Journal of cellular biochemistry最新文献_第2页

RETRACTION: MicroRNA-141 Binds to the Nerve Growth Factor Receptor Associated Protein 1 Gene and Restores the Erectile Function of Diabetic Rats through Down-Regulating the Nerve Growth Factor/Neurotrophin Receptor P75 (NGF/p75NTR) Signaling 缩回：MicroRNA-141结合神经生长因子受体相关蛋白1基因，通过下调神经生长因子/神经营养因子受体P75 （NGF/p75NTR）信号通路恢复糖尿病大鼠勃起功能。

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2026-09-10 DOI: 10.1002/jcb.70121

引用次数: 0

Targeting FOXP3 and Regulatory T Cells in Systemic Lupus Erythematosus: Emerging Therapeutic Strategies and Clinical Prospects 靶向FOXP3和调节性T细胞治疗系统性红斑狼疮：新的治疗策略和临床前景

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2026-09-08 DOI: 10.1002/jcb.70124

Shushu Du, Wenqi Xu, Lili Zhao, Xiaofei Shi, Rongzeng Liu

{"title":"Targeting FOXP3 and Regulatory T Cells in Systemic Lupus Erythematosus: Emerging Therapeutic Strategies and Clinical Prospects","authors":"Shushu Du, Wenqi Xu, Lili Zhao, Xiaofei Shi, Rongzeng Liu","doi":"10.1002/jcb.70124","DOIUrl":"10.1002/jcb.70124","url":null,"abstract":"<div>\u0000 \u0000 Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with multi-system involvement, and its pathogenesis is complex, involving abnormalities of multiple immune cells and molecules. In recent years, the role of the transcription factor Forkhead Box P3 (FOXP3) in SLE has attracted much attention. FOXP3, a crucial indicator of regulatory T cells (Tregs), is essential for maintaining immune tolerance and suppressing excessive immune responses. This review systematically elucidates the multi-tiered regulatory networks that control FOXP3 expression at the transcriptional, epigenetic, and post-translational levels. It further examines the specific phenotypic alterations and molecular mechanisms responsible for the dysregulation of Treg quantity, function, and stability within the SLE milieu, including factors such as interleukin (IL)-2 deficiency, cytokine storms, and epigenetic abnormalities. Building upon this foundation, the article explores a range of emerging therapeutic strategies targeting FOXP3 and Tregs as central elements, highlighting recent advances and clinical translation prospects in low-dose IL-2 therapy, adoptive Treg cell transfer, and epigenetic drug interventions. Ultimately, we propose that the precise modulation and enhancement of Treg function to restore stable immune tolerance in SLE patients constitutes a novel therapeutic paradigm, transitioning from broad immunosuppression toward targeted immune modulation. This strategy holds significant promise for fundamentally improving the therapeutic landscape of this complex autoimmune disorder.\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"127 9","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148912130","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

H3K18 Lactylation Promotes Cell Proliferation in T-Cell Acute Lymphoblastic Leukemia H3K18乳酸化促进t细胞急性淋巴母细胞白血病细胞增殖

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2026-09-02 DOI: 10.1002/jcb.70120

Lingling Feng, Xia Jin, Juan Zhang, Zong Zhai, Xiaohua Zhang, Yi Wang

{"title":"H3K18 Lactylation Promotes Cell Proliferation in T-Cell Acute Lymphoblastic Leukemia","authors":"Lingling Feng, Xia Jin, Juan Zhang, Zong Zhai, Xiaohua Zhang, Yi Wang","doi":"10.1002/jcb.70120","DOIUrl":"https://doi.org/10.1002/jcb.70120","url":null,"abstract":"<div>\u0000 \u0000 The Warburg effect-induced lactate production in T-cell acute lymphoblastic leukemia (T-ALL) cell proliferation is well established, however, the role of lactate-mediated protein lactylation in this process remains poorly understood. In this study, we demonstrated that inhibiting lactate levels through the lactate dehydrogenase A (LDHA) inhibitor significantly reduced both cell proliferation and protein lactylation levels in T-ALL cells. Lactate deficiency led to a marked decrease in protein lactylation, accompanied by impaired cell proliferation. Meanwhile, lactate deficiency also induced the S‑phase cell cycle arrest and reduced DNA synthesis, which collectively impaired cell proliferation. Mechanistically, we observed that the decreased expression of lactylation in histone H3 at lysine 18 (H3K18lac) reduced the enrichment of this mark on the promoter region of neurotrophic receptor tyrosine kinase 3 (NTRK3), which supported the cell proliferation of T-ALL cells. Moreover, the overexpression of NTRK3 rescued the lactate deficiency-induced proliferation inhibition of T-ALL cells. Furthermore, exogenous lactate supplementation dramatically restored the decreased cell proliferation in T-ALL cells and restored H3K18lac levels. Our findings reveal a novel role of lactate-mediated protein lactylation in regulating T-ALL cell proliferation.\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"127 9","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148872061","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}

