Journal of Molecular Cell Biology最新文献_第9页

Distinct roles of two SEC scaffold proteins, AFF1 and AFF4, in regulating RNA polymerase II transcription elongation. 两种 SEC 支架蛋白 AFF1 和 AFF4 在调节 RNA 聚合酶 II 转录伸长过程中的不同作用。

IF 5.3 2区生物学

Journal of Molecular Cell Biology Pub Date : 2024-01-17 DOI: 10.1093/jmcb/mjad049

Zhuanzhuan Che, Xiaoxu Liu, Qian Dai, Ke Fang, Chenghao Guo, Junjie Yue, Haitong Fang, Peng Xie, Zhuojuan Luo, Chengqi Lin

{"title":"Distinct roles of two SEC scaffold proteins, AFF1 and AFF4, in regulating RNA polymerase II transcription elongation.","authors":"Zhuanzhuan Che, Xiaoxu Liu, Qian Dai, Ke Fang, Chenghao Guo, Junjie Yue, Haitong Fang, Peng Xie, Zhuojuan Luo, Chengqi Lin","doi":"10.1093/jmcb/mjad049","DOIUrl":"10.1093/jmcb/mjad049","url":null,"abstract":"The super elongation complex (SEC) containing positive transcription elongation factor b plays a critical role in regulating transcription elongation. AFF1 and AFF4, two members of the AF4/FMR2 family, act as central scaffold proteins of SEC and are associated with various human diseases. However, their precise roles in transcriptional control remain unclear. Here, we investigate differences in the genomic distribution patterns of AFF1 and AFF4 around transcription start sites (TSSs). AFF1 mainly binds upstream of the TSS, while AFF4 is enriched downstream of the TSS. Notably, disruption of AFF4 results in slow elongation and early termination in a subset of AFF4-bound active genes, whereas AFF1 deletion leads to fast elongation and transcriptional readthrough in the same subset of genes. Additionally, AFF1 knockdown increases AFF4 levels at chromatin, and vice versa. In summary, these findings demonstrate that AFF1 and AFF4 function antagonistically to regulate RNA polymerase II transcription.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11113081/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9922959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

CAMSAP2 and CAMSAP3 localize at microtubule intersections to regulate the spatial distribution of microtubules. CAMSAP2 和 CAMSAP3 定位于微管交汇处，调节微管的空间分布。

IF 5.3 2区生物学

Journal of Molecular Cell Biology Pub Date : 2024-01-17 DOI: 10.1093/jmcb/mjad050

Rui Zhang, Lusheng Gu, Wei Chen, Nobutoshi Tanaka, Zhengrong Zhou, Honglin Xu, Tao Xu, Wei Ji, Xin Liang, Wenxiang Meng

{"title":"CAMSAP2 and CAMSAP3 localize at microtubule intersections to regulate the spatial distribution of microtubules.","authors":"Rui Zhang, Lusheng Gu, Wei Chen, Nobutoshi Tanaka, Zhengrong Zhou, Honglin Xu, Tao Xu, Wei Ji, Xin Liang, Wenxiang Meng","doi":"10.1093/jmcb/mjad050","DOIUrl":"10.1093/jmcb/mjad050","url":null,"abstract":"Microtubule networks support many cellular processes and exhibit a highly ordered architecture. However, due to the limited axial resolution of conventional light microscopy, the structural features of these networks cannot be resolved in three-dimensional (3D) space. Here, we used customized ultra-high-resolution interferometric single-molecule localization microscopy to characterize the microtubule networks in Caco2 cells. We found that the calmodulin-regulated spectrin-associated proteins (CAMSAPs) localize at a portion of microtubule intersections. Further investigation showed that depletion of CAMSAP2 and CAMSAP3 leads to the narrowing of the inter-microtubule distance. Mechanistically, CAMSAPs recognize microtubule defects, which often occur near microtubule intersections, and then recruit katanin to remove the damaged microtubules. Therefore, the CAMSAP-katanin complex is a regulatory module for the distance between microtubules. Taken together, our results characterize the architecture of cellular microtubule networks in high resolution and provide molecular insights into how the 3D structure of microtubule networks is controlled.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11156519/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10332748","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Regulation of endogenous retroviruses in murine embryonic stem cells and early embryos. 小鼠胚胎干细胞和早期胚胎中内源性逆转录病毒的调控。

