Journal of Molecular Cell Biology最新文献_第9页

Sex- and age-specific associations between abdominal fat and non-alcoholic fatty liver disease: a prospective cohort study. 腹部脂肪与非酒精性脂肪肝之间的性别和年龄特异性关联:一项前瞻性队列研究

IF 5.3 2区生物学

Journal of Molecular Cell Biology Pub Date : 2024-04-10 DOI: 10.1093/jmcb/mjad069

Hongli Chen, Yuexing Liu, Dan Liu, Yebei Liang, Zhijun Zhu, Keqing Dong, Huating Li, Yuqian Bao, Jiarui Wu, Xuhong Hou, Weiping Jia

{"title":"Sex- and age-specific associations between abdominal fat and non-alcoholic fatty liver disease: a prospective cohort study.","authors":"Hongli Chen, Yuexing Liu, Dan Liu, Yebei Liang, Zhijun Zhu, Keqing Dong, Huating Li, Yuqian Bao, Jiarui Wu, Xuhong Hou, Weiping Jia","doi":"10.1093/jmcb/mjad069","DOIUrl":"10.1093/jmcb/mjad069","url":null,"abstract":"Obesity is closely related to non-alcoholic fatty liver disease (NAFLD). Although sex differences in body fat distribution have been well demonstrated, little is known about the sex-specific associations between adipose tissue and the development of NAFLD. Using community-based cohort data, we evaluated the associations between magnetic resonance imaging quantified areas of abdominal adipose tissue, including visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT), and incident NAFLD in 2830 participants (1205 males and 1625 females) aged 55-70 years. During a 4.6-year median follow-up, the cumulative incidence rates of NAFLD increased with areas of VAT and SAT both in males and in females. Further analyses showed that the above-mentioned positive associations were stronger in males than in females, especially in participants under 60 years old. In contrast, these sex differences disappeared in those over 60 years old. Furthermore, the risk of developing NAFLD increased non-linearly with increasing fat area in a sex-specific pattern. Additionally, sex-specific potential mediators, such as insulin resistance, lipid metabolism, inflammation, and adipokines, may exist in the associations between adipose tissue and NAFLD. This study showed that the associations between abdominal fat and the risk of NAFLD were stratified by sex and age, highlighting the potential need for sex- and age-specific management of NAFLD.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11161703/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138460469","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

JunB condensation attenuates vascular endothelial damage under hyperglycemic condition. JunB 缩合可减轻高血糖条件下的血管内皮损伤。

IF 5.5 2区生物学

Journal of Molecular Cell Biology Pub Date : 2024-04-10 DOI: 10.1093/jmcb/mjad072

Xuxia Ren, Zexu Cui, Qiaoqiao Zhang, Zhiguang Su, Wei Xu, Jinhui Wu, Hao Jiang

引用次数: 0

The interplay between the muscle and liver in the regulation of glucolipid metabolism. 肌肉和肝脏在调节糖脂代谢中的相互作用。

IF 5.5 2区生物学

Journal of Molecular Cell Biology Pub Date : 2024-04-10 DOI: 10.1093/jmcb/mjad073

Cheng Chen, Liping Xie, Mingliang Zhang, Shama, Kenneth King Yip Cheng, Weiping Jia

引用次数: 0

The capsid revolution. 衣壳革命。

IF 5.3 2区生物学

Journal of Molecular Cell Biology Pub Date : 2024-04-10 DOI: 10.1093/jmcb/mjad076

Ian A Taylor, Ariberto Fassati

引用次数: 0

Glycogen synthase kinase 3 signaling in neural regeneration in vivo. 糖原合成酶激酶3信号在体内神经再生中的作用。

IF 5.3 2区生物学

Journal of Molecular Cell Biology Pub Date : 2024-04-10 DOI: 10.1093/jmcb/mjad075

Jing Zhang, Shu-Guang Yang, Feng-Quan Zhou

{"title":"Glycogen synthase kinase 3 signaling in neural regeneration in vivo.","authors":"Jing Zhang, Shu-Guang Yang, Feng-Quan Zhou","doi":"10.1093/jmcb/mjad075","DOIUrl":"10.1093/jmcb/mjad075","url":null,"abstract":"Glycogen synthase kinase 3 (GSK3) signaling plays important and broad roles in regulating neural development in vitro and in vivo. Here, we reviewed recent findings of GSK3-regulated axon regeneration in vivo in both the peripheral and central nervous systems and discussed a few controversial findings in the field. Overall, current evidence indicates that GSK3β signaling serves as an important downstream mediator of the PI3K-AKT pathway to regulate axon regeneration in parallel with the mTORC1 pathway. Specifically, the mTORC1 pathway supports axon regeneration mainly through its role in regulating cap-dependent protein translation, whereas GSK3β signaling might be involved in regulating N6-methyladenosine mRNA methylation-mediated, cap-independent protein translation. In addition, GSK3 signaling also plays a key role in reshaping the neuronal transcriptomic landscape during neural regeneration. Finally, we proposed some research directions to further elucidate the molecular mechanisms underlying the regulatory function of GSK3 signaling and discover novel GSK3 signaling-related therapeutic targets. Together, we hope to provide an updated and insightful overview of how GSK3 signaling regulates neural regeneration in vivo.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11063957/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138498637","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

