Journal of Molecular Cell Biology最新文献_第3页

CD46 regulates hepatitis B virus entry by modulating cell-surface NTCP levels through cis-interaction. CD46通过顺式相互作用调节细胞表面NTCP水平调控乙型肝炎病毒的进入。

IF 6 2区生物学

Journal of Molecular Cell Biology Pub Date : 2026-07-03 DOI: 10.1093/jmcb/mjaf055

Kei Miyakawa, Yusuke Nakai, Taichi Kameya, Hironori Nishitsuji, Koichi Watashi, Makoto Takeda, Tsukasa Seya, Kunitada Shimotohno, Yayoi Kimura, Akihide Ryo

{"title":"CD46 regulates hepatitis B virus entry by modulating cell-surface NTCP levels through cis-interaction.","authors":"Kei Miyakawa, Yusuke Nakai, Taichi Kameya, Hironori Nishitsuji, Koichi Watashi, Makoto Takeda, Tsukasa Seya, Kunitada Shimotohno, Yayoi Kimura, Akihide Ryo","doi":"10.1093/jmcb/mjaf055","DOIUrl":"10.1093/jmcb/mjaf055","url":null,"abstract":"Hepatitis B virus (HBV) infection remains a major global health challenge. While sodium taurocholate co-transporting polypeptide (NTCP) is the primary receptor for HBV entry, the molecular mechanisms regulating NTCP-mediated viral entry remain incompletely understood. Here, we identified CD46 as a crucial regulatory factor for NTCP membrane expression. We found that CD46 interacted with NTCP in cis at the plasma membrane through proximity-based labeling screening. The depletion of CD46 significantly reduced cell-surface NTCP levels and HBV infection in hepatocytes. Anti-CD46 monoclonal antibodies, particularly clone E4.3, inhibited HBV infection by triggering NTCP internalization from the plasma membrane to intracellular vesicles. The antiviral effect of CD46 antibodies was also confirmed in primary human hepatocytes. Our study reveals a previously unknown mechanism regulating NTCP-mediated HBV entry and suggests CD46 as a potential therapeutic target for HBV infection.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13424813/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145810384","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

Sublytic C5b-9 induces S100A8/A9 expression via SMYD4-dependent SOX7-K159 methylation in the glomerular mesangial cells of Thy-1 nephritis rats. 亚溶C5b-9通过smyd4依赖性SOX7-K159甲基化诱导Thy-1肾炎大鼠肾小球系膜细胞中S100A8/A9的表达。

IF 6 2区生物学

Journal of Molecular Cell Biology Pub Date : 2026-07-03 DOI: 10.1093/jmcb/mjag003

Yajuan Gong, Mingyu Peng, Yuhua Dong, Tao Wang, Junjin Liao, Yu Li, Jing Zhang, Yingwei Wang, Wen Qiu

{"title":"Sublytic C5b-9 induces S100A8/A9 expression via SMYD4-dependent SOX7-K159 methylation in the glomerular mesangial cells of Thy-1 nephritis rats.","authors":"Yajuan Gong, Mingyu Peng, Yuhua Dong, Tao Wang, Junjin Liao, Yu Li, Jing Zhang, Yingwei Wang, Wen Qiu","doi":"10.1093/jmcb/mjag003","DOIUrl":"10.1093/jmcb/mjag003","url":null,"abstract":"Rat Thy-1 nephritis (Thy-1N) is a model for human mesangioproliferative glomerulonephritis (MsPGN). Although sublytic C5b-9 has been reported to affect pro-inflammatory cytokine expression in glomerular mesangial cells (GMCs), the induction of other pro-inflammatory mediators remains unclear. In this study, we demonstrated that SET and MYND domain-containing protein 4 (SMYD4), SRY-related HMG-box gene 7 (SOX7), S100 calcium-binding protein A8 (S100A8), and S100A9 were overexpressed in the renal tissues of Thy-1N rats and in the GMCs stimulated by sublytic C5b-9. Mechanistically, SOX7 triggered S100A8/A9 gene transcription through binding to S100A8 promoter (+21 to +31 nt) and S100A9 promoter (-1698 to -1688 nt), and SMYD4 mediated SOX7 methylation at K159, a new methylation site, enhancing SOX7 function and S100A8/A9 transcription. The animal experiments confirmed that silencing SMYD4, SOX7, or S100A8/A9 gene could inhibit GMC proliferation, extracellular matrix accumulation, and proteinuria in Thy-1N rats. Moreover, silencing SMYD4 gene could inhibit renal SOX7-K159me2/3, and silencing SMYD4 or SOX7 gene could inhibit renal S100A8/A9 production. Meanwhile, the SOX7-K159 methylation inhibitory peptide exhibited the similar intervention effects as SMYD4 and SOX7 knockdown in Thy-1N rats. In addition, the expression levels of SMYD4, SOX7, SOX7-K159me2/3, and S100A8/A9 all increased in the renal tissues of MsPGN patients. Collectively, our findings suggest that SMYD4-mediated SOX7-K159me2/3 partly contributes to sublytic C5b-9-induced S100A8/A9 expression in Thy-1N rats, which provides a novel insight into human MsPGN pathogenesis.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13659770/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146180689","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

