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RADICAL: a rationally designed ion channel activated by ligand for chemogenetics. RADICAL:通过配体激活的合理设计的离子通道,用于化学遗传学。
IF 13.6 1区 生物学
Protein & Cell Pub Date : 2025-02-01 DOI: 10.1093/procel/pwae048
Heng Zhang, Zhiwei Zheng, Xiaoying Chen, Lizhen Xu, Chen Guo, Jiawei Wang, Yihui Cui, Fan Yang
{"title":"RADICAL: a rationally designed ion channel activated by ligand for chemogenetics.","authors":"Heng Zhang, Zhiwei Zheng, Xiaoying Chen, Lizhen Xu, Chen Guo, Jiawei Wang, Yihui Cui, Fan Yang","doi":"10.1093/procel/pwae048","DOIUrl":"10.1093/procel/pwae048","url":null,"abstract":"","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":" ","pages":"136-142"},"PeriodicalIF":13.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786721/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142120399","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
Lcn2 secreted by macrophages through NLRP3 signaling pathway induced severe pneumonia. 巨噬细胞通过 NLRP3 信号通路分泌的 Lcn2 可诱发重症肺炎。
IF 13.6 1区 生物学
Protein & Cell Pub Date : 2025-02-01 DOI: 10.1093/procel/pwae045
Mingya Liu, Feifei Qi, Jue Wang, Fengdi Li, Qi Lv, Ran Deng, Xujian Liang, Shasha Zhou, Pin Yu, Yanfeng Xu, Yaqing Zhang, Yiwei Yan, Ming Liu, Shuyue Li, Guocui Mou, Linlin Bao
{"title":"Lcn2 secreted by macrophages through NLRP3 signaling pathway induced severe pneumonia.","authors":"Mingya Liu, Feifei Qi, Jue Wang, Fengdi Li, Qi Lv, Ran Deng, Xujian Liang, Shasha Zhou, Pin Yu, Yanfeng Xu, Yaqing Zhang, Yiwei Yan, Ming Liu, Shuyue Li, Guocui Mou, Linlin Bao","doi":"10.1093/procel/pwae045","DOIUrl":"10.1093/procel/pwae045","url":null,"abstract":"","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":" ","pages":"148-155"},"PeriodicalIF":13.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786722/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142047110","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
Alzheimer's disease: insights into pathology, molecular mechanisms, and therapy. 阿尔茨海默病:对病理学、分子机制和治疗的见解。
IF 13.6 1区 生物学
Protein & Cell Pub Date : 2025-02-01 DOI: 10.1093/procel/pwae026
Qiuyang Zheng, Xin Wang
{"title":"Alzheimer's disease: insights into pathology, molecular mechanisms, and therapy.","authors":"Qiuyang Zheng, Xin Wang","doi":"10.1093/procel/pwae026","DOIUrl":"10.1093/procel/pwae026","url":null,"abstract":"<p><p>Alzheimer's disease (AD), the leading cause of dementia, is characterized by the accumulation of amyloid plaques and neurofibrillary tangles in the brain. This condition casts a significant shadow on global health due to its complex and multifactorial nature. In addition to genetic predispositions, the development of AD is influenced by a myriad of risk factors, including aging, systemic inflammation, chronic health conditions, lifestyle, and environmental exposures. Recent advancements in understanding the complex pathophysiology of AD are paving the way for enhanced diagnostic techniques, improved risk assessment, and potentially effective prevention strategies. These discoveries are crucial in the quest to unravel the complexities of AD, offering a beacon of hope for improved management and treatment options for the millions affected by this debilitating disease.</p>","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":" ","pages":"83-120"},"PeriodicalIF":13.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786724/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140909164","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
Cas7 meets Cas14: a strategic partnership in the type VII CRISPR-Cas. Cas7与Cas14: VII型CRISPR-Cas的战略合作伙伴关系
IF 13.6 1区 生物学