Impaired dNKAP function drives genome instability and tumorigenic growth in Drosophila epithelia. 受损的dNKAP功能驱动果蝇上皮基因组不稳定和致瘤性生长。

IF 5.5 2区生物学

Journal of Molecular Cell Biology Pub Date : 2024-04-10 DOI: 10.1093/jmcb/mjad078

Ting Guo, Chen Miao, Zhonghua Liu, Jingwei Duan, Yanbin Ma, Xiao Zhang, Weiwei Yang, Maoguang Xue, Qiannan Deng, Pengfei Guo, Yongmei Xi, Xiaohang Yang, Xun Huang, Wanzhong Ge

{"title":"Impaired dNKAP function drives genome instability and tumorigenic growth in Drosophila epithelia.","authors":"Ting Guo, Chen Miao, Zhonghua Liu, Jingwei Duan, Yanbin Ma, Xiao Zhang, Weiwei Yang, Maoguang Xue, Qiannan Deng, Pengfei Guo, Yongmei Xi, Xiaohang Yang, Xun Huang, Wanzhong Ge","doi":"10.1093/jmcb/mjad078","DOIUrl":"10.1093/jmcb/mjad078","url":null,"abstract":"Mutations or dysregulated expression of NF-kappaB-activating protein (NKAP) family genes have been found in human cancers. How NKAP family gene mutations promote tumor initiation and progression remains to be determined. Here, we characterized dNKAP, the Drosophila homolog of NKAP, and showed that impaired dNKAP function causes genome instability and tumorigenic growth in a Drosophila epithelial tumor model. dNKAP-knockdown wing imaginal discs exhibit tumorigenic characteristics, including tissue overgrowth, cell-invasive behavior, abnormal cell polarity, and cell adhesion defects. dNKAP knockdown causes both R-loop accumulation and DNA damage, indicating the disruption of genome integrity. Further analysis showed that dNKAP knockdown induces c-Jun N-terminal kinase (JNK)-dependent apoptosis and causes aberrant cell proliferation in distinct cell populations. Activation of the Notch and JAK/STAT signaling pathways contributes to the tumorigenic growth of dNKAP-knockdown tissues. Furthermore, JNK signaling is essential for dNKAP depletion-mediated cell invasion. Transcriptome analysis of dNKAP-knockdown tissues confirmed the misregulation of signaling pathways involved in promoting tumorigenesis and revealed abnormal regulation of metabolic pathways. dNKAP knockdown and oncogenic Ras, Notch, or Yki mutations show synergies in driving tumorigenesis, further supporting the tumor-suppressive role of dNKAP. In summary, this study demonstrates that dNKAP plays a tumor-suppressive role by preventing genome instability in Drosophila epithelia and thus provides novel insights into the roles of human NKAP family genes in tumor initiation and progression.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.5,"publicationDate":"2024-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11070879/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138498638","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

IDeAS: an interactive database for dysregulated alternative splicing in cancers across Chinese and western patients. 想法:一个关于中国和西方患者癌症中失调的选择性剪接的交互式数据库。

IF 5.5 2区生物学

Journal of Molecular Cell Biology Pub Date : 2024-04-10 DOI: 10.1093/jmcb/mjad074

Hanwen Zhou, Liyun Yuan, Yuanhu Ju, Yue Hu, Siqi Wang, Ruifang Cao, Zefeng Wang, Guoqing Zhang

引用次数: 0

Morphomics via next-generation electron microscopy. 通过新一代电子显微镜进行形态组学研究。

IF 5.3 2区生物学

Journal of Molecular Cell Biology Pub Date : 2024-04-10 DOI: 10.1093/jmcb/mjad081

Raku Son, Kenji Yamazawa, Akiko Oguchi, Mitsuo Suga, Masaru Tamura, Motoko Yanagita, Yasuhiro Murakawa, Satoshi Kume

引用次数: 0

Inhibition of GLUD1 mediated by LASP1 and SYVN1 contributes to hepatitis B virus X protein-induced hepatocarcinogenesis LASP1 和 SYVN1 介导的 GLUD1 抑制作用有助于乙型肝炎病毒 X 蛋白诱导的肝癌发生