cGAS: bridging immunity and metabolic regulation. 桥接免疫和代谢调节。

IF 6 2区生物学

Journal of Molecular Cell Biology Pub Date : 2026-07-03 DOI: 10.1093/jmcb/mjaf018

Jing Wang, Wen Meng

引用次数: 0

ITIH5 drives adipocyte differentiation and obesity-associated metabolic dysregulation via PI3K/AKT signaling activation. ih5通过PI3K/AKT信号激活驱动脂肪细胞分化和肥胖相关代谢失调

IF 6 2区生物学

Journal of Molecular Cell Biology Pub Date : 2026-07-03 DOI: 10.1093/jmcb/mjag016

Dan Li, Maoxiang Xu, Jie Li, Mengliu Yang, Gangyi Yang, Ling Li

{"title":"ITIH5 drives adipocyte differentiation and obesity-associated metabolic dysregulation via PI3K/AKT signaling activation.","authors":"Dan Li, Maoxiang Xu, Jie Li, Mengliu Yang, Gangyi Yang, Ling Li","doi":"10.1093/jmcb/mjag016","DOIUrl":"10.1093/jmcb/mjag016","url":null,"abstract":"Obesity markedly increases the risk of type 2 diabetes, highlighting the urgent need for novel therapeutic targets. The inter-alpha-trypsin inhibitor heavy chain 5 (ITIH5), which is predominantly produced by the adipose tissue, has emerged as a potential regulatory factor in obesity; however, the specific underlying mechanisms remain unclear. In this study, we identified ITIH5 as a key factor upregulated in obesity and closely associated with adipocyte differentiation and metabolic regulation. ITIH5 expression was significantly elevated in the adipose tissue of obese mice. In vitro experiments revealed that ITIH5 knockdown suppressed 3T3-L1 adipocyte differentiation, lipid accumulation, and inflammatory cytokine secretion, whereas ITIH5 overexpression markedly enhanced these effects. Mechanistically, activation of the PI3K/AKT signaling pathway was found to mediate ITIH5-induced adipogenic differentiation and lipid synthesis. Consistent with these findings, in vivo knockdown of ITIH5 in the inguinal white adipose tissue alleviated high-fat diet-induced obesity, reduced adipocyte hypertrophy, improved glucose tolerance, and increased energy expenditure. Conversely, overexpression of ITIH5 aggravated metabolic dysfunction. Collectively, these findings indicate that ITIH5 promotes adipogenesis and obesity progression via the PI3K/AKT pathway, providing a potential therapeutic target for obesity intervention.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13344428/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147839193","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

Structural insights into the organization of the human Erlin complex. 对人类厄林复合体组织结构的洞见。

IF 6 2区生物学

Journal of Molecular Cell Biology Pub Date : 2026-07-03 DOI: 10.1093/jmcb/mjaf060

