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Ion channel function of polycystin-2/polycystin-1 heteromer revealed by structure-guided mutagenesis 结构引导诱变揭示多囊蛋白2/多囊蛋白1异构体的离子通道功能。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2025-05-12 DOI: 10.1002/1873-3468.70059
Tobias Staudner, Juthamas Khamseekaew, M. Gregor Madej, Linda Geiges, Bardha Azemi, Christine Ziegler, Christoph Korbmacher, Alexandr V. Ilyaskin
{"title":"Ion channel function of polycystin-2/polycystin-1 heteromer revealed by structure-guided mutagenesis","authors":"Tobias Staudner,&nbsp;Juthamas Khamseekaew,&nbsp;M. Gregor Madej,&nbsp;Linda Geiges,&nbsp;Bardha Azemi,&nbsp;Christine Ziegler,&nbsp;Christoph Korbmacher,&nbsp;Alexandr V. Ilyaskin","doi":"10.1002/1873-3468.70059","DOIUrl":"10.1002/1873-3468.70059","url":null,"abstract":"<p>Mutations in polycystin-1 (PC1) or polycystin-2 (PC2) cause autosomal-dominant polycystic kidney disease (ADPKD). Structural data suggest that one PC1 and three PC2 form heterotetrameric ion channels with an ion permeation pathway blocked by PC1 (R4100, R4107, and H4111) and PC2 (L677, N681) residues. Here, we demonstrate that replacing these residues with alanines results in a gain-of-function (GOF) PC2/PC1 construct with distinct selectivity properties compared to PC2 homomers. We also show preferential formation of PC2/PC1 heteromeric complexes over PC2 homomers. Re-interpretation of published PC2/PC1 cryo-electron microscopy data, combined with cysteine modification experiments, suggests that the pore-forming domain of PC1 adopts a canonical TRP channel-like conformation. This novel PC2/PC1 GOF construct offers the opportunity to investigate the functional impact of ADPKD mutations.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 12","pages":"1649-1668"},"PeriodicalIF":3.5,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.70059","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144005190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Decoding the dual role of autophagy in cancer through transcriptional and epigenetic regulation. 通过转录和表观遗传调控解码自噬在癌症中的双重作用。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2025-05-09 DOI: 10.1002/1873-3468.70060
Young Suk Yu, Ik Soo Kim, Sung Hee Baek
{"title":"Decoding the dual role of autophagy in cancer through transcriptional and epigenetic regulation.","authors":"Young Suk Yu, Ik Soo Kim, Sung Hee Baek","doi":"10.1002/1873-3468.70060","DOIUrl":"https://doi.org/10.1002/1873-3468.70060","url":null,"abstract":"<p><p>Autophagy is a conserved catabolic process that is essential for maintaining cellular homeostasis by degrading and recycling damaged organelles and misfolded proteins. In cancer, autophagy exhibits a context-dependent dual role: In early stages, autophagy acts as a tumor suppressor by preserving genomic integrity and limiting oxidative stress. In advanced stages, autophagy supports tumor progression by facilitating metabolic adaptation, therapy resistance, immune evasion, and metastasis. This review highlights the molecular mechanisms underlying this dual function and focuses on the transcriptional and epigenetic regulation of autophagy in cancer cells. Key transcription factors, including the MiT/TFE family, FOXO family, and p53, as well as additional regulators, are discussed in the context of stress-responsive pathways mediated by mTORC1 and AMPK. A deeper understanding of the transcriptional and epigenetic regulation of autophagy in cancer is crucial for developing context-specific therapeutic strategies to either promote or inhibit autophagy depending on the cancer stage, thereby improving clinical outcomes in cancer treatment.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144004617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Autophagy in cancer and protein conformational disorders. 癌症中的自噬和蛋白质构象紊乱。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2025-05-08 DOI: 10.1002/1873-3468.70061
Sergio Attanasio