IF 5.3 2区生物学

Journal of Molecular Cell Biology Pub Date : 2024-01-17 DOI: 10.1093/jmcb/mjad052

Xinyi Lu

引用次数: 0

Stability and function of RCL1 are dependent on the interaction with BMS1. RCL1 的稳定性和功能取决于与 BMS1 的相互作用。

IF 5.5 2区生物学

Journal of Molecular Cell Biology Pub Date : 2024-01-05 DOI: 10.1093/jmcb/mjad046

Yong Wang, Zhenyu Zhao, Hongyan Yu, Hui Shi, Boxiang Tao, Yinan He, Jun Chen, Jinrong Peng, Meifu Gan, Li Jan Lo

{"title":"Stability and function of RCL1 are dependent on the interaction with BMS1.","authors":"Yong Wang, Zhenyu Zhao, Hongyan Yu, Hui Shi, Boxiang Tao, Yinan He, Jun Chen, Jinrong Peng, Meifu Gan, Li Jan Lo","doi":"10.1093/jmcb/mjad046","DOIUrl":"10.1093/jmcb/mjad046","url":null,"abstract":"During ribosome biogenesis, the small subunit (SSU) processome is responsible for 40S assembly. The BMS1/RCL1 complex is a core component of the SSU processome that plays an important role in 18S rRNA processing and maturation. Genetic studies using zebrafish mutants indicate that both Bms1-like (Bms1l) and Rcl1 are essential for digestive organ development. In spite of vital functions of this complex, the mutual dependence of these two nucleolar proteins for the stability and function remains elusive. In this study, we identified an RCL1-interacting domain in BMS1, which is conserved in zebrafish and humans. Moreover, both the protein stability and nucleolar entry of RCL1 depend on its interaction with BMS1, otherwise RCL1 degraded through the ubiquitination-proteasome pathway. Functional studies revealed that overexpression of RCL1 in BMS1-knockdown cells can partially rescue the defects in 18S rRNA processing and cell proliferation, and hepatocyte-specific overexpression of Rcl1 can resume zebrafish liver development in the bms1l substitution mutant bms1lsq163/sq163but not in the knockout mutant bms1lzju1/zju1, which is attributed to the nucleolar entry of Rcl1 in the former mutant. Our data demonstrate that BMS1 and RCL1 interaction is essential for not only pre-rRNA processing but also the communication between ribosome biogenesis and cell cycle regulation.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.5,"publicationDate":"2024-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11023236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9834332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Cholinergic α7 nAChR signaling suppresses SARS-CoV-2 infection and inflammation in lung epithelial cells. 胆碱能α7 nAChR信号抑制SARS-CoV-2感染和肺上皮细胞炎症。

IF 5.5 2区生物学

Journal of Molecular Cell Biology Pub Date : 2024-01-05 DOI: 10.1093/jmcb/mjad048

Jing Wen, Jing Sun, Yanhong Tang, Jincun Zhao, Xiao Su

引用次数: 0

Estrogen receptor α-mediated signaling inhibits type I interferon response to promote breast carcinogenesis. 雌激素受体α介导的信号传导抑制 I 型干扰素反应，从而促进乳腺癌的发生。

IF 5.5 2区生物学

Journal of Molecular Cell Biology Pub Date : 2024-01-05 DOI: 10.1093/jmcb/mjad047

Li-Bo Cao, Zi-Lun Ruan, Yu-Lin Yang, Nian-Chao Zhang, Chuan Gao, Cheguo Cai, Jing Zhang, Ming-Ming Hu, Hong-Bing Shu