Protein & Cell Pub Date : 2025-02-01 DOI: 10.1093/procel/pwae056
Yao Liu, Senfeng Zhang, Chunyi Hu
{"title":"Cas7 meets Cas14: a strategic partnership in the type VII CRISPR-Cas.","authors":"Yao Liu, Senfeng Zhang, Chunyi Hu","doi":"10.1093/procel/pwae056","DOIUrl":"10.1093/procel/pwae056","url":null,"abstract":"","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":"16 2","pages":"79-82"},"PeriodicalIF":13.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786720/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144216673","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 upgraded nuclease prime editor platform enables high-efficiency singled or multiplexed knock-in/knockout of genes in mouse and sheep zygotes. 升级的核酸酶引物编辑平台能够高效地在小鼠和绵羊受精卵中进行单敲或多重敲入/敲除基因。
IF 21.1 1区 生物学
Protein & Cell Pub Date : 2025-01-20 DOI: 10.1093/procel/pwaf006
Weijia Mao,Pei Wang,Lei Zhou,Dongxu Li,Xiangyang Li,Xin Lou,Xingxu Huang,Feng Wang,Yanli Zhang,Jianghuai Liu,Yongjie Wan
{"title":"An upgraded nuclease prime editor platform enables high-efficiency singled or multiplexed knock-in/knockout of genes in mouse and sheep zygotes.","authors":"Weijia Mao,Pei Wang,Lei Zhou,Dongxu Li,Xiangyang Li,Xin Lou,Xingxu Huang,Feng Wang,Yanli Zhang,Jianghuai Liu,Yongjie Wan","doi":"10.1093/procel/pwaf006","DOIUrl":"https://doi.org/10.1093/procel/pwaf006","url":null,"abstract":"","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":"107 1","pages":""},"PeriodicalIF":21.1,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142991833","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
FOXO3-engineered human mesenchymal stem cells efficiently enhance post-ischemic stroke functional rehabilitation. foxo3工程人间充质干细胞有效促进缺血性脑卒中后功能康复。
IF 21.1 1区 生物学
Protein & Cell Pub Date : 2025-01-17 DOI: 10.1093/procel/pwaf004
Fangshuo Zheng,Jinghui Lei,Zan He,Taixin Ning,Shuhui Sun,Yusheng Cai,Qian Zhao,Shuai Ma,Weiqi Zhang,Jing Qu,Guang-Hui Liu,Si Wang
{"title":"FOXO3-engineered human mesenchymal stem cells efficiently enhance post-ischemic stroke functional rehabilitation.","authors":"Fangshuo Zheng,Jinghui Lei,Zan He,Taixin Ning,Shuhui Sun,Yusheng Cai,Qian Zhao,Shuai Ma,Weiqi Zhang,Jing Qu,Guang-Hui Liu,Si Wang","doi":"10.1093/procel/pwaf004","DOIUrl":"https://doi.org/10.1093/procel/pwaf004","url":null,"abstract":"","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":"56 1","pages":""},"PeriodicalIF":21.1,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142989314","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
The Icarian flight of antibody-drug conjugates: target selection amidst complexity and tackling adverse impacts. 抗体-药物偶联物的伊卡利亚飞行:复杂中的靶标选择和处理不利影响。
IF 21.1 1区 生物学
Protein & Cell Pub Date : 2025-01-15 DOI: 10.1093/procel/pwaf002
Han Liu,Hongye Zeng,Xiaojing Qin,Wenjing Ning,Lin Xu,Shiting Yang,Xue Liu,Wenxin Luo,Ningshao Xia
{"title":"The Icarian flight of antibody-drug conjugates: target selection amidst complexity and tackling adverse impacts.","authors":"Han Liu,Hongye Zeng,Xiaojing Qin,Wenjing Ning,Lin Xu,Shiting Yang,Xue Liu,Wenxin Luo,Ningshao Xia","doi":"10.1093/procel/pwaf002","DOIUrl":"https://doi.org/10.1093/procel/pwaf002","url":null,"abstract":"Antibody-drug conjugates (ADCs) represent a promising class of targeted cancer therapeutics that combine the specificity of monoclonal antibodies with the potency of cytotoxic payloads. Despite their therapeutic potential, the use of ADCs faces significant challenges, including off/on-target toxicity and resistance development. This review examines the current landscape of ADC development, focusing on the critical aspects of target selection and antibody engineering. We discuss