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Correction to: Enhancing prime editing efficiency and flexibility with tethered and split pegRNAs. 更正:利用系留和分离 pegRNA 提高素材编辑效率和灵活性。
IF 21.1 1区 生物学
Protein & Cell Pub Date : 2024-02-01 DOI: 10.1093/procel/pwad025
{"title":"Correction to: Enhancing prime editing efficiency and flexibility with tethered and split pegRNAs.","authors":"","doi":"10.1093/procel/pwad025","DOIUrl":"10.1093/procel/pwad025","url":null,"abstract":"","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":21.1,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10833442/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9888664","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
Aging-induced YTHDF aggregates impair mitochondrial function by trapping mitochondrial RNAs and suppressing their expression in the brain. 衰老诱导的YTHDF聚集体通过捕获线粒体RNA并抑制其在大脑中的表达来损害线粒体功能。
IF 21.1 1区 生物学
Protein & Cell Pub Date : 2024-02-01 DOI: 10.1093/procel/pwad041
Juan Zhang, Dingfeng Li, Keqiang He, Qiang Liu, Zhongwen Xie
{"title":"Aging-induced YTHDF aggregates impair mitochondrial function by trapping mitochondrial RNAs and suppressing their expression in the brain.","authors":"Juan Zhang, Dingfeng Li, Keqiang He, Qiang Liu, Zhongwen Xie","doi":"10.1093/procel/pwad041","DOIUrl":"10.1093/procel/pwad041","url":null,"abstract":"","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":21.1,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10833457/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9807472","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
A single-nucleus transcriptomic atlas of primate liver aging uncovers the pro-senescence role of SREBP2 in hepatocytes. 灵长类动物肝脏衰老的单核转录组图谱揭示了 SREBP2 在肝细胞中的促衰老作用。
IF 21.1 1区 生物学
Protein & Cell Pub Date : 2024-02-01 DOI: 10.1093/procel/pwad039
Shanshan Yang, Chengyu Liu, Mengmeng Jiang, Xiaoqian Liu, Lingling Geng, Yiyuan Zhang, Shuhui Sun, Kang Wang, Jian Yin, Shuai Ma, Si Wang, Juan Carlos Izpisua Belmonte, Weiqi Zhang, Jing Qu, Guang-Hui Liu
{"title":"A single-nucleus transcriptomic atlas of primate liver aging uncovers the pro-senescence role of SREBP2 in hepatocytes.","authors":"Shanshan Yang, Chengyu Liu, Mengmeng Jiang, Xiaoqian Liu, Lingling Geng, Yiyuan Zhang, Shuhui Sun, Kang Wang, Jian Yin, Shuai Ma, Si Wang, Juan Carlos Izpisua Belmonte, Weiqi Zhang, Jing Qu, Guang-Hui Liu","doi":"10.1093/procel/pwad039","DOIUrl":"10.1093/procel/pwad039","url":null,"abstract":"<p><p>Aging increases the risk of liver diseases and systemic susceptibility to aging-related diseases. However, cell type-specific changes and the underlying mechanism of liver aging in higher vertebrates remain incompletely characterized. Here, we constructed the first single-nucleus transcriptomic landscape of primate liver aging, in which we resolved cell type-specific gene expression fluctuation in hepatocytes across three liver zonations and detected aberrant cell-cell interactions between hepatocytes and niche cells. Upon in-depth dissection of this rich dataset, we identified impaired lipid metabolism and upregulation of chronic inflammation-related genes prominently associated with declined liver functions during aging. In particular, hyperactivated sterol regulatory element-binding protein (SREBP) signaling was a hallmark of the aged liver, and consequently, forced activation of SREBP2 in human primary hepatocytes recapitulated in vivo aging phenotypes, manifesting as impaired detoxification and accelerated cellular senescence. This study expands our knowledge of primate liver aging and informs the development of diagnostics and therapeutic interventions for liver aging and associated diseases.</p>","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":21.1,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10833472/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9684335","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
Correction to: Oncogenic miR-19a and miR-19b co-regulate tumor suppressor MTUS1 to promote cell proliferation and migration in lung cancer. 更正为致癌 miR-19a 和 miR-19b 共同调节肿瘤抑制因子 MTUS1,促进肺癌细胞的增殖和迁移。
