Molecular and Cellular Biology最新文献_第4页

Transcription Factor 23 is an Essential Determinant of Murine Term Parturition. 转录因子 23 是小鼠临产的重要决定因素

IF 3.2 2区生物学

Molecular and Cellular Biology Pub Date : 2024-01-01 Epub Date: 2024-07-16 DOI: 10.1080/10985549.2024.2376146

Fatma M Minisy, Hossam H Shawki, Tsubasa Fujita, Ahmed M Moustafa, Rumeysa Sener, Youske Nishio, Issei S Shimada, Shinji Saitoh, Mayumi Sugiura-Ogasawara, Hisashi Oishi

{"title":"Transcription Factor 23 is an Essential Determinant of Murine Term Parturition.","authors":"Fatma M Minisy, Hossam H Shawki, Tsubasa Fujita, Ahmed M Moustafa, Rumeysa Sener, Youske Nishio, Issei S Shimada, Shinji Saitoh, Mayumi Sugiura-Ogasawara, Hisashi Oishi","doi":"10.1080/10985549.2024.2376146","DOIUrl":"10.1080/10985549.2024.2376146","url":null,"abstract":"Pregnancy involving intricate tissue transformations governed by the progesterone hormone (P4). P4 signaling via P4 receptors (PRs) is vital for endometrial receptivity, decidualization, myometrial quiescence, and labor initiation. This study explored the role of TCF23 as a downstream target of PR during pregnancy. TCF23 was found to be expressed in female reproductive organs, predominantly in uterine stromal and smooth muscle cells. Tcf23 expression was high during midgestation and was specifically regulated by P4, but not estrogen. The Tcf23 knockout (KO) mouse was generated and analyzed. Female KO mice aged 4-6 months exhibited subfertility, reduced litter size, and defective parturition. Uterine histology revealed disrupted myometrial structure, altered collagen organization, and disarrayed smooth muscle sheets at the conceptus sites of KO mice. RNA-Seq analysis of KO myometrium revealed dysregulation of genes associated with cell adhesion and extracellular matrix organization. TCF23 potentially modulates TCF12 activity to mediate cell-cell adhesion and matrix modulation in smooth muscle cells. Overall, TCF23 deficiency leads to impaired myometrial remodeling, causing parturition delay and fetal demise. This study sheds light on the critical role of TCF23 as a dowstream mediator of PR in uterine remodeling, reflecting the importance of cell-cell communication and matrix dynamics in myometrial activation and parturition.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"316-333"},"PeriodicalIF":3.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11296541/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141627155","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

NatB Protects Procaspase-8 from UBR4-Mediated Degradation and Is Required for Full Induction of the Extrinsic Apoptosis Pathway. NatB 保护 Procaspase-8 免受 UBR4 介导的降解，是全面诱导凋亡外途径的必要条件

IF 3.2 2区生物学

Molecular and Cellular Biology Pub Date : 2024-01-01 Epub Date: 2024-08-04 DOI: 10.1080/10985549.2024.2382453

Joana P Guedes, Jean Baptiste Boyer, Jasmine Elurbide, Beatriz Carte, Virginie Redeker, Laila Sago, Thierry Meinnel, Manuela Côrte-Real, Carmela Giglione, Rafael Aldabe

