Protein & Cell最新文献_第2页

MultiKano: an automatic cell type annotation tool for single-cell multi-omics data based on Kolmogorov-Arnold network and data augmentation.

IF 13.6 1区生物学

Protein & Cell Pub Date : 2024-12-10 DOI: 10.1093/procel/pwae069

Siyu Li, Xinhao Zhuang, Songbo Jia, Songming Tang, Liming Yan, Heyang Hua, Yuhang Jia, Xuelin Zhang, Yan Zhang, Qingzhu Yang, Shengquan Chen

引用次数: 0

Aberrant outputs of cerebellar nuclei and targeted rescue of social deficits in an autism mouse model. 自闭症小鼠模型中小脑核的异常输出和社交障碍的定向拯救

IF 13.6 1区生物学

Protein & Cell Pub Date : 2024-12-02 DOI: 10.1093/procel/pwae040

Xin-Yu Cai, Xin-Tai Wang, Jing-Wen Guo, Fang-Xiao Xu, Kuang-Yi Ma, Zhao-Xiang Wang, Yue Zhao, Wei Xie, Martijn Schonewille, Chris De Zeeuw, Wei Chen, Ying Shen

{"title":"Aberrant outputs of cerebellar nuclei and targeted rescue of social deficits in an autism mouse model.","authors":"Xin-Yu Cai, Xin-Tai Wang, Jing-Wen Guo, Fang-Xiao Xu, Kuang-Yi Ma, Zhao-Xiang Wang, Yue Zhao, Wei Xie, Martijn Schonewille, Chris De Zeeuw, Wei Chen, Ying Shen","doi":"10.1093/procel/pwae040","DOIUrl":"10.1093/procel/pwae040","url":null,"abstract":"The cerebellum is heavily connected with other brain regions, sub-serving not only motor but also nonmotor functions. Genetic mutations leading to cerebellar dysfunction are associated with mental diseases, but cerebellar outputs have not been systematically studied in this context. Here, we present three dimensional distributions of 50,168 target neurons of cerebellar nuclei (CN) from wild-type mice and Nlgn3R451C mutant mice, a mouse model for autism. Our results derived from 36 target nuclei show that the projections from CN to thalamus, midbrain and brainstem are differentially affected by Nlgn3R451C mutation. Importantly, Nlgn3R451C mutation altered the innervation power of CN→zona incerta (ZI) pathway, and chemogenetic inhibition of a neuronal subpopulation in the ZI that receives inputs from the CN rescues social defects in Nlgn3R451C mice. Our study highlights potential role of cerebellar outputs in the pathogenesis of autism and provides potential new therapeutic strategy for this disease.","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":" ","pages":"872-888"},"PeriodicalIF":13.6,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11637611/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141767133","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

Macrophages suppress cardiac reprogramming of fibroblasts in vivo via IFN-mediated intercellular self-stimulating circuit. 巨噬细胞通过 IFN 介导的细胞间自我刺激回路抑制体内成纤维细胞的心脏重编程。