IF 21.1 1区 生物学
Protein & Cell Pub Date : 2024-01-13 DOI: 10.1093/procel/pwad062
{"title":"Correction to: Oncogenic miR-19a and miR-19b co-regulate tumor suppressor MTUS1 to promote cell proliferation and migration in lung cancer.","authors":"","doi":"10.1093/procel/pwad062","DOIUrl":"https://doi.org/10.1093/procel/pwad062","url":null,"abstract":"","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":21.1,"publicationDate":"2024-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139465601","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
BMP7 expression in mammalian cortical radial glial cells increases the length of the neurogenic period. 哺乳动物皮质放射状胶质细胞中 BMP7 的表达可增加神经源期的长度。
IF 21.1 1区 生物学
Protein & Cell Pub Date : 2024-01-03 DOI: 10.1093/procel/pwad036
Zhenmeiyu Li, Guoping Liu, Lin Yang, Mengge Sun, Zhuangzhi Zhang, Zhejun Xu, Yanjing Gao, Xin Jiang, Zihao Su, Xiaosu Li, Zhengang Yang
{"title":"BMP7 expression in mammalian cortical radial glial cells increases the length of the neurogenic period.","authors":"Zhenmeiyu Li, Guoping Liu, Lin Yang, Mengge Sun, Zhuangzhi Zhang, Zhejun Xu, Yanjing Gao, Xin Jiang, Zihao Su, Xiaosu Li, Zhengang Yang","doi":"10.1093/procel/pwad036","DOIUrl":"10.1093/procel/pwad036","url":null,"abstract":"<p><p>The seat of human intelligence is the human cerebral cortex, which is responsible for our exceptional cognitive abilities. Identifying principles that lead to the development of the large-sized human cerebral cortex will shed light on what makes the human brain and species so special. The remarkable increase in the number of human cortical pyramidal neurons and the size of the human cerebral cortex is mainly because human cortical radial glial cells, primary neural stem cells in the cortex, generate cortical pyramidal neurons for more than 130 days, whereas the same process takes only about 7 days in mice. The molecular mechanisms underlying this difference are largely unknown. Here, we found that bone morphogenic protein 7 (BMP7) is expressed by increasing the number of cortical radial glial cells during mammalian evolution (mouse, ferret, monkey, and human). BMP7 expression in cortical radial glial cells promotes neurogenesis, inhibits gliogenesis, and thereby increases the length of the neurogenic period, whereas Sonic Hedgehog (SHH) signaling promotes cortical gliogenesis. We demonstrate that BMP7 signaling and SHH signaling mutually inhibit each other through regulation of GLI3 repressor formation. We propose that BMP7 drives the evolutionary expansion of the mammalian cortex by increasing the length of the neurogenic period.</p>","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":21.1,"publicationDate":"2024-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10762677/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9593016","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: 1
Human ESC-derived vascular cells promote vascular regeneration in a HIF-1α dependent manner. 人 ESC 衍生血管细胞以 HIF-1α 依赖性方式促进血管再生。
IF 21.1 1区 生物学
Protein & Cell Pub Date : 2024-01-03 DOI: 10.1093/procel/pwad027
Jinghui Lei, Xiaoyu Jiang, Daoyuan Huang, Ying Jing, Shanshan Yang, Lingling Geng, Yupeng Yan, Fangshuo Zheng, Fang Cheng, Weiqi Zhang, Juan Carlos Izpisua Belmonte, Guang-Hui Liu, Si Wang, Jing Qu
{"title":"Human ESC-derived vascular cells promote vascular regeneration in a HIF-1α dependent manner.","authors":"Jinghui Lei, Xiaoyu Jiang, Daoyuan Huang, Ying Jing, Shanshan Yang, Lingling Geng, Yupeng Yan, Fangshuo Zheng, Fang Cheng, Weiqi Zhang, Juan Carlos Izpisua Belmonte, Guang-Hui Liu, Si Wang, Jing Qu","doi":"10.1093/procel/pwad027","DOIUrl":"10.1093/procel/pwad027","url":null,"abstract":"<p><p>Hypoxia-inducible factor (HIF-1α), a core transcription factor responding to changes in cellular oxygen levels, is closely associated with a wide range of physiological and pathological conditions. However, its differential impacts on vascular cell types and molecular programs modulating human vascular homeostasis and regeneration remain largely elusive. Here, we applied CRISPR/Cas9-mediated gene