{"title":"NatB Protects Procaspase-8 from UBR4-Mediated Degradation and Is Required for Full Induction of the Extrinsic Apoptosis Pathway.","authors":"Joana P Guedes, Jean Baptiste Boyer, Jasmine Elurbide, Beatriz Carte, Virginie Redeker, Laila Sago, Thierry Meinnel, Manuela Côrte-Real, Carmela Giglione, Rafael Aldabe","doi":"10.1080/10985549.2024.2382453","DOIUrl":"10.1080/10985549.2024.2382453","url":null,"abstract":"N-terminal acetyltransferase B (NatB) is a major contributor to the N-terminal acetylome and is implicated in several key cellular processes including apoptosis and proteostasis. However, the molecular mechanisms linking NatB-mediated N-terminal acetylation to apoptosis and its relationship with protein homeostasis remain elusive. In this study, we generated mouse embryonic fibroblasts (MEFs) with an inactivated catalytic subunit of NatB (Naa20-/-) to investigate the impact of NatB deficiency on apoptosis regulation. Through quantitative N-terminomics, label-free quantification, and targeted proteomics, we demonstrated that NatB does not influence the proteostasis of all its substrates. Instead, our focus on putative NatB-dependent apoptotic factors revealed that NatB serves as a protective shield against UBR4 and UBR1 Arg/N-recognin-mediated degradation. Notably, Naa20-/- MEFs exhibited reduced responsiveness to an extrinsic pro-apoptotic stimulus, a phenotype that was partially reversible upon UBR4 Arg/N-recognin silencing and consequent inhibition of procaspase-8 degradation. Collectively, our results shed light on how the interplay between NatB-mediated acetylation and the Arg/N-degron pathway appears to impact apoptosis regulation, providing new perspectives in the field including in therapeutic interventions.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"358-371"},"PeriodicalIF":3.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11376409/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141889774","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

De Novo Missense Variations of ATP8B2 Impair Its Phosphatidylcholine Flippase Activity. ATP8B2 的新缺义变异会削弱其磷脂酰胆碱翻转酶活性

IF 3.2 2区生物学

Molecular and Cellular Biology Pub Date : 2024-01-01 Epub Date: 2024-09-02 DOI: 10.1080/10985549.2024.2391829

Hiroyuki Takatsu, Narumi Nishimura, Yusuke Kosugi, Haruo Ogawa, Kazuhisa Nakayama, Estelle Colin, Konrad Platzer, Rami Abou Jamra, Silke Redler, Clément Prouteau, Alban Ziegler, Hye-Won Shin

{"title":"De Novo Missense Variations of ATP8B2 Impair Its Phosphatidylcholine Flippase Activity.","authors":"Hiroyuki Takatsu, Narumi Nishimura, Yusuke Kosugi, Haruo Ogawa, Kazuhisa Nakayama, Estelle Colin, Konrad Platzer, Rami Abou Jamra, Silke Redler, Clément Prouteau, Alban Ziegler, Hye-Won Shin","doi":"10.1080/10985549.2024.2391829","DOIUrl":"10.1080/10985549.2024.2391829","url":null,"abstract":"P4-ATPases comprise a family of lipid flippases that translocate lipids from the exoplasmic (or luminal) to the cytoplasmic leaflet of biological membranes. Of the 14 known human P4-ATPases, ATP8B2 is a phosphatidylcholine flippase at the plasma membrane, but its physiological function is not well understood. Although ATP8B2 could interact with both CDC50A and CDC50B, it required only the CDC50A interaction for its exit from the endoplasmic reticulum and subsequent transport to the plasma membrane. Three de novo monoallelic missense variations of ATP8B2 were found in patients with intellectual disability. None of these variations affected the interaction of ATP8B2 with CDC50A or its localization to the plasma membrane. However, variations of either of two amino acid residues, which are conserved in all P4-ATPases, significantly reduced the phosphatidylcholine flippase activity of ATP8B2. Furthermore, mutations in the corresponding residues of ATP8B1 and ATP11C were found to decrease their flippase activities toward phosphatidylcholine and phosphatidylserine, respectively. These results indicate that the conserved amino acid residues are crucial for the enzymatic activities of the P4-ATPases.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"473-488"},"PeriodicalIF":3.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11529410/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142109409","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

Control of Intestinal Stemness and Cell Lineage by Histone Variant H2A.Z Isoforms. 组蛋白变体 H2A.Z 同工酶对肠道干性和细胞系的控制

IF 3.2 2区生物学

Molecular and Cellular Biology Pub Date : 2024-01-01 Epub Date: 2024-08-18 DOI: 10.1080/10985549.2024.2387720

Jérémie Rispal, Clémence Rives, Virginie Jouffret, Caroline Leoni, Louise Dubois, Martine Chevillard-Briet, Didier Trouche, Fabrice Escaffit