{"title":"Estrogen receptor α-mediated signaling inhibits type I interferon response to promote breast carcinogenesis.","authors":"Li-Bo Cao, Zi-Lun Ruan, Yu-Lin Yang, Nian-Chao Zhang, Chuan Gao, Cheguo Cai, Jing Zhang, Ming-Ming Hu, Hong-Bing Shu","doi":"10.1093/jmcb/mjad047","DOIUrl":"10.1093/jmcb/mjad047","url":null,"abstract":"Estrogen receptor α (ERα) is an important driver and therapeutic target in ∼70% of breast cancers. How ERα drives breast carcinogenesis is not fully understood. In this study, we show that ERα is a negative regulator of type I interferon (IFN) response. Activation of ERα by its natural ligand estradiol inhibits IFN-β-induced transcription of downstream IFN-stimulated genes (ISGs), whereas ERα deficiency or the stimulation with its antagonist fulvestrant has opposite effects. Mechanistically, ERα induces the expression of the histone 2A variant H2A.Z to restrict the engagement of the IFN-stimulated gene factor 3 (ISGF3) complex to the promoters of ISGs and also interacts with STAT2 to disrupt the assembly of the ISGF3 complex. These two events mutually lead to the inhibition of ISG transcription induced by type I IFNs. In a xenograft mouse model, fulvestrant enhances the ability of IFN-β to suppress ERα+ breast tumor growth. Consistently, clinical data analysis reveals that ERα+ breast cancer patients with higher levels of ISGs exhibit higher long-term survival rates. Taken together, our findings suggest that ERα inhibits type I IFN response via two distinct mechanisms to promote breast carcinogenesis.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.5,"publicationDate":"2024-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11066933/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9775957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

The transcriptional activator Klf5 recruits p300-mediated H3K27ac for maintaining trophoblast stem cell pluripotency. 转录激活因子 Klf5 可通过 p300 介导的 H3K27ac 来维持滋养层干细胞的全能性。

IF 5.5 2区生物学

Journal of Molecular Cell Biology Pub Date : 2024-01-05 DOI: 10.1093/jmcb/mjad045

Chengli Dou, Linhui Wu, Jingjing Zhang, Hainan He, Tian Xu, Zhisheng Yu, Peng Su, Xia Zhang, Junling Wang, Yi-Liang Miao, Jilong Zhou

{"title":"The transcriptional activator Klf5 recruits p300-mediated H3K27ac for maintaining trophoblast stem cell pluripotency.","authors":"Chengli Dou, Linhui Wu, Jingjing Zhang, Hainan He, Tian Xu, Zhisheng Yu, Peng Su, Xia Zhang, Junling Wang, Yi-Liang Miao, Jilong Zhou","doi":"10.1093/jmcb/mjad045","DOIUrl":"10.1093/jmcb/mjad045","url":null,"abstract":"The effective proliferation and differentiation of trophoblast stem cells (TSCs) is indispensable for the development of the placenta, which is the key to maintaining normal fetal growth during pregnancy. Kruppel-like factor 5 (Klf5) is implicated in the activation of pluripotency gene expression in embryonic stem cells (ESCs), yet its function in TSCs is poorly understood. Here, we showed that Klf5 knockdown resulted in the downregulation of core TSC-specific genes, consequently causing rapid differentiation of TSCs. Consistently, Klf5-depleted embryos lost the ability to establish TSCs in vitro. At the molecular level, Klf5 preferentially occupied the proximal promoter regions and maintained an open chromatin architecture of key TSC-specific genes. Deprivation of Klf5 impaired the enrichment of p300, a major histone acetyl transferase of H3 lysine 27 acetylation (H3K27ac), and further reduced the occupancy of H3K27ac at promoter regions, leading to decreased transcriptional activity of TSC pluripotency genes. Thus, our findings highlight a novel mechanism of Klf5 in regulating the self-renewal and differentiation of TSCs and provide a reference for understanding placental development and improving pregnancy rates.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.5,"publicationDate":"2024-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10768793/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9927286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Transcriptional pausing induced by ionizing radiation enables the acquisition of radioresistance in nasopharyngeal carcinoma. 电离辐射诱导的转录暂停可使鼻咽癌获得放射抗性。