Xiaoxiao Jia, Guoyun Liu, Haiwen Li, Hongwu Qian

{"title":"Structural insights into the organization of the human Erlin complex.","authors":"Xiaoxiao Jia, Guoyun Liu, Haiwen Li, Hongwu Qian","doi":"10.1093/jmcb/mjaf060","DOIUrl":"10.1093/jmcb/mjaf060","url":null,"abstract":"The endoplasmic reticulum lipid raft proteins (Erlins) belong to the stomatin-prohibitin-flotillin-HflC/K (SPFH) family and form highly oligomeric platforms that mediate the degradation of activated inositol 1,4,5-trisphosphate receptors by facilitating their interaction with the E3 ligase RNF170. However, the molecular mechanisms underlying this process remain unclear. Here, we successfully reconstituted the Erlin1-Erlin2 complex and its complex with RNF170 by overexpressing these components in HEK293F cells. We also isolated the Erlin2 oligomer by solely expressing Erlin2 in the cells. Using cryo-electron microscopy, we determined the structures of the Erlin1-Erlin2 complex, the Erlin1-Erlin2-RNF170 complex, and the Erlin2 oligomer at resolutions of 3.29 Å, 3.05 Å, and 2.12 Å, respectively. Both the Erlin1-Erlin2 complex and the Erlin2 oligomer exhibit similar cage-like architectures, with the Erlin1-Erlin2 complex containing 13 pairs of Erlin1 and Erlin2 subunits, whereas the Erlin2 oligomer comprises 26 Erlin2. Although RNF170 was clearly identified during protein purification, it was invisible in the final 3D reconstruction, suggesting a high degree of flexibility between RNF170 and the Erlin complex. Multiple water molecules were identified in the Erlin2 oligomer, underscoring their critical roles in facilitating the high degree of oligomerization of the Erlin2 complex. Taken together, our structural investigation elucidates the molecular basis for the assembly of the Erlin complex and provides a framework for further investigation.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13449098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145889514","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

Unraveling the mystery of parathyroid oxyphil cells in uremic SHPT: ongoing challenges and multi-omics advances. 揭示尿毒症SHPT中甲状旁腺氧细胞的奥秘：持续的挑战和多组学进展。

IF 6 2区生物学

Journal of Molecular Cell Biology Pub Date : 2026-07-03 DOI: 10.1093/jmcb/mjaf061

Jianping Mao, Jing Chen

{"title":"Unraveling the mystery of parathyroid oxyphil cells in uremic SHPT: ongoing challenges and multi-omics advances.","authors":"Jianping Mao, Jing Chen","doi":"10.1093/jmcb/mjaf061","DOIUrl":"10.1093/jmcb/mjaf061","url":null,"abstract":"The parathyroid gland, a pivotal organ regulating calcium and phosphorus homeostasis, harbors two primary cell types: chief cells and the enigmatic oxyphil cells. While scarce in healthy individuals, oxyphil cells undergo pronounced proliferation in uremic secondary hyperparathyroidism (SHPT), and their abundance is strongly associated with resistance to first-line therapies like calcitriol and calcimimetics. This correlation underscores a critical clinical challenge, yet the origin, functional role, and mechanisms driving oxyphil cell proliferation have remained poorly understood. Integrated multi-omics studies have decisively illuminated the underlying mechanisms, revealing uremic milieu-driven transdifferentiation from chief cells to oxyphil cells and the pivotal role of mitochondrial biogenesis activation in this process. This paradigm shift redefines oxyphil cells from passive entities to metabolically hyperactive, autonomous units capable of heightening parathyroid hormone synthesis and secretion. The core mechanism of therapy resistance is explained by the profound downregulation of key regulatory receptors, rendering them insensitive to conventional drugs. This review synthesizes current knowledge and, more importantly, highlights how integrated multi-omics approaches are illuminating the pathobiology of oxyphil cells, providing groundbreaking insights into their function, origin, and proliferation mechanisms. We conclude that these advances are pivotal for developing novel therapeutic strategies to overcome treatment resistance in uremic SHPT.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13463627/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145889468","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

