Protein & Cell最新文献

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":null,"pages":null},"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

Syn3, a newly developed cyclic peptide and BDNF signaling enhancer, ameliorates retinal ganglion cell degeneration in diabetic retinopathy. Syn3 是一种新开发的环肽和 BDNF 信号增强剂，可改善糖尿病视网膜病变中视网膜神经节细胞的退化。

IF 13.6 1区生物学

Protein & Cell Pub Date : 2024-11-01 DOI: 10.1093/procel/pwae028

Ke-Ran Li, Meng-Jia Huan, Jin Yao, Jia-Jun Li, Yuan Cao, Suyu Wang, Mandar T Naik, Yuan Fang, John Marshall, Chang-Gong Lan, Cong Cao

引用次数: 0

Integrative analysis of transcriptome, DNA methylome, and chromatin accessibility reveals candidate therapeutic targets in hypertrophic cardiomyopathy. 转录组、DNA 甲基化组和染色质可及性的综合分析揭示了肥厚型心肌病的候选治疗靶点。

IF 13.6 1区生物学

Protein & Cell Pub Date : 2024-11-01 DOI: 10.1093/procel/pwae032

Junpeng Gao, Mengya Liu, Minjie Lu, Yuxuan Zheng, Yan Wang, Jingwei Yang, Xiaohui Xue, Yun Liu, Fuchou Tang, Shuiyun Wang, Lei Song, Lu Wen, Jizheng Wang

{"title":"Integrative analysis of transcriptome, DNA methylome, and chromatin accessibility reveals candidate therapeutic targets in hypertrophic cardiomyopathy.","authors":"Junpeng Gao, Mengya Liu, Minjie Lu, Yuxuan Zheng, Yan Wang, Jingwei Yang, Xiaohui Xue, Yun Liu, Fuchou Tang, Shuiyun Wang, Lei Song, Lu Wen, Jizheng Wang","doi":"10.1093/procel/pwae032","DOIUrl":"10.1093/procel/pwae032","url":null,"abstract":"Hypertrophic cardiomyopathy (HCM) is the most common inherited heart disease and is characterized by primary left ventricular hypertrophy usually caused by mutations in sarcomere genes. The mechanism underlying cardiac remodeling in HCM remains incompletely understood. An investigation of HCM through integrative analysis at multi-omics levels will be helpful for treating HCM. DNA methylation and chromatin accessibility, as well as gene expression, were assessed by nucleosome occupancy and methylome sequencing (NOMe-seq) and RNA-seq, respectively, using the cardiac tissues of HCM patients. Compared with those of the controls, the transcriptome, DNA methylome, and chromatin accessibility of the HCM myocardium showed multifaceted differences. At the transcriptome level, HCM hearts returned to the fetal gene program through decreased sarcomeric and metabolic gene expression and increased extracellular matrix gene expression. In the DNA methylome, hypermethylated and hypomethylated differentially methylated regions were identified in HCM. At the chromatin accessibility level, HCM hearts showed changes in different genome elements. Several transcription factors, including SP1 and EGR1, exhibited a fetal-like pattern of binding motifs in nucleosome-depleted regions in HCM. In particular, the inhibition of SP1 or EGR1 in an HCM mouse model harboring sarcomere mutations markedly alleviated the HCM phenotype of the mutant mice and reversed fetal gene reprogramming. Overall, this study not only provides a high-precision multi-omics map of HCM heart tissue but also sheds light on the therapeutic strategy by intervening in the fetal gene reprogramming in HCM.","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":13.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11528543/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141082074","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

Antiviral activity of lipoxygenase against severe fever with thrombocytopenia syndrome virus. 脂氧合酶对严重发热伴血小板减少综合征病毒的抗病毒活性

IF 13.6 1区生物学

Protein & Cell Pub Date : 2024-10-29 DOI: 10.1093/procel/pwae061

Shuang Li, Xiaojie Zheng, Yunfa Zhang, Lingyu Zhang, Tong Yang, Hao Li, Caiyu Zhou, Xiao-Ai Zhang, Li-Zeng Gao, Wei Liu

引用次数: 0

Microbiome, metabolome and transcriptome analyses in esophageal squamous cell carcinoma: Insights into immune modulation by F. nucleatum. 食管鳞状细胞癌的微生物组、代谢组和转录组分析：洞察核酸酵母菌的免疫调节作用。

IF 13.6 1区生物学

Protein & Cell Pub Date : 2024-10-29 DOI: 10.1093/procel/pwae063

Xue Zhang, Jing Han, Yudong Wang, Li Feng, Zhisong Fan, Yu Su, Wenya Song, Lan Wang, Long Wang, Hui Jin, Jiayin Liu, Dan Li, Guiying Li, Yan Liu, Jing Zuo, Zhiyu Ni

引用次数: 0

JMJD1C forms condensates to facilitate a RUNX1-dependent gene expression program shared by multiple types of AML cells. JMJD1C 形成凝聚体，促进多种类型急性髓细胞白血病细胞共有的 RUNX1 依赖性基因表达程序。