IF 5.5 2区生物学

Journal of Molecular Cell Biology Pub Date : 2024-01-05 DOI: 10.1093/jmcb/mjad044

Honglu Liu, Huanyi Fu, Chunhong Yu, Na Zhang, Canhua Huang, Lu Lv, Chunhong Hu, Fang Chen, Zhiqiang Xiao, Zhuohua Zhang, Huasong Lu, Kai Yuan

{"title":"Transcriptional pausing induced by ionizing radiation enables the acquisition of radioresistance in nasopharyngeal carcinoma.","authors":"Honglu Liu, Huanyi Fu, Chunhong Yu, Na Zhang, Canhua Huang, Lu Lv, Chunhong Hu, Fang Chen, Zhiqiang Xiao, Zhuohua Zhang, Huasong Lu, Kai Yuan","doi":"10.1093/jmcb/mjad044","DOIUrl":"10.1093/jmcb/mjad044","url":null,"abstract":"Lesions on the DNA template can impact transcription via distinct regulatory pathways. Ionizing radiation (IR) as the mainstay modality for many malignancies elicits most of the cytotoxicity by inducing a variety of DNA damages in the genome. How the IR treatment alters the transcription cycle and whether it contributes to the development of radioresistance remain poorly understood. Here, we report an increase in the paused RNA polymerase II (RNAPII), as indicated by the phosphorylation at serine 5 residue of its C-terminal domain, in recurrent nasopharyngeal carcinoma (NPC) patient samples after IR treatment and cultured NPC cells developing IR resistance. Reducing the pool of paused RNAPII by either inhibiting TFIIH-associated CDK7 or stimulating the positive transcription elongation factor b, a CDK9-CycT1 heterodimer, attenuates IR resistance of NPC cells. Interestingly, the poly(ADP-ribosyl)ation of CycT1, which disrupts its phase separation, is elevated in the IR-resistant cells. Mutation of the major poly(ADP-ribosyl)ation sites of CycT1 decreases RNAPII pausing and restores IR sensitivity. Genome-wide chromatin immunoprecipitation followed by sequencing analyses reveal that several genes involved in radiation response and cell cycle control are subject to the regulation imposed by the paused RNAPII. Particularly, we identify the NIMA-related kinase NEK7 under such regulation as a new radioresistance factor, whose downregulation results in the increased chromosome instability, enabling the development of IR resistance. Overall, our results highlight a novel link between the alteration in the transcription cycle and the acquisition of IR resistance, opening up new opportunities to increase the efficacy of radiotherapy and thwart radioresistance in NPC.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.5,"publicationDate":"2024-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10960568/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9746355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

ARTC1-mediated VAPB ADP-ribosylation regulates calcium homeostasis. ARTC1 介导的 VAPB ADP-ribosylation 调节钙稳态。

IF 5.5 2区生物学

Journal of Molecular Cell Biology Pub Date : 2024-01-05 DOI: 10.1093/jmcb/mjad043

Xueyao Ma, Mengyuan Li, Yi Liu, Xuefang Zhang, Xiaoyun Yang, Yun Wang, Yipeng Li, Jiayue Wang, Xiuhua Liu, Zhenzhen Yan, Xiaochun Yu, Chen Wu

