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Correction to: DJ-1 is dispensable for human stem cell homeostasis. 更正:DJ-1对人类干细胞稳态是不可缺少的。
IF 21.1 1区 生物学
Protein & Cell Pub Date : 2025-05-20 DOI: 10.1093/procel/pwaf034
{"title":"Correction to: DJ-1 is dispensable for human stem cell homeostasis.","authors":"","doi":"10.1093/procel/pwaf034","DOIUrl":"https://doi.org/10.1093/procel/pwaf034","url":null,"abstract":"","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":"1 1","pages":""},"PeriodicalIF":21.1,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144103525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
Correction to: RBM46 is essential for gametogenesis and functions in post-transcriptional roles affecting meiotic cohesin subunits. 修正:RBM46对配子发生和影响减数分裂内聚亚基的转录后作用至关重要。
IF 21.1 1区 生物学
Protein & Cell Pub Date : 2025-05-20 DOI: 10.1093/procel/pwaf038
{"title":"Correction to: RBM46 is essential for gametogenesis and functions in post-transcriptional roles affecting meiotic cohesin subunits.","authors":"","doi":"10.1093/procel/pwaf038","DOIUrl":"https://doi.org/10.1093/procel/pwaf038","url":null,"abstract":"","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":"31 1","pages":""},"PeriodicalIF":21.1,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144103531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
Correction to: Single-cell profiling reveals a potent role of quercetin in promoting hair regeneration. 更正:单细胞分析揭示了槲皮素在促进头发再生方面的有效作用。
IF 21.1 1区 生物学
Protein & Cell Pub Date : 2025-05-20 DOI: 10.1093/procel/pwaf035
{"title":"Correction to: Single-cell profiling reveals a potent role of quercetin in promoting hair regeneration.","authors":"","doi":"10.1093/procel/pwaf035","DOIUrl":"https://doi.org/10.1093/procel/pwaf035","url":null,"abstract":"","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":"41 1","pages":""},"PeriodicalIF":21.1,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144103526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
Correction to: A single-nucleus transcriptomic atlas of primate testicular aging reveals exhaustion of the spermatogonial stem cell reservoir and loss of Sertoli cell homeostasis. 更正:灵长类动物睾丸衰老的单核转录组图谱揭示了精原干细胞储存库的衰竭和支持细胞稳态的丧失。
IF 13.6 1区 生物学
Protein & Cell Pub Date : 2025-05-20 DOI: 10.1093/procel/pwaf033
{"title":"Correction to: A single-nucleus transcriptomic atlas of primate testicular aging reveals exhaustion of the spermatogonial stem cell reservoir and loss of Sertoli cell homeostasis.","authors":"","doi":"10.1093/procel/pwaf033","DOIUrl":"https://doi.org/10.1093/procel/pwaf033","url":null,"abstract":"","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":" ","pages":""},"PeriodicalIF":13.6,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144111546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
EZH2 in non-cancerous diseases: Expanding horizons. EZH2在非癌性疾病中的作用:拓展视野。
IF 21.1 1区 生物学
Protein & Cell Pub Date : 2025-05-19 DOI: 10.1093/procel/pwaf032
Renjing Jin,Jianlin Zhang,Yuqing Wang,Ziyu Chen,Xuan He,Xintong Zhang,Zhen Tan,Celina G Kleer,Ye Li,Deli Wang,Lixiang Xue
{"title":"EZH2 in non-cancerous diseases: Expanding horizons.","authors":"Renjing Jin,Jianlin Zhang,Yuqing Wang,Ziyu Chen,Xuan He,Xintong Zhang,Zhen Tan,Celina G Kleer,Ye Li,Deli Wang,Lixiang Xue","doi":"10.1093/procel/pwaf032","DOIUrl":"https://doi.org/10.1093/procel/pwaf032","url":null,"abstract":"Enhancer of Zeste homolog 2 (EZH2), a histone methyltransferase within polycomb repressive complex 2 (PRC2), plays a crucial role in epigenetic regulation by silencing gene expression through trimethylation of histone 3 at lysine 27 (H3K27me3). Beyond its well-documented oncogenic functions, emerging research has revealed EZH2's involvement in various non-cancerous pathologies. For instance, EZH2 is critical in regulating immune responses, particularly in modulating T cell differentiation and cytokine production, which affects inflammation and immune homeostasis. EZH2 also controls fibroblast activation and extracellular matrix (ECM) remodeling, influencing critical processes such