IF 13.6 1区生物学

Protein & Cell Pub Date : 2024-12-02 DOI: 10.1093/procel/pwae013

Hao Wang, Junbo Yang, Yihong Cai, Yang Zhao

{"title":"Macrophages suppress cardiac reprogramming of fibroblasts in vivo via IFN-mediated intercellular self-stimulating circuit.","authors":"Hao Wang, Junbo Yang, Yihong Cai, Yang Zhao","doi":"10.1093/procel/pwae013","DOIUrl":"10.1093/procel/pwae013","url":null,"abstract":"Direct conversion of cardiac fibroblasts (CFs) to cardiomyocytes (CMs) in vivo to regenerate heart tissue is an attractive approach. After myocardial infarction (MI), heart repair proceeds with an inflammation stage initiated by monocytes infiltration of the infarct zone establishing an immune microenvironment. However, whether and how the MI microenvironment influences the reprogramming of CFs remains unclear. Here, we found that in comparison with cardiac fibroblasts (CFs) cultured in vitro, CFs that transplanted into infarct region of MI mouse models resisted to cardiac reprogramming. RNA-seq analysis revealed upregulation of interferon (IFN) response genes in transplanted CFs, and subsequent inhibition of the IFN receptors increased reprogramming efficiency in vivo. Macrophage-secreted IFN-β was identified as the dominant upstream signaling factor after MI. CFs treated with macrophage-conditioned medium containing IFN-β displayed reduced reprogramming efficiency, while macrophage depletion or blocking the IFN signaling pathway after MI increased reprogramming efficiency in vivo. Co-IP, BiFC and Cut-tag assays showed that phosphorylated STAT1 downstream of IFN signaling in CFs could interact with the reprogramming factor GATA4 and inhibit the GATA4 chromatin occupancy in cardiac genes. Furthermore, upregulation of IFN-IFNAR-p-STAT1 signaling could stimulate CFs secretion of CCL2/7/12 chemokines, subsequently recruiting IFN-β-secreting macrophages. Together, these immune cells further activate STAT1 phosphorylation, enhancing CCL2/7/12 secretion and immune cell recruitment, ultimately forming a self-reinforcing positive feedback loop between CFs and macrophages via IFN-IFNAR-p-STAT1 that inhibits cardiac reprogramming in vivo. Cumulatively, our findings uncover an intercellular self-stimulating inflammatory circuit as a microenvironmental molecular barrier of in situ cardiac reprogramming that needs to be overcome for regenerative medicine applications.","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":" ","pages":"906-929"},"PeriodicalIF":13.6,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11637486/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140294305","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: Macrophages suppress cardiac reprogramming of fibroblasts in vivo via IFN-mediated intercellular self-stimulating circuit. 更正为巨噬细胞通过 IFN 介导的细胞间自我刺激回路抑制体内成纤维细胞的心脏重编程。

IF 13.6 1区生物学

Protein & Cell Pub Date : 2024-12-02 DOI: 10.1093/procel/pwae038

引用次数: 0

Endothelial-to-Osteoblast Conversion maintains bone homeostasis through Kindlin-2/Piezo1/TGFβ/Runx2 axis.

IF 13.6 1区生物学

Protein & Cell Pub Date : 2024-12-02 DOI: 10.1093/procel/pwae066

Guixing Ma, Yingying Han, Wanze Tang, Bo Zhou, Litong Chen, Zhen Ding, Siyuan Cheng, Di Chen, Huiling Cao

引用次数: 0

A third dose of inactivated vaccine augments the potency, breadth, and duration of anamnestic responses against SARS-CoV-2. 第三剂灭活疫苗可增强对 SARS-CoV-2 的过敏反应的效力、广度和持续时间。

IF 13.6 1区生物学

Protein & Cell Pub Date : 2024-12-02 DOI: 10.1093/procel/pwae033

Zijing Jia, Kang Wang, Minxiang Xie, Jiajing Wu, Yaling Hu, Yunjiao Zhou, Ayijiang Yisimayi, Wangjun Fu, Lei Wang, Pan Liu, Kaiyue Fan, Ruihong Chen, Lin Wang, Jing Li, Yao Wang, Xiaoqin Ge, Qianqian Zhang, Jianbo Wu, Nan Wang, Wei Wu, Yidan Gao, Jingyun Miao, Yinan Jiang, Lili Qin, Ling Zhu, Weijin Huang, Yanjun Zhang, Huan Zhang, Baisheng Li, Qiang Gao, Xiaoliang Sunney Xie, Youchun Wang, Yunlong Cao, Qiao Wang, Xiangxi Wang

引用次数: 0

Dissecting caspase-2-mediated cell death: from intrinsic PIDDosome activation to chemical modulation. 剖析caspase-2介导的细胞死亡：从内在PIDDosome激活到化学调制。

IF 13.6 1区生物学

Protein & Cell Pub Date : 2024-12-02 DOI: 10.1093/procel/pwae020

Mengxue Zeng, Kun Wang, Qingcui Wu, Jingjin Ding, Dan Xie, Xiangbing Qi, Feng Shao