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Impacts of N-glycanase1 (NGLY1) Down Regulation on the Function of Mitochondria n -甘聚糖酶1 （NGLY1）下调对线粒体功能的影响。

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2026-08-24 DOI: 10.1002/jcb.70119

Yanwen Chen, Ruijie Liu, Shaoxing Zhang, Yuxin Zhang, Qiange Lin, Yilin Ye, Shuying Yuan, Xinrong Lu, Linfei Wang, Li Chen, Guiqin Sun

引用次数: 0

Expression of Concern: Sweroside Alleviates Hepatic Steatosis in Part by Activating Ampk/Mtor-Mediated Autophagy in Mice 表达关注：甜苷通过激活Ampk/ mtor介导的小鼠自噬，部分缓解肝脂肪变性

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2026-08-20 DOI: 10.1002/jcb.70118

{"title":"Expression of Concern: Sweroside Alleviates Hepatic Steatosis in Part by Activating Ampk/Mtor-Mediated Autophagy in Mice","authors":"","doi":"10.1002/jcb.70118","DOIUrl":"https://doi.org/10.1002/jcb.70118","url":null,"abstract":"EXPRESSION OF CONCERN: Y. Ding, Y. Chen, K. Hu, Q. Yang, Y. Li, and M. Huang, “Sweroside Alleviates Hepatic Steatosis in Part by Activating AMPK/mTOR-Mediated Autophagy in Mice,” Journal of Cellular Biochemistry 124, no. 7 (2023): 1012-1022, https://doi.org/10.1002/jcb.30428.This Expression of Concern is for the above article, published online on 03 June 2023 in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, Lucie Kalvodova; and Wiley Periodicals LLC.The Expression of Concern has been issued due to methodological concerns identified during the assessment of a correction request submitted by the authors. The authors contacted the journal to report errors in Figure 1H arising from the inadvertent incorporation of incorrect image elements. During the subsequent review, verification of the raw data underlying the study revealed that, for the majority of the Western blot figures published in the article, the loading control images were derived from membranes other than those used to probe the corresponding proteins of interest. The authors provided images reported as deriving from replicate experiments not included in the published article, in which the loading controls were obtained from the same membranes as the proteins of interest. However, when requested to provide the underlying raw data to support these data, the authors did no longer respond to the journal's requests. Therefore, the journal has decided to issue an Expression of Concern to inform and alert the readers.","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"127 8","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.70118","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148784832","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

METTL14 Promotes Cuproptosis-Associated Changes in Rats With Myocardial Ischemia-Reperfusion Injury METTL14促进心肌缺血再灌注损伤大鼠铜沉淀相关变化

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2026-08-13 DOI: 10.1002/jcb.70109