as cell differentiation, tissue repair and energy homeostasis. Additionally, EZH2's epigenetic regulation of neuroinflammatory processes is linked to neuronal health and survival. Recent advancements in EZH2 inhibitor therapies demonstrate promising potential for treating a range of non-cancerous conditions, with preclinical trials suggesting efficacy in mitigating disease progression. This review highlights the expanding functional scope of EZH2, emphasizing its epigenetic mechanisms and the therapeutic opportunities for targeting EZH2 in non-cancerous diseases.","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":"10 1","pages":""},"PeriodicalIF":21.1,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144087523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
Glutamine signaling specifically activates c-Myc and Mcl-1 to Facilitate cancer cell proliferation and survival. 谷氨酰胺信号特异性激活c-Myc和Mcl-1促进癌细胞增殖和存活。
IF 21.1 1区 生物学
Protein & Cell Pub Date : 2025-05-04 DOI: 10.1093/procel/pwaf029
Meng Wang,Fu-Shen Guo,Dai-Sen Hou,Hui-Lu Zhang,Xiang-Tian Chen,Yan-Xin Shen,Zi-Fan Guo,Zhi-Fang Zheng,Yu-Peng Hu,Pei-Zhun Du,Chen-Ji Wang,Yan Lin,Yi-Yuan Yuan,Shi-Min Zhao,Wei Xu
{"title":"Glutamine signaling specifically activates c-Myc and Mcl-1 to Facilitate cancer cell proliferation and survival.","authors":"Meng Wang,Fu-Shen Guo,Dai-Sen Hou,Hui-Lu Zhang,Xiang-Tian Chen,Yan-Xin Shen,Zi-Fan Guo,Zhi-Fang Zheng,Yu-Peng Hu,Pei-Zhun Du,Chen-Ji Wang,Yan Lin,Yi-Yuan Yuan,Shi-Min Zhao,Wei Xu","doi":"10.1093/procel/pwaf029","DOIUrl":"https://doi.org/10.1093/procel/pwaf029","url":null,"abstract":"Glutamine provides carbon and nitrogen to support the proliferation of cancer cells. However, the precise reason why cancer cells are particularly dependent on glutamine remains unclear. In this study, we report that glutamine modulates the tumor suppressor F-box and WD repeat domain-containing 7 (FBW7) to promote cancer cell proliferation and survival. Specifically, lysine 604 (K604) in the sixth of the seven substrate-recruiting WD repeats of FBW7 undergoes glutaminylation (Gln-K604) by glutaminyl tRNA synthetase (QARS). Gln-K604 inhibits SCFFBW7-mediated degradation of c-Myc and Mcl-1, enhances glutamine utilization, and stimulates nucleotide and DNA biosynthesis through the activation of c-Myc. Additionally, Gln-K604 promotes resistance to apoptosis by activating Mcl-1. In contrast, SIRT1 deglutaminylates Gln-K604, thereby reversing its effects. Cancer cells lacking Gln-K604 exhibit overexpression of c-Myc and Mcl-1 and display resistance to chemotherapy-induced apoptosis. Silencing both c-MYC and MCL-1 in these cells sensitizes them to chemotherapy. These findings indicate that the glutamine-mediated signal via Gln-K604 is a key driver of cancer progression and suggest potential strategies for targeted cancer therapies based on varying Gln-K604 status.","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":"25 1","pages":""},"PeriodicalIF":21.1,"publicationDate":"2025-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143921014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
Integrative transcriptomic and epigenomic analysis identifies BCL6B as a novel regulator of human pluripotent stem cell to endothelial differentiation. 综合转录组学和表观基因组学分析发现BCL6B是人类多能干细胞向内皮分化的一种新的调节因子。
IF 13.6 1区 生物学
Protein & Cell Pub Date : 2025-05-03 DOI: 10.1093/procel/pwaf039
Yonglin Zhu, Jinyang Liu, Jia Wang, Shuangyuan Ding, Hui Qiu, Xia Chen, Jianying Guo, Peiliang Wang, Xingwu Zhang, Fengzhi Zhang, Rujin Huang, Fuyu Duan, Lin Wang, Jie Na
{"title":"Integrative transcriptomic and epigenomic analysis identifies BCL6B as a novel regulator of human pluripotent stem cell to endothelial differentiation.","authors":"Yonglin Zhu, Jinyang Liu, Jia Wang, Shuangyuan Ding, Hui Qiu, Xia Chen, Jianying Guo, Peiliang Wang, Xingwu Zhang, Fengzhi Zhang, Rujin Huang, Fuyu Duan, Lin Wang, Jie Na","doi":"10.1093/procel/pwaf039","DOIUrl":"https://doi.org/10.1093/procel/pwaf039","url":null,"abstract":"","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":" ","pages":""},"PeriodicalIF":13.6,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144009251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
