Cell Biology International最新文献_第8页

The p. Arg¹⁸⁰⁰His Mutation of Factor VIII Results in Moderate Hemophilia A Due to Defective Processing and Stability of Functional Protein. 由于功能蛋白加工和稳定性缺陷，p. Arg1800His因子VIII突变导致中度血友病A。

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-05-01 DOI: 10.1002/cbin.70164

Han Wang, Jiaqi Tian, Ming Zhang, Liyuan Zhang, Chunxia Liu, Lu Niu, Wenjuan Jia

{"title":"The p. Arg1800His Mutation of Factor VIII Results in Moderate Hemophilia A Due to Defective Processing and Stability of Functional Protein.","authors":"Han Wang, Jiaqi Tian, Ming Zhang, Liyuan Zhang, Chunxia Liu, Lu Niu, Wenjuan Jia","doi":"10.1002/cbin.70164","DOIUrl":"10.1002/cbin.70164","url":null,"abstract":"Haemophilia A (HA) is a rare congenital, recessive X-linked bleeding disorders caused by the lack or deficiency of clotting factor VIII (FVIII). Missense variants, which can alter protein structure, conformation and immunogenicity, are found in nearly all individuals with mild or moderate hemophilia A but in fewer than 20% of those with the severe form. Here, we identified a 26-year-old man with a hemizygous F8 mutation (NM_000132.4(F8):c.5399 G > A (p. Arg1800His)) through direct sequencing of all exons of the F8 gene, which is established to cause a lack of FVIII:c (%) in circulating blood and leads to moderate HA. In addition, we also provide evidence for the reduced active FVIII (FVIII:c (%)) caused by p. Arg1800His mutation. In detail, we show that p. Arg1800His mutation may activate the unfolded protein response through IRE1a-XBP1 pathway and reduce stability of FVIII. Results from co-immunoprecipitation assays showed that p. Arg1800His mutation decreases the interaction between FVIII and PDIA5. Furthermore, unbiased molecular dynamics simulations highlight the importance of Arg1800 in the interactions FVIII and von Willebrand factor. These findings demonstrate the crucial role of Arg1800 in the correct biogenesis of FVIII and shed light on molecular mechanisms through which missense mutations in FVIII contribute to the development of moderate hemophilia A.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 5","pages":"e70164"},"PeriodicalIF":3.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147940140","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

osr1 as a Novel Marker for ICC-Like Cells Development in Zebrafish. osr1作为斑马鱼icc样细胞发育的新标志物

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-05-01 DOI: 10.1002/cbin.70162

Wenmin Yang, Xiaoqin Tan, Peng He, Zhongwei He, Yunfeng Zhang, TingTing Tian, Yan Li, Ting Yu, Furong Li, Mingzhou Zhang, Xiaoliang Liu, Chi Liu

{"title":"osr1 as a Novel Marker for ICC-Like Cells Development in Zebrafish.","authors":"Wenmin Yang, Xiaoqin Tan, Peng He, Zhongwei He, Yunfeng Zhang, TingTing Tian, Yan Li, Ting Yu, Furong Li, Mingzhou Zhang, Xiaoliang Liu, Chi Liu","doi":"10.1002/cbin.70162","DOIUrl":"10.1002/cbin.70162","url":null,"abstract":"Interstitial cells of Cajal (ICCs) are essential for maintaining normal intestinal function, and their dysfunction is closely associated with various gastrointestinal diseases. However, the developmental process of ICCs and their role in intestinal development remain unclear. In this study, we analyzed single-cell transcriptome data and found that odd-skipped-related 1 (OSR1) is expressed in the intestinal tissues of humans and zebrafish. Additionally, OSR1 expression was reduced in tissue biopsies obtained from IBD patients. To further explore the function of osr1 in intestinal development and disease, we generated transgenic lines Tg(osr1:mCherry) and Tg(osr1:eGFP). Furthermore, we found that these transgenic fish could label interstitial cells of Cajal-like cells (ICC-like cells) from 48 h post-fertilization (hpf) to adulthood. osr1-positive ICC-like cells form a network structure that envelops the intestine and coordinates its development. Moreover, mutations in osr1 lead to developmental defects in the intestine, characterized by disrupted ICC-like cells network structure, intestinal wall hypoplasia, and increased intestinal permeability, potentially mediated through the regulation of yap1. Overall, our findings indicate that osr1 acts as a novel marker gene for ICC-like cells and plays a crucial role in intestinal development.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 5","pages":"e70162"},"PeriodicalIF":3.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147927055","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