{"title":"ARTC1-mediated VAPB ADP-ribosylation regulates calcium homeostasis.","authors":"Xueyao Ma, Mengyuan Li, Yi Liu, Xuefang Zhang, Xiaoyun Yang, Yun Wang, Yipeng Li, Jiayue Wang, Xiuhua Liu, Zhenzhen Yan, Xiaochun Yu, Chen Wu","doi":"10.1093/jmcb/mjad043","DOIUrl":"10.1093/jmcb/mjad043","url":null,"abstract":"Mono-ADP-ribosylation (MARylation) is a post-translational modification that regulates a variety of biological processes, including DNA damage repair, cell proliferation, metabolism, and stress and immune responses. In mammals, MARylation is mainly catalyzed by ADP-ribosyltransferases (ARTs), which consist of two groups: ART cholera toxin-like (ARTCs) and ART diphtheria toxin-like (ARTDs, also known as PARPs). The human ARTC (hARTC) family is composed of four members: two active mono-ADP-ARTs (hARTC1 and hARTC5) and two enzymatically inactive enzymes (hARTC3 and hARTC4). In this study, we systematically examined the homology, expression, and localization pattern of the hARTC family, with a particular focus on hARTC1. Our results showed that hARTC3 interacted with hARTC1 and promoted the enzymatic activity of hARTC1 by stabilizing hARTC1. We also identified vesicle-associated membrane protein-associated protein B (VAPB) as a new target of hARTC1 and pinpointed Arg50 of VAPB as the ADP-ribosylation site. Furthermore, we demonstrated that knockdown of hARTC1 impaired intracellular calcium homeostasis, highlighting the functional importance of hARTC1-mediated VAPB Arg50 ADP-ribosylation in regulating calcium homeostasis. In summary, our study identified a new target of hARTC1 in the endoplasmic reticulum and suggested that ARTC1 plays a role in regulating calcium signaling.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.5,"publicationDate":"2024-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10928986/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10051793","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

The bacterial effector SidN/Lpg1083 promotes cell death by targeting Lamin-B2. 细菌效应物 SidN/Lpg1083 通过靶向 Lamin-B2 促进细胞死亡。

IF 5.5 2区生物学

Journal of Molecular Cell Biology Pub Date : 2023-11-27 DOI: 10.1093/jmcb/mjad036

Jiajia Gao, Wenwen Xu, Feng Tang, Minrui Xu, Qin Zhou, Xingyuan Yang, Nannan Zhang, Jinming Ma, Qi Yang, Xiaofang Chen, Ximing Qin, Honghua Ge

{"title":"The bacterial effector SidN/Lpg1083 promotes cell death by targeting Lamin-B2.","authors":"Jiajia Gao, Wenwen Xu, Feng Tang, Minrui Xu, Qin Zhou, Xingyuan Yang, Nannan Zhang, Jinming Ma, Qi Yang, Xiaofang Chen, Ximing Qin, Honghua Ge","doi":"10.1093/jmcb/mjad036","DOIUrl":"10.1093/jmcb/mjad036","url":null,"abstract":"To facilitate survival, replication, and dissemination, the intracellular pathogen Legionella pneumophila relies on its unique type IVB secretion system (T4SS) to deliver over 330 effectors to hijack host cell pathways in a spatiotemporal manner. The effectors and their host targets are largely unexplored due to their low sequence identity to the known proteins and functional redundancy. The T4SS effector SidN (Lpg1083) is secreted into host cells during the late infection period. However, to the best of our knowledge, the molecular characterization of SidN has not been studied. Herein, we identified SidN as a nuclear envelope-localized effector. Its structure adopts a novel fold, and the N-terminal domain is crucial for its specific subcellular localization. Furthermore, we found that SidN is transported by eukaryotic karyopherin Importin-13 into the nucleus, where it attaches to the N-terminal region of Lamin-B2 to interfere with the integrity of the nuclear envelope, causing nuclear membrane disruption and eventually cell death. Our work provides new insights into the structure and function of an L. pneumophila effector protein, and suggests a potential strategy utilized by the pathogen to promote host cell death and then escape from the host for secondary infection.","PeriodicalId":16433,"journal":{"name":"Journal of Molecular Cell Biology","volume":" ","pages":""},"PeriodicalIF":5.5,"publicationDate":"2023-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10729856/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9547765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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