{"title":"Control of Intestinal Stemness and Cell Lineage by Histone Variant H2A.Z Isoforms.","authors":"Jérémie Rispal, Clémence Rives, Virginie Jouffret, Caroline Leoni, Louise Dubois, Martine Chevillard-Briet, Didier Trouche, Fabrice Escaffit","doi":"10.1080/10985549.2024.2387720","DOIUrl":"10.1080/10985549.2024.2387720","url":null,"abstract":"The histone variant H2A.Z plays important functions in the regulation of gene expression. In mammals, it is encoded by two genes, giving rise to two highly related isoforms named H2A.Z.1 and H2A.Z.2, which can have similar or antagonistic functions depending on the promoter. Knowledge of the physiopathological consequences of such functions emerges, but how the balance between these isoforms regulates tissue homeostasis is not fully understood. Here, we investigated the relative role of H2A.Z isoforms in intestinal epithelial homeostasis. Through genome-wide analysis of H2A.Z genomic localization in differentiating Caco-2 cells, we uncovered an enrichment of H2A.Z isoforms on the bodies of genes which are induced during enterocyte differentiation, stressing the potential importance of H2A.Z isoforms dynamics in this process. Through a combination of in vitro and in vivo experiments, we further demonstrated the two isoforms cooperate for stem and progenitor cells proliferation, as well as for secretory lineage differentiation. However, we found that they antagonistically regulate enterocyte differentiation, with H2A.Z.1 preventing terminal differentiation and H2A.Z.2 favoring it. Altogether, these data indicate that H2A.Z isoforms are critical regulators of intestine homeostasis and may provide a paradigm of how the balance between two isoforms of the same chromatin structural protein can control physiopathological processes.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"455-472"},"PeriodicalIF":3.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11529411/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142000367","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 Ribosome Assembly Factor LSG1 Interacts with Vesicle-Associated Membrane Protein-Associated Proteins (VAPs). 核糖体组装因子 LSG1 与囊泡相关膜蛋白相关蛋白（VAPs）相互作用

IF 3.2 2区生物学

Molecular and Cellular Biology Pub Date : 2024-01-01 Epub Date: 2024-08-12 DOI: 10.1080/10985549.2024.2384600

Putri Sutjita, Sharmishtha Musalgaonkar, Jeffrey Recchia-Rife, Lisa Huang, Blerta Xhemalce, Arlen W Johnson

引用次数: 0

Functional Roles of H3K4 Methylation in Transcriptional Regulation. H3K4 甲基化在转录调控中的功能作用

IF 3.2 2区生物学

Molecular and Cellular Biology Pub Date : 2024-01-01 Epub Date: 2024-08-18 DOI: 10.1080/10985549.2024.2388254

Haoming Yu, Bluma J Lesch

引用次数: 0

Reduced Protein Import via TIM23 SORT Drives Disease Pathology in TIMM50-Associated Mitochondrial Disease. TIMM50 相关线粒体疾病中，通过 TIM23 SORT 的蛋白质导入减少导致了疾病病理变化。

IF 3.2 2区生物学

Molecular and Cellular Biology Pub Date : 2024-01-01 Epub Date: 2024-06-03 DOI: 10.1080/10985549.2024.2353652

Jordan J Crameri, Catherine S Palmer, Tegan Stait, Thomas D Jackson, Matthew Lynch, Adriane Sinclair, Leah E Frajman, Alison G Compton, David Coman, David R Thorburn, Ann E Frazier, Diana Stojanovski