{"title":"Dissecting caspase-2-mediated cell death: from intrinsic PIDDosome activation to chemical modulation.","authors":"Mengxue Zeng, Kun Wang, Qingcui Wu, Jingjin Ding, Dan Xie, Xiangbing Qi, Feng Shao","doi":"10.1093/procel/pwae020","DOIUrl":"10.1093/procel/pwae020","url":null,"abstract":"Caspase-2, a highly conserved member of the caspase family, is considered an initiator caspase that triggers apoptosis in response to some cellular stresses. Previous studies suggest that an intracellular multi-protein complex PIDDosome, induced by genotoxic stress, serves as a platform for caspase-2 activation. Due to caspase-2's inability to process effector caspases, however, the mechanism underlying caspase-2-mediated cell death upon PIDDosome activation remains unclear. Here, we conducted an unbiased genome-wide genetic screen and identified that the Bcl2 family protein BID is required for PIDDosome-induced, caspase-2-mediated apoptosis. PIDDosome-activated caspase-2 directly and functionally processes BID to signal the mitochondrial pathway for apoptosis induction. In addition, a designed chemical screen identified a compound, HUHS015, which specifically activates caspase-2-mediated apoptosis. HUHS015-stimulated apoptosis also requires BID but is independent of the PIDDosome. Through extensive structure-activity relationship efforts, we identified a derivative with a potency of ~60 nmol/L in activating caspase-2-mediated apoptosis. The HUHS015-series of compounds act as efficient agonists that directly target the interdomain linker in caspase-2, representing a new mode of initiator caspase activation. Human and mouse caspase-2 differ in two crucial residues in the linker, rendering a selectivity of the agonists for human caspase-2. The caspase-2 agonists are valuable tools to explore the physiological roles of caspase-2-mediated cell death and a base for developing small-molecule drugs for relevant diseases.","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":" ","pages":"889-905"},"PeriodicalIF":13.6,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11637483/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140869069","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: Adenosine-to-inosine RNA editing in cancer: molecular mechanisms and downstream targets. 更正：癌症中的腺苷转肌苷 RNA 编辑：分子机制和下游靶点。

IF 13.6 1区生物学

Protein & Cell Pub Date : 2024-11-08 DOI: 10.1093/procel/pwae062

引用次数: 0

p21/Zbtb18 repress the expression of cKit to regulate the self-renewal of hematopoietic stem cells. p21/Zbtb18 抑制 cKit 的表达，从而调节造血干细胞的自我更新。

IF 13.6 1区生物学

Protein & Cell Pub Date : 2024-11-01 DOI: 10.1093/procel/pwae022

Nini Wang, Shangda Yang, Yu Li, Fanglin Gou, Yanling Lv, Xiangnan Zhao, Yifei Wang, Chang Xu, Bin Zhou, Fang Dong, Zhenyu Ju, Tao Cheng, Hui Cheng

{"title":"p21/Zbtb18 repress the expression of cKit to regulate the self-renewal of hematopoietic stem cells.","authors":"Nini Wang, Shangda Yang, Yu Li, Fanglin Gou, Yanling Lv, Xiangnan Zhao, Yifei Wang, Chang Xu, Bin Zhou, Fang Dong, Zhenyu Ju, Tao Cheng, Hui Cheng","doi":"10.1093/procel/pwae022","DOIUrl":"10.1093/procel/pwae022","url":null,"abstract":"The maintenance of hematopoietic stem cells (HSCs) is a complex process involving numerous cell-extrinsic and -intrinsic regulators. The first member of the cyclin-dependent kinase family of inhibitors to be identified, p21, has been reported to perform a wide range of critical biological functions, including cell cycle regulation, transcription, differentiation, and so on. Given the previous inconsistent results regarding the functions of p21 in HSCs in a p21-knockout mouse model, we employed p21-tdTomato (tdT) mice to further elucidate its role in HSCs during homeostasis. The results showed that p21-tdT+ HSCs exhibited increased self-renewal capacity compared to p21-tdT- HSCs. Zbtb18, a transcriptional repressor, was upregulated in p21-tdT+ HSCs, and its knockdown significantly impaired the reconstitution capability of HSCs. Furthermore, p21 interacted with ZBTB18 to co-repress the expression of cKit in HSCs and thus regulated the self-renewal of HSCs. Our data provide novel insights into the physiological role and mechanisms of p21 in HSCs during homeostasis independent of its conventional role as a cell cycle inhibitor.","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":" ","pages":"840-857"},"PeriodicalIF":13.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11528518/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140892325","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 13.6 1区生物学

Protein & Cell Pub Date : 2024-11-01 DOI: 10.1093/procel/pwad062

引用次数: 0