA+ macrophages contribute to atherosclerotic plaque formation.","authors":"Menglu Li, Lili Wu, Yuxin Wen, Anni Wang, Xiao Zhou, Lijie Ren, Qiongyu Lu, Fengchan Li, Li Zhu, Chaojun Tang","doi":"10.1007/s00018-025-05655-3","DOIUrl":"10.1007/s00018-025-05655-3","url":null,"abstract":"Macrophages play differential roles in the pathogenesis of atherosclerosis due to their different phenotypes. Although α-SMA+ macrophages have been found to present in bone marrow and atherosclerotic plaques, their role in atherosclerosis remains unclear. By performing partial carotid ligation (PCL) on monocyte/macrophage lineage-tracked mice, we observed bone marrow-derived α-SMA+ macrophages in the subendothelium and atherosclerotic plaques under disturbed flow conditions. The functional role of α-SMA+ macrophages in atherosclerotic plaque formation was examined using macrophage-specific Acta2 knockout (Acta2MKO) mice generated by crossing Acta2f/f transgenic mice with LysM-Cre mice. The size of the aortic plaques was 77.43% smaller in Acta2MKO mice than in Acta2f/f mice following adeno-associated virus-mutant PCSK9 injection and high-fat diet (HFD) feeding for 12 weeks. A significant reduction in lipid deposition, macrophage infiltration and the α-SMA+ area was observed in the aortic roots of Acta2MKO mice compared with Acta2f/f mice. Mechanistically, using Acta2-overexpressing Raw264.7 cells (Acta2hi cells) and bone marrow-derived macrophages (BMDMs) from Acta2MKO mice (Acta2MKO BMDMs), we showed that macrophage α-SMA increased the expression of the scavenger receptor SR-A, induced Ox-LDL binding and uptake, and reduced the level of the cholesterol transporter ABCA1, potentially via the AKT pathway. Together, our results indicate that bone marrow-derived α-SMA+ macrophages contribute to atherosclerotic plaque formation due to dysregulated cholesterol uptake and efflux, providing potential targets for the prevention and treatment of atherosclerosis.","PeriodicalId":10007,"journal":{"name":"Cellular and Molecular Life Sciences","volume":"82 1","pages":"134"},"PeriodicalIF":6.2,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11955436/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143751459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Correction: Histone demethylase KDM4A regulates adipogenic and osteogenic differentiation via epigenetic regulation of C/EBPα and canonical Wnt signaling. 纠正：组蛋白去甲基化酶KDM4A通过表观遗传调控C/EBPα和典型Wnt信号传导调节成脂和成骨分化。

IF 6.2 2区生物学

Cellular and Molecular Life Sciences Pub Date : 2025-03-28 DOI: 10.1007/s00018-024-05569-6

Qi Qi, Yi Wang, Xiaochen Wang, Junying Yang, Yan Xie, Jie Zhou, Xiaoxia Li, Baoli Wang

引用次数: 0