{"title":"Reduced Protein Import via TIM23 SORT Drives Disease Pathology in TIMM50-Associated Mitochondrial Disease.","authors":"Jordan J Crameri, Catherine S Palmer, Tegan Stait, Thomas D Jackson, Matthew Lynch, Adriane Sinclair, Leah E Frajman, Alison G Compton, David Coman, David R Thorburn, Ann E Frazier, Diana Stojanovski","doi":"10.1080/10985549.2024.2353652","DOIUrl":"10.1080/10985549.2024.2353652","url":null,"abstract":"TIMM50 is a core subunit of the TIM23 complex, the mitochondrial inner membrane translocase responsible for the import of pre-sequence-containing precursors into the mitochondrial matrix and inner membrane. Here we describe a mitochondrial disease patient who is homozygous for a novel variant in TIMM50 and establish the first proteomic map of mitochondrial disease associated with TIMM50 dysfunction. We demonstrate that TIMM50 pathogenic variants reduce the levels and activity of endogenous TIM23 complex, which significantly impacts the mitochondrial proteome, resulting in a combined oxidative phosphorylation (OXPHOS) defect and changes to mitochondrial ultrastructure. Using proteomic data sets from TIMM50 patient fibroblasts and a TIMM50 HEK293 cell model of disease, we reveal that laterally released substrates imported via the TIM23SORT complex pathway are most sensitive to loss of TIMM50. Proteins involved in OXPHOS and mitochondrial ultrastructure are enriched in the TIM23SORT substrate pool, providing a biochemical mechanism for the specific defects in TIMM50-associated mitochondrial disease patients. These results highlight the power of using proteomics to elucidate molecular mechanisms of disease and uncovering novel features of fundamental biology, with the implication that human TIMM50 may have a more pronounced role in lateral insertion than previously understood.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"226-244"},"PeriodicalIF":3.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11204040/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141200293","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

Expression of Interferon Epsilon in Mucosal Epithelium is Regulated by Elf3. 粘膜上皮细胞中干扰素 Epsilon 的表达受 Elf3 的调控

IF 3.2 2区生物学

Molecular and Cellular Biology Pub Date : 2024-01-01 Epub Date: 2024-07-08 DOI: 10.1080/10985549.2024.2366207

Ka Yee Fung, Eveline D de Geus, Le Ying, Helen Cumming, Nollaig Bourke, Samuel C Foster, Paul J Hertzog

{"title":"Expression of Interferon Epsilon in Mucosal Epithelium is Regulated by Elf3.","authors":"Ka Yee Fung, Eveline D de Geus, Le Ying, Helen Cumming, Nollaig Bourke, Samuel C Foster, Paul J Hertzog","doi":"10.1080/10985549.2024.2366207","DOIUrl":"10.1080/10985549.2024.2366207","url":null,"abstract":"Interferon epsilon (IFNε) is a unique type I interferon (IFN) that shows distinct constitutive expression in reproductive tract epithelium. Understanding how IFNε expression is regulated is critical for the mechanism of action in protecting the mucosa from infection. Combined computational and experimental investigation of the promoter of IFNε predicted transcription factor binding sites for the ETS family of transcription factors. We demonstrate here that Ifnε is regulated by Elf3, an epithelial restricted member of the ETS family. It is co-expressed with IFNε at the epithelium of uterus, lung and intestine, and we focused on regulation of IFNε expression in the uterus. Promoter reporter studies demonstrated that Elf3 was a strong driver of Ifnε expression; knockdown of Elf3 reduced expression levels of IFNε; Elf3 regulated Ifnε expression and chromatin immunoprecipitation (ChIP) confirmed the direct binding of Elf3 to the IFNε promoter. These data show that Elf3 is important in regulating protective mucosal immunity by driving constitutive expression of IFNε to protect mucosal tissues from infection in at least three organ systems.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"334-343"},"PeriodicalIF":3.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11296529/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141555189","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

FoxP1 Represses MEF2A in Striated Muscle. FoxP1 抑制横纹肌中的 MEF2A

IF 3.2 2区生物学

Molecular and Cellular Biology Pub Date : 2024-01-01 Epub Date: 2024-03-14 DOI: 10.1080/10985549.2024.2323959