{"title":"Autophagy in cancer and protein conformational disorders.","authors":"Sergio Attanasio","doi":"10.1002/1873-3468.70061","DOIUrl":"https://doi.org/10.1002/1873-3468.70061","url":null,"abstract":"<p><p>Autophagy is a catabolic process by which cells maintain cellular homeostasis through the degradation of dysfunctional cytoplasmic components, such as toxic misfolded proteins and damaged organelles, within the lysosome. It is a multistep process that is tightly regulated by nutrient, energy, and stress-sensing mechanisms. Autophagy plays a pivotal role in various biological processes, including protein and organelle quality control, defense against pathogen infections, cell metabolism, and immune surveillance. As a result, autophagy dysfunction is linked to a variety of pathological conditions. The role of autophagy in cancer is complex and dynamic. Depending on the context, autophagy can have both tumor-suppressive and pro-tumorigenic effects. In contrast, its role is more clearly defined in protein conformational disorders, where autophagy serves as a mechanism to reduce toxic protein aggregation, thereby improving cellular homeostasis. Because autophagy-based therapies hold promising potential for the treatment of cancer and protein conformational disorders, this review will highlight the latest findings and advancements in these areas.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143970482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Modifications in FLAP's second cytosolic loop influence 5-LOX interaction, inhibitor binding, and leukotriene formation. FLAP第二细胞质环的修饰影响5-LOX相互作用、抑制剂结合和白三烯形成。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2025-05-08 DOI: 10.1002/1873-3468.70066
Erik Romp, Katharina Rataj, Stefanie König, Marcia E Newcomer, Oliver Werz, Ulrike Garscha
{"title":"Modifications in FLAP's second cytosolic loop influence 5-LOX interaction, inhibitor binding, and leukotriene formation.","authors":"Erik Romp, Katharina Rataj, Stefanie König, Marcia E Newcomer, Oliver Werz, Ulrike Garscha","doi":"10.1002/1873-3468.70066","DOIUrl":"https://doi.org/10.1002/1873-3468.70066","url":null,"abstract":"<p><p>Leukotrienes, synthesized via the 5-lipoxygenase (5-LOX) pathway in the arachidonic acid cascade, are critical in inflammation. Effective leukotriene production requires interaction between 5-LOX and 5-LOX-activating protein (FLAP) at the nuclear membrane. This study used site-directed mutagenesis to explore amino acid residues in FLAP's inhibitor binding pocket and cytosolic loops, assessing their impact on 5-LOX product formation, the FLAP inhibitor MK886's efficacy, 5-LOX translocation, and 5-LOX/FLAP complex formation. Mutations in the second cytosolic loop, especially at residue S108, reduced MK886 potency and disrupted 5-LOX/FLAP complex formation. These results highlight the second cytosolic loop of FLAP in the 5-LOX/FLAP interaction and proper leukotriene formation and suggest that targeting this region could aid in the development of new FLAP inhibitors with improved pharmacokinetics.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143975801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Lytic photoreceptor cell death caused by Rab escort protein deficiency in Drosophila. 拉布护卫蛋白缺乏引起果蝇裂解性光感受器细胞死亡。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2025-05-05 DOI: 10.1002/1873-3468.70056
Shogo Sasaki, Rina Satoh, Takunori Satoh, Akiko K Satoh
{"title":"Lytic photoreceptor cell death caused by Rab escort protein deficiency in Drosophila.","authors":"Shogo Sasaki, Rina Satoh, Takunori Satoh, Akiko K Satoh","doi":"10.1002/1873-3468.70056","DOIUrl":"https://doi.org/10.1002/1873-3468.70056","url":null,"abstract":"<p><p>Choroideremia (CHM) is a rare X-linked recessive form of inherited retinal degeneration caused by the deficiency of the Rab escort protein 1 (REP1)-encoding CHM gene. REP1 is essential for the post-translational prenylation of the key players in intracellular membrane trafficking, the Rab GTPases. In this study, we aimed to analyze the mechanisms of retinal degeneration caused by Rep deficiency using the Drosophila retina as a model system. Rab GTPases lost their membrane association ability and diffused into the cytoplasm, and the accumulation of unprenylated Rab6 and Rab7 was observed in Rep-deficient photoreceptors. Notably, Rep-deficient photoreceptors underwent progressive cell death via cell swelling and rupture rather than apoptosis. These findings provide new insight to seek a therapeutic approach to CHM. Impact statement Choroideremia is an inherited retinal degeneration caused by a deficiency of Rab escort protein 1 (Rep-1). We used the Drosophila retina as a model to study the mechanism of retinal degeneration in Rep-deficiency and found that Rep-deficient photoreceptors undergo progressive cell death via cell swelling and rupture rather than apoptosis.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143989125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Amy and Friends: improving the lives of individuals affected by DNA repair disorders 艾米和朋友们：改善受DNA修复障碍影响的个体的生活。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2025-05-05 DOI: 10.1002/1873-3468.70049
Jayne Hughes, Donata Orioli, Lavinia Arseni