FcεRIγ reinforces double-negative T cell-mediated antibody-dependent cellular cytotoxicity against tumor cells. FcεRIγ增强双阴性T细胞介导的抗体依赖细胞对肿瘤细胞的细胞毒性。

IF 6 2区生物学

Journal of Molecular Cell Biology Pub Date : 2026-07-03 DOI: 10.1093/jmcb/mjaf059

Shuai Shao, Xiaotong Han, Tianzhen Zhang, Lu Yang, Mingyang Li, Zihan Zhang, Xiaonan Du, Hua Jin, Songlin Wang, Yingchi Yang, Zhongtao Zhang, Guangyong Sun, Dong Zhang, Dan Tian

{"title":"FcεRIγ reinforces double-negative T cell-mediated antibody-dependent cellular cytotoxicity against tumor cells.","authors":"Shuai Shao, Xiaotong Han, Tianzhen Zhang, Lu Yang, Mingyang Li, Zihan Zhang, Xiaonan Du, Hua Jin, Songlin Wang, Yingchi Yang, Zhongtao Zhang, Guangyong Sun, Dong Zhang, Dan Tian","doi":"10.1093/jmcb/mjaf059","DOIUrl":"10.1093/jmcb/mjaf059","url":null,"abstract":"Double-negative T (DNT) cells (TCRαβ+CD4-CD8-NK1.1-/CD56-) exhibit strong tumor-killing capabilities. Our single-cell transcriptome analysis has revealed high Fcer1g expression in DNT cells, but its role in tumor immunity remains unclear. In this study, we demonstrated that IgG1 stimulation significantly upregulated IgG Fc receptors and cytotoxic molecules in DNT cells, enhancing their cytotoxicity against MC38 tumor cells in vitro. FcεRIγ-deficient DNT cells failed to respond effectively to IgG1 stimulation. Inhibiting the downstream spleen tyrosine kinase (Syk) of FcεRIγ reduced cytotoxicity of DNT cells and phosphorylation levels of molecules such as AKT and NF-κB. In a subcutaneous tumor model, combined treatment with DNT cells and tumor-specific antibodies more effectively inhibited tumor growth compared to DNT cells alone, while FcεRIγ-deficient DNT cells combined with antibodies showed no significant difference in efficacy compared to DNT cells alone, suggesting that DNT cells enhance tumor cell killing via FcεRIγ-mediated antibody-dependent cellular cytotoxicity (ADCC). These results indicate that DNT cells mediate antitumor ADCC effects through high FcεRIγ expression. Binding of IgG1 to FcεRIγ activates the FcεRIγ/Syk/AKT/NF-κB pathway, consequently enhancing tumor cell killing. Thus, DNT cells may play a significant role in cancer immunity, providing a basis for novel immune cell and antibody combination therapies.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13435804/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145889470","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

Integrated single-nucleus transcriptomic and chromatin accessibility analysis reveals key molecular basis of human testicular aging. 综合单核转录组学和染色质可及性分析揭示了人类睾丸衰老的关键分子基础。

IF 6 2区生物学

Journal of Molecular Cell Biology Pub Date : 2026-07-03 DOI: 10.1093/jmcb/mjag001

Weihao Sun, Hongyu Liu, Guanyu Ren, Pengcheng Pang, Zhuanghui Feng, Lei Wang, Shuguang Piao, Miaoxia He, Haoyu Shen, Jinsong Li, Xin Li, Chenghua Yang, Linhui Wang, Zhiyong Liu