editing of human embryonic stem cells and directed differentiation to generate HIF-1α-deficient human vascular cells including vascular endothelial cells, vascular smooth muscle cells, and mesenchymal stem cells (MSCs), as a platform for discovering cell type-specific hypoxia-induced response mechanisms. Through comparative molecular profiling across cell types under normoxic and hypoxic conditions, we provide insight into the indispensable role of HIF-1α in the promotion of ischemic vascular regeneration. We found human MSCs to be the vascular cell type most susceptible to HIF-1α deficiency, and that transcriptional inactivation of ANKZF1, an effector of HIF-1α, impaired pro-angiogenic processes. Altogether, our findings deepen the understanding of HIF-1α in human angiogenesis and support further explorations of novel therapeutic strategies of vascular regeneration against ischemic damage.</p>","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":21.1,"publicationDate":"2024-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10762672/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9432828","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
Innovative insights into extrachromosomal circular DNAs in gynecologic tumors and reproduction. 对妇科肿瘤和生殖中染色体外环状 DNA 的创新见解。
IF 21.1 1区 生物学
Protein & Cell Pub Date : 2024-01-03 DOI: 10.1093/procel/pwad032
Ning Wu, Ling Wei, Zhipeng Zhu, Qiang Liu, Kailong Li, Fengbiao Mao, Jie Qiao, Xiaolu Zhao
{"title":"Innovative insights into extrachromosomal circular DNAs in gynecologic tumors and reproduction.","authors":"Ning Wu, Ling Wei, Zhipeng Zhu, Qiang Liu, Kailong Li, Fengbiao Mao, Jie Qiao, Xiaolu Zhao","doi":"10.1093/procel/pwad032","DOIUrl":"10.1093/procel/pwad032","url":null,"abstract":"<p><p>Originating but free from chromosomal DNA, extrachromosomal circular DNAs (eccDNAs) are organized in circular form and have long been found in unicellular and multicellular eukaryotes. Their biogenesis and function are poorly understood as they are characterized by sequence homology with linear DNA, for which few detection methods are available. Recent advances in high-throughput sequencing technologies have revealed that eccDNAs play crucial roles in tumor formation, evolution, and drug resistance as well as aging, genomic diversity, and other biological processes, bringing it back to the research hotspot. Several mechanisms of eccDNA formation have been proposed, including the breakage-fusion-bridge (BFB) and translocation-deletion-amplification models. Gynecologic tumors and disorders of embryonic and fetal development are major threats to human reproductive health. The roles of eccDNAs in these pathological processes have been partially elucidated since the first discovery of eccDNA in pig sperm and the double minutes in ovarian cancer ascites. The present review summarized the research history, biogenesis, and currently available detection and analytical methods for eccDNAs and clarified their functions in gynecologic tumors and reproduction. We also proposed the application of eccDNAs as drug targets and liquid biopsy markers for prenatal diagnosis and the early detection, prognosis, and treatment of gynecologic tumors. This review lays theoretical foundations for future investigations into the complex regulatory networks of eccDNAs in vital physiological and pathological processes.</p>","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":21.1,"publicationDate":"2024-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10762679/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9524639","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
Correction to: SIRT7 antagonizes human stem cell aging as a heterochromatin stabilizer. 更正:SIRT7作为异染色质稳定剂拮抗人类干细胞衰老
IF 21.1 1区 生物学
Protein & Cell Pub Date : 2024-01-03 DOI: 10.1093/procel/pwad037
{"title":"Correction to: SIRT7 antagonizes human stem cell aging as a heterochromatin stabilizer.","authors":"","doi":"10.1093/procel/pwad037","DOIUrl":"10.1093/procel/pwad037","url":null,"abstract":"","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":21.1,"publicationDate":"2024-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10762660/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9779322","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