Shengqiang Zeng, Dezhi Hong, Liu Yang, Yanqing Wu

{"title":"METTL14 Promotes Cuproptosis-Associated Changes in Rats With Myocardial Ischemia-Reperfusion Injury","authors":"Shengqiang Zeng, Dezhi Hong, Liu Yang, Yanqing Wu","doi":"10.1002/jcb.70109","DOIUrl":"https://doi.org/10.1002/jcb.70109","url":null,"abstract":"<div>\u0000 \u0000 To investigate the role and mechanism of METTL14-mediated regulation of cuproptosis in myocardial ischemia-reperfusion injury (MI/RI). An MI/RI rat model was established. H9C2 cells were cultured and subjected to hypoxia/reoxygenation (H/R) modeling. Cells were transfected with siRNAs targeting METTL14 and ATP7A. Cell viability was detected by CCK-8 assay. Intracellular Cu2+ levels were measured using a biochemical kit. The interaction between METTL14 and ATP7A mRNA was verified by RNA immunoprecipitation (RIP) assay. Adenovirus containing si-METTL14 was constructed and injected into rats, followed by the induction of the MI/RI model. Cardiac function was evaluated by measuring ejection fraction (EF) and fractional shortening (FS) using echocardiography. Rat myocardial tissues were collected for Hematoxylin and Eosin (HE) staining. The mRNA expression of m6A regulatory enzymes was detected by quantitative PCR (qPCR). Cu2+ levels in myocardial tissue were measured using a biochemical assay kit. The expression of cuproptosis-related proteins was assessed by Western blot. MI/RI rats showed significantly decreased FS and EF values, with necrosis and hemorrhage, increased Cu2+ content, elevated mRNA levels of FTO, METTL3, ALKBH5, and METTL14, decreased ATP7A protein expression, and increased protein expression of FDX1, LIAS, and DLAT in the myocardial tissue. Intramyocardial injection of adenovirus containing si-METTL14 reversed the MI/RI-induced changes. In vitro, decreased cell viability, increased Cu2+ content, decreased ATP7A protein expression, and increased FDX1, LIAS, and DLAT protein expression were observed in H/R stimulated H9C2 cells, which were remarkably rescued by si-METTL14. Moreover, co-transfection with both si-METTL14 and si-ATP7A reversed effects induced by si-METTL14 alone. METTL14 promotes cuproptosis-associated changes and exacerbates MI/RI.\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"127 8","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148753806","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

Elucidating the Antiglycation Potential of Plumbagin Against Methylglyoxal-Induced Glycation of Bovine Liver Catalase 阐明白桦素对甲基乙二醛诱导的牛肝过氧化氢酶糖化的抗糖化电位。

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2026-08-09 DOI: 10.1002/jcb.70117

Faiza Iram, Ayesha Aiman, Deepanshi Vijh, Gourav Choudhir, Md. Imtaiyaz Hassan, Asimul Islam

{"title":"Elucidating the Antiglycation Potential of Plumbagin Against Methylglyoxal-Induced Glycation of Bovine Liver Catalase","authors":"Faiza Iram, Ayesha Aiman, Deepanshi Vijh, Gourav Choudhir, Md. Imtaiyaz Hassan, Asimul Islam","doi":"10.1002/jcb.70117","DOIUrl":"10.1002/jcb.70117","url":null,"abstract":"<div>\u0000 \u0000 Non-enzymatic glycosylation of proteins leads to the formation of advanced glycation end products (AGEs), implicated in oxidative stress and the progression of several chronic diseases. Among the reactive carbonyl compounds, methylglyoxal (MGO) is highly potent in inducing glycoxidative damage by modifying proteins. Herein, we investigated the protective effect of plumbagin, a naphthoquinone derived from Plumbago zeylanica, to counteract MGO-induced glycation of catalase, employing integrated biophysical and computational approaches. AGE-specific fluorescence at 335 and 370 nm, ThT dye fluorescence, and microscopic visualizations confirmed that plumbagin markedly reduces AGEs formation and aggregation. Fluorescence quenching experiments revealed a stable catalase-plumbagin complex formation having binding affinity (Ka): 0.205 × 106 M−1 and a stoichiometry of one binding site (n ≈ 1.1), suggesting a single, specific binding pocket. Isothermal titration calorimetry (ITC) confirmed an exothermic, enthalpy-driven interaction. Molecular dynamics simulations (MDS) analysis displayed a more compact and ordered conformation of complex, as evidenced by reduced Rg, SASA, and RMSF values. H-bonds stabilized the complex without altering the catalytic residues (His74, Asn147, Tyr357). PCA and FEL showed complex remained confined to a single deep energy minimum, indicating enhanced thermodynamic stability. These findings highlight plumbagin as a potent multifunctional compound capable of mitigating MGO-induced glycation.\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"127 8","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148701354","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

Integrated Bioinformatic and Experimental Analysis Reveals the Molecular Mechanisms Underlying KDM1B/LSD2 Inhibition as a Therapeutic Strategy in Human Lung Adenocarcinoma 综合生物信息学和实验分析揭示了KDM1B/LSD2抑制作为人肺腺癌治疗策略的分子机制。

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2026-08-03 DOI: 10.1002/jcb.70115