strategies to increase ADC efficacy and safety, including multitarget approaches, pH-dependent antibodies, and masked peptide technologies. The importance of comprehensive antigen expression profiling in both tumor and normal tissues is emphasized, highlighting the role of advanced technologies, such as single-cell sequencing and artificial intelligence (AI), in optimizing target selection. Furthermore, we explore combination therapies and innovations in linker‒payload chemistry, which may provide approaches for expanding the therapeutic window of ADCs. These advances pave the way for the development of more precise and effective cancer treatments, potentially extending ADC applications beyond oncology.","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":"127 1","pages":""},"PeriodicalIF":21.1,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142989315","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
Lentivirus-modified hematopoietic stem cell gene therapy for advanced symptomatic juvenile metachromatic leukodystrophy: a long-term follow-up pilot study. 慢病毒修饰造血干细胞基因疗法治疗晚期症状性幼年变色性白质营养不良症:长期跟踪试点研究。
IF 13.6 1区 生物学
Protein & Cell Pub Date : 2025-01-04 DOI: 10.1093/procel/pwae037
Zhao Zhang, Hua Jiang, Li Huang, Sixi Liu, Xiaoya Zhou, Yun Cai, Ming Li, Fei Gao, Xiaoting Liang, Kam-Sze Tsang, Guangfu Chen, Chui-Yan Ma, Yuet-Hung Chai, Hongsheng Liu, Chen Yang, Mo Yang, Xiaoling Zhang, Shuo Han, Xin Du, Ling Chen, Wuh-Liang Hwu, Jiacai Zhuo, Qizhou Lian
{"title":"Lentivirus-modified hematopoietic stem cell gene therapy for advanced symptomatic juvenile metachromatic leukodystrophy: a long-term follow-up pilot study.","authors":"Zhao Zhang, Hua Jiang, Li Huang, Sixi Liu, Xiaoya Zhou, Yun Cai, Ming Li, Fei Gao, Xiaoting Liang, Kam-Sze Tsang, Guangfu Chen, Chui-Yan Ma, Yuet-Hung Chai, Hongsheng Liu, Chen Yang, Mo Yang, Xiaoling Zhang, Shuo Han, Xin Du, Ling Chen, Wuh-Liang Hwu, Jiacai Zhuo, Qizhou Lian","doi":"10.1093/procel/pwae037","DOIUrl":"10.1093/procel/pwae037","url":null,"abstract":"<p><p>Metachromatic leukodystrophy (MLD) is an inherited disease caused by a deficiency of the enzyme arylsulfatase A (ARSA). Lentivirus-modified autologous hematopoietic stem cell gene therapy (HSCGT) has recently been approved for clinical use in pre and early symptomatic children with MLD to increase ARSA activity. Unfortunately, this advanced therapy is not available for most patients with MLD who have progressed to more advanced symptomatic stages at diagnosis. Patients with late-onset juvenile MLD typically present with a slower neurological progression of symptoms and represent a significant burden to the economy and healthcare system, whereas those with early onset infantile MLD die within a few years of symptom onset. We conducted a pilot study to determine the safety and benefit of HSCGT in patients with postsymptomatic juvenile MLD and report preliminary results. The safety profile of HSCGT was favorable in this long-term follow-up over 9 years. The most common adverse events (AEs) within 2 months of HSCGT were related to busulfan conditioning, and all AEs resolved. No HSCGT-related AEs and no evidence of distorted hematopoietic differentiation during long-term follow-up for up to 9.6 years. Importantly, to date, patients have maintained remarkably improved ARSA activity with a stable disease state, including increased Functional Independence Measure (FIM) score and decreased magnetic resonance imaging (MRI) lesion score. This long-term follow-up pilot study suggests that HSCGT is safe and provides clinical benefit to patients with postsymptomatic juvenile MLD.</p>","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":" ","pages":"16-27"},"PeriodicalIF":13.6,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141446854","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