ATRX Knockdown Enhances Irradiation-Induced Mitotic Catastrophe in p53-Deficient Cancer Cells. ATRX敲低增强辐照诱导的p53缺陷癌细胞有丝分裂灾难。

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-05-01 DOI: 10.1002/cbin.70161

Lijing Qin, Rongrong Liu, Weiqiang Xu, Lei Yu, Wen Li, Xinru Lian, Zhicheng Wang

{"title":"ATRX Knockdown Enhances Irradiation-Induced Mitotic Catastrophe in p53-Deficient Cancer Cells.","authors":"Lijing Qin, Rongrong Liu, Weiqiang Xu, Lei Yu, Wen Li, Xinru Lian, Zhicheng Wang","doi":"10.1002/cbin.70161","DOIUrl":"10.1002/cbin.70161","url":null,"abstract":"Induction of mitotic catastrophe (MC), a tumor suppressor mechanism to maintain genomic stability, with exogenous agents is a promising therapeutic endpoint. During cell division, mitotic defects and DNA damage can lead to mitotic failure and eventual MC. Alpha-thalassemia/mental retardation syndrome X-linked (ATRX) play an important role in DNA replication and damage repair, in addition to enhancing sister chromatid cohesion to maintain mitosis. However, the effects of ATRX knockdown (KD) on irradiation-induced MC and the underlying mechanism remain unclear. Therefore, the aim of the present study was to clarify the effects and mechanisms of ATRX KD on irradiation-induced MC in p53-wild type, p53-deficient and p53-mutant cancer cells. The results showed that irradiation induced G2/M phase arrest in three cells, while ATRX KD induced additional G1 phase arrest and S phase delay in irradiated HCT116 p53+/+ cells. Notably, ATRX KD induced typical characteristics of MC exclusively in p53-deficient (HCT116 p53-/-) and p53-mutant (MDA-MB-231) cells but not in p53-proficient HCT116 counterparts. This effect was mechanistically linked to the downregulation of spindle assembly checkpoint (SAC) and chromosomal passenger complex (CPC) component proteins, which exacerbated irradiation-induced MC and consequently enhanced radiation-induced proliferation inhibition and apoptosis in HCT116 p53-/- cells.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 5","pages":"e70161"},"PeriodicalIF":3.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147863670","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

Lipoxin A4 and Resolvin D1 Preserve Neural Inductive Capacity of Dental Pulp Stem Cells Cultured Under Inflammatory Conditions. 脂素A4和Resolvin D1维持炎症条件下培养的牙髓干细胞的神经诱导能力。

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-05-01 DOI: 10.1002/cbin.70163

Ana Paula Turrioni, Geovana Pires da Silva, Yan Xu, Alpdogan Kantarci, Hatice Hasturk, Ricardo A Battaglino, Leslie R Morse