Biallelic variants in RBM42 cause a multisystem disorder with neurological, facial, cardiac, and musculoskeletal involvement. RBM42 的双叶变体会导致神经、面部、心脏和肌肉骨骼受累的多系统疾病。
IF 21.1 1区 生物学
Protein & Cell Pub Date : 2024-01-03 DOI: 10.1093/procel/pwad034
Yiyao Chen, Bingxin Yang, Xiaoyu Merlin Zhang, Songchang Chen, Minhui Wang, Liya Hu, Nina Pan, Shuyuan Li, Weihui Shi, Zhenhua Yang, Li Wang, Yajing Tan, Jian Wang, Yanlin Wang, Qinghe Xing, Zhonghua Ma, Jinsong Li, He-Feng Huang, Jinglan Zhang, Chenming Xu
{"title":"Biallelic variants in RBM42 cause a multisystem disorder with neurological, facial, cardiac, and musculoskeletal involvement.","authors":"Yiyao Chen, Bingxin Yang, Xiaoyu Merlin Zhang, Songchang Chen, Minhui Wang, Liya Hu, Nina Pan, Shuyuan Li, Weihui Shi, Zhenhua Yang, Li Wang, Yajing Tan, Jian Wang, Yanlin Wang, Qinghe Xing, Zhonghua Ma, Jinsong Li, He-Feng Huang, Jinglan Zhang, Chenming Xu","doi":"10.1093/procel/pwad034","DOIUrl":"10.1093/procel/pwad034","url":null,"abstract":"<p><p>Here, we report a previously unrecognized syndromic neurodevelopmental disorder associated with biallelic loss-of-function variants in the RBM42 gene. The patient is a 2-year-old female with severe central nervous system (CNS) abnormalities, hypotonia, hearing loss, congenital heart defects, and dysmorphic facial features. Familial whole-exome sequencing (WES) reveals that the patient has two compound heterozygous variants, c.304C>T (p.R102*) and c.1312G>A (p.A438T), in the RBM42 gene which encodes an integral component of splicing complex in the RNA-binding motif protein family. The p.A438T variant is in the RRM domain which impairs RBM42 protein stability in vivo. Additionally, p.A438T disrupts the interaction of RBM42 with hnRNP K, which is the causative gene for Au-Kline syndrome with overlapping disease characteristics seen in the index patient. The human R102* or A438T mutant protein failed to fully rescue the growth defects of RBM42 ortholog knockout ΔFgRbp1 in Fusarium while it was rescued by the wild-type (WT) human RBM42. A mouse model carrying Rbm42 compound heterozygous variants, c.280C>T (p.Q94*) and c.1306_1308delinsACA (p.A436T), demonstrated gross fetal developmental defects and most of the double mutant animals died by E13.5. RNA-seq data confirmed that Rbm42 was involved in neurological and myocardial functions with an essential role in alternative splicing (AS). Overall, we present clinical, genetic, and functional data to demonstrate that defects in RBM42 constitute the underlying etiology of a new neurodevelopmental disease which links the dysregulation of global AS to abnormal embryonic development.</p>","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":21.1,"publicationDate":"2024-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10762670/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9603681","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
An orally-available monovalent SMAC mimetic compound as a broad-spectrum antiviral. 一种可口服的单价 SMAC 拟态化合物,是一种广谱抗病毒药物。
IF 21.1 1区 生物学
Protein & Cell Pub Date : 2024-01-03 DOI: 10.1093/procel/pwad033
Miao Mei, Maria Antonietta Impagnatiello, Jun Jiao, Ulrich Reiser, Ulrike Tontsch-Grunt, Ju Zhang, Paul Nicklin, Bingke Yu, Yu Wang, Yuan He, Xu Tan
{"title":"An orally-available monovalent SMAC mimetic compound as a broad-spectrum antiviral.","authors":"Miao Mei, Maria Antonietta Impagnatiello, Jun Jiao, Ulrich Reiser, Ulrike Tontsch-Grunt, Ju Zhang, Paul Nicklin, Bingke Yu, Yu Wang, Yuan He, Xu Tan","doi":"10.1093/procel/pwad033","DOIUrl":"10.1093/procel/pwad033","url":null,"abstract":"","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":21.1,"publicationDate":"2024-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10762662/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9603683","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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