Noncoding RNA Terc-53 and hyaluronan receptor Hmmr regulate aging in mice. 非编码 RNA Terc-53 和透明质酸受体 Hmmr 可调节小鼠的衰老。
IF 13.6 1区 生物学
Protein & Cell Pub Date : 2025-01-04 DOI: 10.1093/procel/pwae023
Sipeng Wu, Yiqi Cai, Lixiao Zhang, Xiang Li, Xu Liu, Guangkeng Zhou, Hongdi Luo, Renjian Li, Yujia Huo, Zhirong Zhang, Siyi Chen, Jinliang Huang, Jiahao Shi, Shanwei Ding, Zhe Sun, Zizhuo Zhou, Pengcheng Wang, Geng Wang
{"title":"Noncoding RNA Terc-53 and hyaluronan receptor Hmmr regulate aging in mice.","authors":"Sipeng Wu, Yiqi Cai, Lixiao Zhang, Xiang Li, Xu Liu, Guangkeng Zhou, Hongdi Luo, Renjian Li, Yujia Huo, Zhirong Zhang, Siyi Chen, Jinliang Huang, Jiahao Shi, Shanwei Ding, Zhe Sun, Zizhuo Zhou, Pengcheng Wang, Geng Wang","doi":"10.1093/procel/pwae023","DOIUrl":"10.1093/procel/pwae023","url":null,"abstract":"<p><p>One of the basic questions in the aging field is whether there is a fundamental difference between the aging of lower invertebrates and mammals. A major difference between the lower invertebrates and mammals is the abundancy of noncoding RNAs, most of which are not conserved. We have previously identified a noncoding RNA Terc-53 that is derived from the RNA component of telomerase Terc. To study its physiological functions, we generated two transgenic mouse models overexpressing the RNA in wild-type and early-aging Terc-/- backgrounds. Terc-53 mice showed age-related cognition decline and shortened life span, even though no developmental defects or physiological abnormality at an early age was observed, indicating its involvement in normal aging of mammals. Subsequent mechanistic study identified hyaluronan-mediated motility receptor (Hmmr) as the main effector of Terc-53. Terc-53 mediates the degradation of Hmmr, leading to an increase of inflammation in the affected tissues, accelerating organismal aging. adeno-associated virus delivered supplementation of Hmmr in the hippocampus reversed the cognition decline in Terc-53 transgenic mice. Neither Terc-53 nor Hmmr has homologs in C. elegans. Neither do arthropods express hyaluronan. These findings demonstrate the complexity of aging in mammals and open new paths for exploring noncoding RNA and Hmmr as means of treating age-related physical debilities and improving healthspan.</p>","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":" ","pages":"28-48"},"PeriodicalIF":13.6,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140892318","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
ARID1A IDR targets EWS-FLI1 condensates and finetunes chromatin remodeling. ARID1A IDR以EWS-FLI1凝集物为靶标,对染色质重塑进行微调。
IF 13.6 1区 生物学
Protein & Cell Pub Date : 2025-01-04 DOI: 10.1093/procel/pwae029
Jingdong Xue, Siang Lv, Ming Yu, Yixuan Pan, Ningzhe Li, Xiang Xu, Qi Zhang, Mengyuan Peng, Fang Liu, Xuxu Sun, Yimin Lao, Yanhua Yao, Juan Song, Jun Wu, Bing Li
{"title":"ARID1A IDR targets EWS-FLI1 condensates and finetunes chromatin remodeling.","authors":"Jingdong Xue, Siang Lv, Ming Yu, Yixuan Pan, Ningzhe Li, Xiang Xu, Qi Zhang, Mengyuan Peng, Fang Liu, Xuxu Sun, Yimin Lao, Yanhua Yao, Juan Song, Jun Wu, Bing Li","doi":"10.1093/procel/pwae029","DOIUrl":"10.1093/procel/pwae029","url":null,"abstract":"","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":" ","pages":"64-71"},"PeriodicalIF":13.6,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140959284","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
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