{"title":"Integrated single-nucleus transcriptomic and chromatin accessibility analysis reveals key molecular basis of human testicular aging.","authors":"Weihao Sun, Hongyu Liu, Guanyu Ren, Pengcheng Pang, Zhuanghui Feng, Lei Wang, Shuguang Piao, Miaoxia He, Haoyu Shen, Jinsong Li, Xin Li, Chenghua Yang, Linhui Wang, Zhiyong Liu","doi":"10.1093/jmcb/mjag001","DOIUrl":"10.1093/jmcb/mjag001","url":null,"abstract":"The human testis, a crucial organ in male reproduction, is mainly responsible for spermatogenesis and androgen production. As men age, testicular function declines, yet the underlying molecular mechanisms are still not well understood. To elucidate the mechanisms of human testicular aging, we performed an integrated analysis of single-nucleus transcriptomes and chromatin accessibility (snRNA-seq and snATAC-seq) on pathologically confirmed non-tumor testicular tissues from young and aged individuals. Our integrated multi-omic analysis reveals significant aging-induced alterations in the testis transcriptome, particularly affecting genes linked to spermatogenesis. Significant aging-related changes were also observed in Sertoli and Leydig cells, with Sertoli cells exhibiting increased sensitivity to environmental influences as age. Furthermore, the expression of Wntless (WLS), a Wnt transporter, was substantially upregulated in Sertoli cells of aged testes, which was correlated with cellular senescence and the disruption of tight junctions. Overexpression of WLS in Sertoli cells significantly accelerated senescence in vitro, implying a potential role for WLS in testicular aging. Our study provides a detailed multi-omic map of the transcriptomic and chromatin accessibility changes in the human testis during aging, offering insights into the cellular and molecular mechanisms behind these changes, and identifying potential therapeutic targets for interventions against aging-related declines in male reproductive health.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13572877/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147389918","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

Zbtb38 transcriptionally activates XIAP to regulate apoptosis in development and cancer. Zbtb38转录激活XIAP调控发育和癌症中的细胞凋亡。

IF 6 2区生物学

Journal of Molecular Cell Biology Pub Date : 2026-07-03 DOI: 10.1093/jmcb/mjag011

Toshiaki Shigeoka, Hiroyuki Nagaoka, Nunuk Aries Nurulita, Shogo Tada, Yasumasa Bessho, Yasumasa Ishida, Eishou Matsuda

{"title":"Zbtb38 transcriptionally activates XIAP to regulate apoptosis in development and cancer.","authors":"Toshiaki Shigeoka, Hiroyuki Nagaoka, Nunuk Aries Nurulita, Shogo Tada, Yasumasa Bessho, Yasumasa Ishida, Eishou Matsuda","doi":"10.1093/jmcb/mjag011","DOIUrl":"10.1093/jmcb/mjag011","url":null,"abstract":"The X-linked inhibitor of apoptosis protein (XIAP) is a key suppressor of apoptosis, crucial for cellular differentiation, embryogenesis, and cancer progression. However, its upstream regulatory mechanisms remain poorly understood. Here, we demonstrate that the zinc finger transcription factor Zbtb38, a negative regulator of apoptosis, modulates XIAP expression in both loss- and gain-of-function experiments, irrespective of p53 expression. Notably, XIAP overexpression rescues the apoptosis induced by Zbtb38 knockdown, indicating that Zbtb38-associated apoptosis is at least partially XIAP-dependent. Mechanistically, Zbtb38 binds to E-box motifs within upstream regulatory regions of XIAP and activates its transcription. During embryonic stem cell differentiation and embryogenesis, Zbtb38 depletion increases apoptosis and reduces XIAP and Bcl-2 expression, underscoring their functional relevance in these processes. Analysis of human tumor datasets reveals a strong positive correlation between ZBTB38 and XIAP expression, with elevated ZBTB38 levels associated with high-grade malignancies. Furthermore, Zbtb38 knockdown induces apoptosis in cancer cells with reduced XIAP expression, regardless of p53 expression. Collectively, these findings uncover a novel Zbtb38-XIAP axis that regulates apoptosis during cellular differentiation, development, and oncogenesis and highlight its therapeutic potential in XIAP-driven and p53-deficient tumors.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13344426/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147473881","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 to: Mutual regulation between SIAH2 and DYRK2 controls hypoxic and genotoxic signaling pathways. 更正：SIAH2和DYRK2之间的相互调节控制缺氧和基因毒性信号通路。

IF 6 2区生物学

Journal of Molecular Cell Biology Pub Date : 2026-07-03 DOI: 10.1093/jmcb/mjag024

引用次数: 0