Kayalvizhi Samuvel Muthiah, Sathan Raj Natarajan, Udesh Dhawan, Yu-Chien Lin, Ren-Jei Chung

{"title":"Integrated Bioinformatic and Experimental Analysis Reveals the Molecular Mechanisms Underlying KDM1B/LSD2 Inhibition as a Therapeutic Strategy in Human Lung Adenocarcinoma","authors":"Kayalvizhi Samuvel Muthiah, Sathan Raj Natarajan, Udesh Dhawan, Yu-Chien Lin, Ren-Jei Chung","doi":"10.1002/jcb.70115","DOIUrl":"10.1002/jcb.70115","url":null,"abstract":"<div>\u0000 \u0000 Lung cancer remains a major global health challenge, and the oncogenic function of KDM1B (Lysine-specific Demethylase 1B) is still poorly characterized. This study employed integrated bioinformatics and experimental approaches to investigate KDM1B's function in lung cancer. Pan-cancer analysis using databases such as TIMER revealed notably elevated KDM1B mRNA expression in LUAD datasets, suggesting its potential as a diagnostic biomarker. A strong association was also found between increased KDM1B levels and immune cell infiltration in LUAD datasets. Protein interaction networks constructed using STRING and Cytoscape revealed close associations between KDM1B and key regulatory genes in NSCLC. KEGG enrichment analysis linked KDM1B to the mTOR signaling, which is critical for cell proliferation and survival. RT-PCR and western blotting for experimental validation showed KDM1B expression was significantly increased in A549 and NCI-H460 lung cancer cells. The deletion of KDM1B inhibits cell growth, induces G0/G1 phase cell cycle arrest, and promotes apoptosis in A54 cells. Moreover, cell proliferation was significantly inhibited by the KDM1B inhibitor, tranylcypromine, and induced G0/G1 phase cell cycle arrest, increased apoptosis, ROS, and glycolytic activity in A549 cells. Collectively, these findings highlight KDM1B as a valuable therapeutic target in lung adenocarcinoma and emphasize its key role in lung cancer development.\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"127 8","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148669537","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}

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Functional Role of ALKBH5 in Kidney Injury: Insights Into Mechanisms and Therapeutic Potential ALKBH5在肾损伤中的功能作用：机制和治疗潜力的见解。

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2026-08-02 DOI: 10.1002/jcb.70114

YiFeng Dong, Danqin Lu, Yiling Wei, Huibo Wang, Cheng Yuan, Lihua Ni

引用次数: 0

EXPRESSION OF CONCERN: Cross-Talk Between T-Ag Presence and pRb Family and p53/p73 Signaling in Mouse and Human Medulloblastoma 关注表达：T-Ag存在与小鼠和人髓母细胞瘤中pRb家族和p53/p73信号传导之间的串扰

IF 3 3区生物学

Journal of cellular biochemistry Pub Date : 2026-07-29 DOI: 10.1002/jcb.70108

{"title":"EXPRESSION OF CONCERN: Cross-Talk Between T-Ag Presence and pRb Family and p53/p73 Signaling in Mouse and Human Medulloblastoma","authors":"","doi":"10.1002/jcb.70108","DOIUrl":"10.1002/jcb.70108","url":null,"abstract":"EXPRESSION OF CONCERN: V. Caracciolo, M. Macaluso, L. D'Agostino, M. Montanari, J. Scheff, K. Reiss, K. Khalili and A. Giordano, “Cross-Talk Between T-Ag Presence and pRb Family and p53/p73 Signaling in Mouse and Human Medulloblastoma,” Journal of Cellular Biochemistry 110, no. 1 (2010): 182–190, https://doi.org/10.1002/jcb.22525.This Expression of Concern is for the above article, published online on March 24, 2010, in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, Lucie Kalvodova; and Wiley Periodicals LLC. The Expression of Concern has been agreed upon following concerns raised by a third party. An investigation identified inconsistencies in the loading controls presented in Figures 4B and 6B. While the α-tubulin panels are identical across both figures, the corresponding lamin A/C controls differ. The authors acknowledged the issue and indicated that the error occurred during figure preparation. However, due to the time elapsed since the publication, they were unable to provide any original data. Although the conclusions are considered unaffected, the editors have decided to issue an Expression of Concern to inform and alert readers.","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"127 8","pages":""},"PeriodicalIF":3.0,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.70108","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148603367","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