CRISPR-based screening pinpoints H2AZ1 as a driver of senescence in human mesenchymal stem cells. 基于 CRISPR 的筛选确定 H2AZ1 是人类间充质干细胞衰老的驱动因素。
IF 13.6 1区 生物学
Protein & Cell Pub Date : 2025-04-18 DOI: 10.1093/procel/pwae035
Ming-Heng Li, Xiaoyu Jiang, Yaobin Jing, Kaowen Yan, Shi-Jia Bi, Si Wang, Shuai Ma, Guang-Hui Liu, Weiqi Zhang, Shuhui Sun, Jing Qu
{"title":"CRISPR-based screening pinpoints H2AZ1 as a driver of senescence in human mesenchymal stem cells.","authors":"Ming-Heng Li, Xiaoyu Jiang, Yaobin Jing, Kaowen Yan, Shi-Jia Bi, Si Wang, Shuai Ma, Guang-Hui Liu, Weiqi Zhang, Shuhui Sun, Jing Qu","doi":"10.1093/procel/pwae035","DOIUrl":"10.1093/procel/pwae035","url":null,"abstract":"","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":" ","pages":"296-305"},"PeriodicalIF":13.6,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12082294/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141420512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
SMAD2/3-SMYD2 and developmental transcription factors cooperate with cell-cycle inhibitors to guide tissue formation. SMAD2/3-SMYD2 和发育转录因子与细胞周期抑制剂合作,引导组织形成。
IF 13.6 1区 生物学
Protein & Cell Pub Date : 2025-04-18 DOI: 10.1093/procel/pwae031
Stefania Militi, Reshma Nibhani, Martin Pook, Siim Pauklin
{"title":"SMAD2/3-SMYD2 and developmental transcription factors cooperate with cell-cycle inhibitors to guide tissue formation.","authors":"Stefania Militi, Reshma Nibhani, Martin Pook, Siim Pauklin","doi":"10.1093/procel/pwae031","DOIUrl":"10.1093/procel/pwae031","url":null,"abstract":"<p><p>Tissue formation and organ homeostasis are achieved by precise coordination of proliferation and differentiation of stem cells and progenitors. While deregulation of these processes can result in degenerative disease or cancer, their molecular interplays remain unclear. Here we show that the switch of human pluripotent stem cell (hPSC) self-renewal to differentiation is associated with the induction of distinct cyclin-dependent kinase inhibitors (CDKIs). In hPSCs, Activin/Nodal/TGFβ signaling maintains CDKIs in a poised state via SMAD2/3-NANOG-OCT4-EZH2-SNON transcriptional complex. Upon gradual differentiation, CDKIs are induced by successive transcriptional complexes between SMAD2/3-SMYD2 and developmental regulators such as EOMES, thereby lengthening the G1 phase. This, in turn, induces SMAD2/3 transcriptional activity by blocking its linker phosphorylation. Such SMAD2/3-CDKI positive feedback loops drive the exit from pluripotency and stepwise cell-fate specification that could be harnessed for producing cells for therapeutic applications. Our study uncovers fundamental mechanisms of how cell-fate specification is interconnected to cell-cycle dynamics and provides insight into autonomous circuitries governing tissue self-formation.</p>","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":" ","pages":"260-285"},"PeriodicalIF":13.6,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12053477/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140959228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
PKM2, the "K+ sink" in the tumor interstitial fluid. PKM2,肿瘤间质中的 "K+汇"。
IF 13.6 1区 生物学
Protein & Cell Pub Date : 2025-04-18 DOI: 10.1093/procel/pwae036
Wenjing Na, Wenfeng Zeng, Kai Song, Youwang Wang, Luoyang Wang, Ziran Zhao, Lingtao Jin, Ping Zhu, Wei Liang
{"title":"PKM2, the \"K+ sink\" in the tumor interstitial fluid.","authors":"Wenjing Na, Wenfeng Zeng, Kai Song, Youwang Wang, Luoyang Wang, Ziran Zhao, Lingtao Jin, Ping Zhu, Wei Liang","doi":"10.1093/procel/pwae036","DOIUrl":"10.1093/procel/pwae036","url":null,"abstract":"","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":" ","pages":"303-308"},"PeriodicalIF":13.6,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12053478/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141443275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
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