{"title":"Amy and Friends: improving the lives of individuals affected by DNA repair disorders","authors":"Jayne Hughes,&nbsp;Donata Orioli,&nbsp;Lavinia Arseni","doi":"10.1002/1873-3468.70049","DOIUrl":"10.1002/1873-3468.70049","url":null,"abstract":"<p>DNA repair disorders are rare genetic conditions characterized by defects in the mechanisms responsible for repairing damaged DNA. DNA damage occurs frequently due to environmental factors, and in healthy cells, repair systems fix this damage to maintain genomic integrity. In individuals with DNA repair disorders, these mechanisms are impaired, leading to accumulated damage, cellular dysfunction, premature aging, and cell death. Symptoms vary depending on the specific repair pathway defect, with examples including Cockayne syndrome (CS), trichothiodystrophy (TTD), and xeroderma pigmentosum. <i>Amy and Friends</i> was founded by Jayne Hughes in the UK in 2007 to support children/young adults and families suffering from CS, TTD, and linked DNA repair disorders. In this second of a new series on patient advocacy, <i>FEBS Letters</i> interviews Founder and CEO Jayne Hughes and molecular geneticist and specialist team member Prof. Donata Orioli on the aims, achievements, and activities of <i>Amy and Friends</i>.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 10","pages":"1339-1345"},"PeriodicalIF":3.5,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.70049","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143963893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Protonophore activity of short-chain fatty acids induces their intracellular accumulation and acidification. 短链脂肪酸的质子团活性诱导其在细胞内积累和酸化。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2025-05-05 DOI: 10.1002/1873-3468.70064
Muwei Jiang, Frans Bianchi, Geert van den Bogaart
{"title":"Protonophore activity of short-chain fatty acids induces their intracellular accumulation and acidification.","authors":"Muwei Jiang, Frans Bianchi, Geert van den Bogaart","doi":"10.1002/1873-3468.70064","DOIUrl":"https://doi.org/10.1002/1873-3468.70064","url":null,"abstract":"<p><p>Short-chain fatty acids (SCFAs), produced by dietary fiber fermentation in the colon, play essential roles in cellular metabolism, with butyrate notably modulating immune responses and epigenetic regulation. Their production contributes to an acidic colonic environment where protonated SCFAs permeate membranes, leading to intracellular acidification and SCFA accumulation. Using our method to measure intracellular pH, we investigated how extracellular pH influences butyrate-induced acidification and immunomodulatory effects in human macrophages. Our data show that butyrate accumulates and acidifies cells at acidic extracellular pH due to the permeability of its protonated form. While inflammatory cytokine production was mildly influenced by extracellular pH, butyrate-induced histone acetylation exhibited a pH dependence, underscoring the importance of considering extracellular pH when assessing the SCFA's functions.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143974533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Spot-14 and its paralog Spot-14R regulate expression of metabolic and thermogenic pathway genes in murine brown and beige adipocytes Spot-14及其类似物Spot-14R调节小鼠棕色和米色脂肪细胞的代谢和产热途径基因的表达。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2025-05-02 DOI: 10.1002/1873-3468.70052
Lidia Itzel Castro-Rodríguez, Cristina Velez-delValle, Claudia Patricia Hernández-Mosqueira, Walid Kuri-Harcuch
{"title":"Spot-14 and its paralog Spot-14R regulate expression of metabolic and thermogenic pathway genes in murine brown and beige adipocytes","authors":"Lidia Itzel Castro-Rodríguez,&nbsp;Cristina Velez-delValle,&nbsp;Claudia Patricia Hernández-Mosqueira,&nbsp;Walid Kuri-Harcuch","doi":"10.1002/1873-3468.70052","DOIUrl":"10.1002/1873-3468.70052","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <p>Spot 14 (S14), encoded by <i>Thrsp</i>, is a thyroid hormone-responsive transcriptional activator that regulates lipogenesis, though its mechanisms remain unclear. We aimed to study the role of S14 on gene expression in adipocytes. We analyzed <i>Thrsp</i> and its paralog <i>Mid1ip1</i> in brown (EB5), beige (EB7), and white (F442A) adipocytes. <i>Thrsp</i> expression was higher in EB5 and EB7 than in F442A and increased with thyroid hormone T3 in EB5 and EB7 but decreased in F442A. <i>Mid1ip1</i> expression rose moderately in EB5 and EB7, influencing lipid metabolism genes. Silencing <i>Thrsp</i> upregulated <i>Mid1ip1</i> in EB7 and reduced thermogenic gene expression in EB5 and EB7. These findings underscore the roles of <i>Thrsp</i> and <i>Mid1ip1</i> in metabolic and thermogenic pathways, highlighting the responsiveness of S14 to thyroid hormones and nutrient signals.