Sydney Steiman, Tetsuaki Miyake, John C McDermott

{"title":"FoxP1 Represses MEF2A in Striated Muscle.","authors":"Sydney Steiman, Tetsuaki Miyake, John C McDermott","doi":"10.1080/10985549.2024.2323959","DOIUrl":"10.1080/10985549.2024.2323959","url":null,"abstract":"Myocyte enhancer factor 2 (MEF2) proteins are involved in multiple developmental, physiological, and pathological processes in vertebrates. Protein-protein interactions underlie the plethora of biological processes impacted by MEF2A, necessitating a detailed characterization of the MEF2A interactome. A nanobody based affinity-purification/mass spectrometry strategy was employed to achieve this goal. Specifically, the MEF2A protein complexes were captured from myogenic lysates using a GFP-tagged MEF2A protein immobilized with a GBP-nanobody followed by LC-MS/MS proteomic analysis to identify MEF2A interactors. After bioinformatic analysis, we further characterized the interaction of MEF2A with a transcriptional repressor, FOXP1. FOXP1 coprecipitated with MEF2A in proliferating myogenic cells which diminished upon differentiation (myotube formation). Ectopic expression of FOXP1 inhibited MEF2A driven myogenic reporter genes (derived from the creatine kinase muscle and myogenin genes) and delayed induction of endogenous myogenin during differentiation. Conversely, FOXP1 depletion enhanced MEF2A transactivation properties and myogenin expression. The FoxP1:MEF2A interaction is also preserved in cardiomyocytes and FoxP1 depletion enhanced cardiomyocyte hypertrophy. FOXP1 prevented MEF2A phosphorylation and activation by the p38MAPK pathway. Overall, these data implicate FOXP1 in restricting MEF2A function in order to avoid premature differentiation in myogenic progenitors and also to possibly prevent re-activation of embryonic gene expression in cardiomyocyte hypertrophy.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"57-71"},"PeriodicalIF":3.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10950271/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140120080","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

ANP32e Binds Histone H2A.Z in a Cell Cycle-Dependent Manner and Regulates Its Protein Stability in the Cytoplasm. ANP32e 以细胞周期依赖性方式结合组蛋白 H2A.Z 并调节其在细胞质中的蛋白稳定性

IF 3.2 2区生物学

Molecular and Cellular Biology Pub Date : 2024-01-01 Epub Date: 2024-03-14 DOI: 10.1080/10985549.2024.2319731

Yasmin Dijkwel, Gene Hart-Smith, Sebastian Kurscheid, David J Tremethick

{"title":"ANP32e Binds Histone H2A.Z in a Cell Cycle-Dependent Manner and Regulates Its Protein Stability in the Cytoplasm.","authors":"Yasmin Dijkwel, Gene Hart-Smith, Sebastian Kurscheid, David J Tremethick","doi":"10.1080/10985549.2024.2319731","DOIUrl":"10.1080/10985549.2024.2319731","url":null,"abstract":"ANP32e, a chaperone of H2A.Z, is receiving increasing attention because of its association with cancer growth and progression. An unanswered question is whether ANP32e regulates H2A.Z dynamics during the cell cycle; this could have clear implications for the proliferation of cancer cells. We confirmed that ANP32e regulates the growth of human U2OS cancer cells and preferentially interacts with H2A.Z during the G1 phase of the cell cycle. Unexpectedly, ANP32e does not mediate the removal of H2A.Z from chromatin, is not a stable component of the p400 remodeling complex and is not strongly associated with chromatin. Instead, most ANP32e is in the cytoplasm. Here, ANP32e preferentially interacts with H2A.Z in the G1 phase in response to an increase in H2A.Z protein abundance and regulates its protein stability. This G1-specific interaction was also observed in the nucleoplasm but was unrelated to any change in H2A.Z abundance. These results challenge the idea that ANP32e regulates the abundance of H2A.Z in chromatin as part of a chromatin remodeling complex. We propose that ANP32e is a molecular chaperone that maintains the soluble pool of H2A.Z by regulating its protein stability and acting as a buffer in response to cell cycle-dependent changes in H2A.Z abundance.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"72-85"},"PeriodicalIF":3.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10950284/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140120079","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