IF 5.5 2区生物学

Journal of Molecular Cell Biology Pub Date : 2024-04-08 DOI: 10.1093/jmcb/mjae014

Hong-Juan You, Qi Li, Li-Hong Ma, Xing Wang, Huan-Yang Zhang, Yu-Xin Wang, En-Si Bao, Yu-Jie Zhong, De-Long Kong, Xiang-Ye Liu, Fan-Yun Kong, Kui-Yang Zheng, Ren-Xian Tang

{"title":"Inhibition of GLUD1 mediated by LASP1 and SYVN1 contributes to hepatitis B virus X protein-induced hepatocarcinogenesis","authors":"Hong-Juan You, Qi Li, Li-Hong Ma, Xing Wang, Huan-Yang Zhang, Yu-Xin Wang, En-Si Bao, Yu-Jie Zhong, De-Long Kong, Xiang-Ye Liu, Fan-Yun Kong, Kui-Yang Zheng, Ren-Xian Tang","doi":"10.1093/jmcb/mjae014","DOIUrl":"https://doi.org/10.1093/jmcb/mjae014","url":null,"abstract":"Glutamate dehydrogenase 1 (GLUD1) is implicated in oncogenesis. However, little is known about the relationship between GLUD1 and hepatocellular carcinoma (HCC). In the present study, we demonstrated that the expression levels of GLUD1 significantly decreased in tumors, which was relevant to the poor prognosis of HCC. Functionally, GLUD1 silencing enhanced the growth and migration of HCC cells. Mechanistically, the upregulation of interleukin-32 through AKT activation contributes to GLUD1 silencing-facilitated hepatocarcinogenesis. The interaction between GLUD1 and AKT, as well as α-ketoglutarate regulated by GLUD1, can suppress AKT activation. In addition, LIM and SH3 protein 1 (LASP1) interacts with GLUD1 and induces GLUD1 degradation via the ubiquitin–proteasome pathway, which relies on the E3 ubiquitin ligase synoviolin (SYVN1), whose interaction with GLUD1 is enhanced by LASP1. In hepatitis B virus (HBV)-related HCC, the HBV X protein (HBX) can suppress GLUD1 with the participation of LASP1 and SYVN1. Collectively, our data suggest that GLUD1 silencing is significantly associated with HCC development, and LASP1 and SYVN1 mediate the inhibition of GLUD1 in HCC, especially in HBV-related tumors.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":"84 1","pages":""},"PeriodicalIF":5.5,"publicationDate":"2024-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140577028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

ELP3 stabilizes c-Myc to promote tumorigenesis. ELP3稳定c-myc以促进肿瘤发生。

IF 5.5 2区生物学

Journal of Molecular Cell Biology Pub Date : 2024-04-04 DOI: 10.1093/jmcb/mjad059

Wentao Zhao, Cong Ouyang, Chen Huang, Jiaojiao Zhang, Qiao Xiao, Fengqiong Zhang, Huihui Wang, Furong Lin, Jinyang Wang, Zhanxiang Wang, Bin Jiang, Qinxi Li

{"title":"ELP3 stabilizes c-Myc to promote tumorigenesis.","authors":"Wentao Zhao, Cong Ouyang, Chen Huang, Jiaojiao Zhang, Qiao Xiao, Fengqiong Zhang, Huihui Wang, Furong Lin, Jinyang Wang, Zhanxiang Wang, Bin Jiang, Qinxi Li","doi":"10.1093/jmcb/mjad059","DOIUrl":"10.1093/jmcb/mjad059","url":null,"abstract":"ELP3, the catalytic subunit of the Elongator complex, is an acetyltransferase and associated with tumor progression. However, the detail of ELP3 oncogenic function remains largely unclear. Here, we found that ELP3 stabilizes c-Myc to promote tumorigenesis in an acetyltransferase-independent manner. Mechanistically, ELP3 competes with the E3-ligase FBXW7β for c-Myc binding, resulting in the inhibition of FBXW7β-mediated ubiquitination and proteasomal degradation of c-Myc. ELP3 knockdown diminishes glycolysis and glutaminolysis and dramatically retards cell proliferation and xenograft growth by downregulating c-Myc, and such effects are rescued by the reconstitution of c-Myc expression. Moreover, ELP3 and c-Myc were found overexpressed with a positive correlation in colorectal cancer and hepatocellular carcinoma. Taken together, we elucidate a new function of ELP3 in promoting tumorigenesis by stabilizing c-Myc, suggesting that inhibition of ELP3 is a potential strategy for treating c-Myc-driven carcinomas.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.5,"publicationDate":"2024-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11054291/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41128250","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