{"title":"Lipoxin A4 and Resolvin D1 Preserve Neural Inductive Capacity of Dental Pulp Stem Cells Cultured Under Inflammatory Conditions.","authors":"Ana Paula Turrioni, Geovana Pires da Silva, Yan Xu, Alpdogan Kantarci, Hatice Hasturk, Ricardo A Battaglino, Leslie R Morse","doi":"10.1002/cbin.70163","DOIUrl":"10.1002/cbin.70163","url":null,"abstract":"Human dental pulp stem cells (DPSCs) exhibit neurogenic differentiation potential; however, inflammatory conditions may impair this process. This study investigated the impact of tumor necrosis factor alpha (TNF-α) on the neurodifferentiation potential of DPSCs and the modulatory role of the pro-resolving lipid mediators lipoxin A4 (LXA4) and resolvin D1 (RvD1). DPSCs were isolated and subjected to neuronal differentiation for 21 days. Cells were treated with different concentrations of TNF-α (1, 10, 25, and 100 ng/mL) and with LXA4 or RvD1 (10 and 100 nM). After 21 days, neuronal differentiation was associated with a reduction in the stem cell marker OCT3/4 (53% in the absence of TNF-α and 48.5% in the presence of TNF-α) and increased expression of the early neuronal marker doublecortin (87% in the absence of TNF-α and 116% in the presence of TNF-α). The intermediate neuronal marker βIII-tubulin increased by 135% in the absence of TNF-α but decreased by 40% in its presence. The reduction in βIII-tubulin induced by 25 ng/mL TNF-α was partially attenuated by treatment with 100 nM RvD1 (p = 0.02) or 10 nM LXA4 (p = 0.02). These findings suggest that LXA4 and RvD1 help preserve the neural differentiation potential of DPSCs cultured under inflammatory conditions.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 5","pages":"e70163"},"PeriodicalIF":3.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13184579/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147970699","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}

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IF 3.1 3区生物学

Cell Biology International Pub Date : 2026-04-16

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IF 3.1 3区生物学

Cell Biology International Pub Date : 2026-04-16

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IF 3.1 3区生物学

Cell Biology International Pub Date : 2026-04-15

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IF 3.1 3区生物学

Cell Biology International Pub Date : 2026-04-15

引用次数: 0

Unlocking Cancer Immunity: Deciphering the Role of Tumor-Associated Macrophages in Modulating Immunosuppressive Tumor Microenvironment 解锁癌症免疫：解读肿瘤相关巨噬细胞在调节免疫抑制肿瘤微环境中的作用。

IF 3.1 3区生物学

Cell Biology International Pub Date : 2026-04-04 DOI: 10.1002/cbin.70156

Durre Aden, Samreen Zaheer, Sufian Zaheer

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Synergistic Combinations for Improved Therapeutic Outcomes in Triple Negative Breast Cancer. 协同组合改善三阴性乳腺癌的治疗效果。

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-04-01 DOI: 10.1002/cbin.70157

Avani Jha, Shashi Kumar Sampangin Venkatesh, Anuradha Singh, Naga Rajiv Lakkaniga

{"title":"Synergistic Combinations for Improved Therapeutic Outcomes in Triple Negative Breast Cancer.","authors":"Avani Jha, Shashi Kumar Sampangin Venkatesh, Anuradha Singh, Naga Rajiv Lakkaniga","doi":"10.1002/cbin.70157","DOIUrl":"10.1002/cbin.70157","url":null,"abstract":"Triple-negative breast cancer (TNBC) is a biologically aggressive and clinically challenging subtype of breast cancer, defined by the absence of hormone receptors and HER2 amplification. This limits the applicability of targeted therapies and contributes to poor prognosis. Emerging evidence underscores the therapeutic importance of rationally designed combination regimens capable of generating synergy by simultaneously engaging complementary oncogenic vulnerabilities. Synergistic combinations, such as dual blockade of PI3K/AKT and MAPK signalling, co-inhibition of DNA repair pathways (PARP with ATR or WEE1), and the integration of immune checkpoint inhibitors with chemotherapy, angiogenesis blockade, or epigenetic modifiers, enhance tumour control by disrupting adaptive resistance, promoting immunogenic cell death and remodelling the tumour microenvironment. These strategies exploit synthetic lethality and reverse immune exclusion, often yielding effects greater than the sum of individual agents. Increasing clinical evidence suggests that synergy-based therapeutic design may improve outcomes in TNBC by converting transient responses into durable remissions. Herein, we review the mechanistic insights and translational data that support synergy-driven polytherapy as a foundational paradigm in the evolving management of TNBC.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 4","pages":"e70157"},"PeriodicalIF":3.5,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147697716","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