IF 21.1 1区生物学

Protein & Cell Pub Date : 2024-10-25 DOI: 10.1093/procel/pwae059

Qian Chen,Saisai Wang,Juqing Zhang,Min Xie,Bin Lu,Jie He,Zhuoran Zhen,Jing Li,Jiajun Zhu,Rong Li,Pilong Li,Haifeng Wang,Christopher Vakoc,Robert G Roeder,Mo Chen

{"title":"JMJD1C forms condensates to facilitate a RUNX1-dependent gene expression program shared by multiple types of AML cells.","authors":"Qian Chen,Saisai Wang,Juqing Zhang,Min Xie,Bin Lu,Jie He,Zhuoran Zhen,Jing Li,Jiajun Zhu,Rong Li,Pilong Li,Haifeng Wang,Christopher Vakoc,Robert G Roeder,Mo Chen","doi":"10.1093/procel/pwae059","DOIUrl":"https://doi.org/10.1093/procel/pwae059","url":null,"abstract":"JMJD1C, a member of the lysine demethylase 3 (KDM3) family, is universally required for the survival of several types of acute myeloid leukemia (AML) cells with different genetic mutations, representing a therapeutic opportunity with broad application. Yet how JMJD1C regulates the leukemic programs of various AML cells is largely unexplored. Here we show that JMJD1C interacts with the master hematopoietic transcription factor RUNX1, which thereby recruits JMJD1C to the genome to facilitate a RUNX1-driven transcriptional program that supports leukemic cell survival. The underlying mechanism hinges on the long N-terminal disordered region of JMJD1C, which harbors two inseparable abilities: condensate formation and direct interaction with RUNX1. This dual capability of JMJD1C may influence enhancer-promoter contacts crucial for the expression of key leukemic genes regulated by RUNX1. Our findings demonstrate a previously unappreciated role for the non-catalytic function of JMJD1C in transcriptional regulation, underlying a mechanism shared by different types of leukemias.","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":21.1,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142490565","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

Stress granules and organelles: Coordinating cellular responses in health and disease. 应激颗粒和细胞器：协调健康和疾病中的细胞反应

IF 21.1 1区生物学

Protein & Cell Pub Date : 2024-10-23 DOI: 10.1093/procel/pwae057

Ying Liu,Yin Li,Peipei Zhang

引用次数: 0

Quantitative real-time in vitro transcription assay (QRIVTA) for transcriptional regulation studies. 用于转录调控研究的定量实时体外转录测定（QRIVTA）。

IF 21.1 1区生物学

Protein & Cell Pub Date : 2024-10-10 DOI: 10.1093/procel/pwae054

Fan Liu,Jing Xu,Xinli Hu,Bo Duan,Bin Xia

引用次数: 0

Skin organoid transplantation promotes tissue repair with scarless in frostbite. 皮肤类器官移植可促进冻伤组织的无疤痕修复。

IF 13.6 1区生物学

Protein & Cell Pub Date : 2024-10-04 DOI: 10.1093/procel/pwae055

Wenwen Wang, Pu Liu, Wendi Zhu, Tianwei Li, Ying Wang, Yujie Wang, Jun Li, Jie Ma, Ling Leng

{"title":"Skin organoid transplantation promotes tissue repair with scarless in frostbite.","authors":"Wenwen Wang, Pu Liu, Wendi Zhu, Tianwei Li, Ying Wang, Yujie Wang, Jun Li, Jie Ma, Ling Leng","doi":"10.1093/procel/pwae055","DOIUrl":"https://doi.org/10.1093/procel/pwae055","url":null,"abstract":"Frostbite is the most common cold injury and is caused by both immediate cold-induced cell death and the gradual development of localized inflammation and tissue ischemia. Delayed healing of frostbite often leads to scar formation, which not only causes psychological distress but also tends to result in the development of secondary malignant tumors. Therefore, a rapid healing method for frostbite wounds is urgently needed. Herein, we used a mouse skin model of frostbite injury to evaluate the recovery process after frostbite. Moreover, single-cell transcriptomics was used to determine the patterns of changes in monocytes, macrophages, epidermal cells and fibroblasts during frostbite. Most importantly, human-induced pluripotent stem cell (hiPSC) -derived skin organoids combining with gelatin-hydrogel were constructed for the treatment of frostbite. The results showed that skin organoid treatment significantly accelerated wound healing by reducing early inflammation after frostbite and increasing the proportions of epidermal stem cells. Moreover, in the later stage of wound healing, skin organoids reduced the overall proportions of fibroblasts, significantly reduced fibroblast-to-myofibroblast transition by regulating the integrin α5β1-FAK pathway, and remodeled the extracellular matrix (ECM) through degradation and reassembly mechanisms, facilitating the restoration of physiological ECM and reducing the abundance of ECM associated with abnormal scar formation. These results highlight the potential application of organoids for promoting the reversal of frostbite-related injury and the recovery of skin functions. This study provides a new therapeutic alternative for patients suffering from disfigurement and skin dysfunction caused by frostbite.","PeriodicalId":20790,"journal":{"name":"Protein & Cell","volume":null,"pages":null},"PeriodicalIF":13.6,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142372700","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