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <div>\u0000 \u0000 <div>\u0000 \u0000 <h3>Impact statement</h3>\u0000 <p>This study reveals that Thyroid Hormone-Induced Protein 8 (THRSP), also known as Spot-14, and its paralog Spot-14R, regulate metabolic and thermogenic gene expression differently in brown and beige adipocytes. These findings provide insights into adipocyte metabolism, offering potential targets for obesity and metabolic disorder treatments.</p>\u0000 </div>\u0000 </div>\u0000 </section>\u0000 </div>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 12","pages":"1760-1780"},"PeriodicalIF":3.5,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.70052","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143986176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Interaction vesicles as emerging mediators of host-pathogen molecular crosstalk and their implications for infection dynamics. 相互作用囊泡作为宿主-病原体分子串扰的新介质及其对感染动力学的影响。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2025-05-01 DOI: 10.1002/1873-3468.70055
Bruna Sabatke, Izadora Volpato Rossi, Marcel I Ramirez
{"title":"Interaction vesicles as emerging mediators of host-pathogen molecular crosstalk and their implications for infection dynamics.","authors":"Bruna Sabatke, Izadora Volpato Rossi, Marcel I Ramirez","doi":"10.1002/1873-3468.70055","DOIUrl":"https://doi.org/10.1002/1873-3468.70055","url":null,"abstract":"<p><p>Extracellular vesicles (EVs) are critical in cell communication, transfer of biomolecules, and host-pathogen interaction. A newly identified subset, \"interaction vesicles\" (iEVs), forms through host-pathogen contact, merging membrane elements from both. These iEVs may arise through multiple mechanisms, including direct cell-cell contact, membrane contact sites, uptake and repackaging of foreign EVs, and post-release fusion of EVs. These hybrid vesicles enable pathogens to modify host environments, aiding immune evasion and infection persistence. However, iEVs may also act in favor of the host, contributing to pathogen recognition and elimination. Advanced techniques, including proteomics and high-resolution microscopy, are beginning to clarify their composition and fusion. Yet, isolating these hybrid EVs remains challenging. Overcoming these barriers could enhance understanding of infection mechanisms and support diagnostic and therapeutic innovation.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143960498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
A cellular system to study responses to a collision between the transcription complex and a protein-bound nick in the DNA template 一种细胞系统，用于研究转录复合体和DNA模板中蛋白质结合缺口之间碰撞的反应。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2025-05-01 DOI: 10.1002/1873-3468.70053
Petra Herring, Morten Roedgaard, Camilla Myrup Holst, Helene Christensen, Birgitta R. Knudsen, Lotte Bjergbaek, Anni Hangaard Andersen
{"title":"A cellular system to study responses to a collision between the transcription complex and a protein-bound nick in the DNA template","authors":"Petra Herring,&nbsp;Morten Roedgaard,&nbsp;Camilla Myrup Holst,&nbsp;Helene Christensen,&nbsp;Birgitta R. Knudsen,&nbsp;Lotte Bjergbaek,&nbsp;Anni Hangaard Andersen","doi":"10.1002/1873-3468.70053","DOIUrl":"10.1002/1873-3468.70053","url":null,"abstract":"<p>We present a transcription-coupled Flp-nick system enabling a stable protein-bound nick mimicking a topoisomerase I–DNA cleavage complex. The nick is introduced at a single site within a controllable <i>LacZ</i> gene inserted into the <i>Saccharomyces cerevisiae</i> genome. This system allows unique single-site studies of a frequently occurring damage within a transcription unit <i>in vivo</i>. As proof of principle, we demonstrate RNA polymerase II accumulation at the damage site when MG132 inhibits the proteasome. Similarly, accumulation occurs when polymerase ubiquitination is abolished by deletion of the ubiquitinase <i>ELC1</i> gene. This indicates that a topoisomerase I–DNA mimicking cleavage complex <i>per se</i> induces RNA polymerase II ubiquitination and degradation. These findings advance understanding of cellular responses to topoisomerase I-targeting drugs used in cancer chemotherapy.</p>","PeriodicalId":12142,"journal":{"name":"FEBS Letters","volume":"599 12","pages":"1749-1759"},"PeriodicalIF":3.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/1873-3468.70053","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143975350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
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