Cell structure and function最新文献_第2页

A high-resolution phase-contrast microscopy system for label-free imaging in living cells 用于活细胞无标记成像的高分辨率相位对比显微系统

IF 1.5 4区生物学

Cell structure and function Pub Date : 2024-05-25 DOI: 10.1247/csf.24018

Kentaro Shimasaki, Yuko Okemoto-Nakamura, Saito Kyoko, Masayoshi Fukasawa, Kaoru Katoh, Kentaro Hanada

引用次数: 0

In vivo evidence for homeostatic regulation of ribosomal protein levels in Drosophila. 果蝇核糖体蛋白水平同态调节的体内证据

IF 2 4区生物学

Cell structure and function Pub Date : 2024-02-16 Epub Date: 2024-01-11 DOI: 10.1247/csf.23088

Daiki Kitamura, Kiichiro Taniguchi, Mai Nakamura, Tatsushi Igaki

{"title":"In vivo evidence for homeostatic regulation of ribosomal protein levels in Drosophila.","authors":"Daiki Kitamura, Kiichiro Taniguchi, Mai Nakamura, Tatsushi Igaki","doi":"10.1247/csf.23088","DOIUrl":"10.1247/csf.23088","url":null,"abstract":"The ribosome is a molecular machine essential for protein synthesis, which is composed of approximately 80 different ribosomal proteins (Rps). Studies in yeast and cell culture systems have revealed that the intracellular level of Rps is finely regulated by negative feedback mechanisms or ubiquitin-proteasome system, which prevents over- or under-abundance of Rps in the cell. However, in vivo evidence for the homeostatic regulation of intracellular Rp levels has been poor. Here, using Drosophila genetics, we show that intracellular Rp levels are regulated by proteasomal degradation of excess Rps that are not incorporated into the ribosome. By establishing an EGFP-fused Rp gene system that can monitor endogenously expressed Rp levels, we found that endogenously expressed EGFP-RpS20 or -RpL5 is eliminated from the cell when RpS20 or RpL5 is exogenously expressed. Notably, the level of endogenously expressed Hsp83, a housekeeping gene, was not affected by exogenous expression of Hsp83, suggesting that the strict negative regulation of excess protein is specific for intracellular Rps. Further analyses revealed that the maintenance of cellular Rp levels is not regulated at the transcriptional level but by proteasomal degradation of excess free Rps as a protein quality control mechanism. Our observations provide not only the in vivo evidence for the homeostatic regulation of Rp levels but also a novel genetic strategy to study in vivo regulation of intracellular Rp levels and its role in tissue homeostasis via cell competition.Key words: ribosomal protein, proteasomal degradation, Drosophila.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":" ","pages":"11-20"},"PeriodicalIF":2.0,"publicationDate":"2024-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11496781/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139416479","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

Coronin-1 promotes directional cell rearrangement in Drosophila wing epithelium. 冠状蛋白-1促进果蝇翅膀上皮细胞定向重排。

IF 2 4区生物学

Cell structure and function Pub Date : 2023-12-20 Epub Date: 2023-11-30 DOI: 10.1247/csf.23049

Keisuke Ikawa, Souta Hiro, Shu Kondo, Shizue Ohsawa, Kaoru Sugimura

{"title":"Coronin-1 promotes directional cell rearrangement in Drosophila wing epithelium.","authors":"Keisuke Ikawa, Souta Hiro, Shu Kondo, Shizue Ohsawa, Kaoru Sugimura","doi":"10.1247/csf.23049","DOIUrl":"10.1247/csf.23049","url":null,"abstract":"Directional cell rearrangement is a critical process underlying correct tissue deformation during morphogenesis. Although the involvement of F-actin regulation in cell rearrangement has been established, the role and regulation of actin binding proteins (ABPs) in this process are not well understood. In this study, we investigated the function of Coronin-1, a WD-repeat actin-binding protein, in controlling directional cell rearrangement in the Drosophila pupal wing. Transgenic flies expressing Coronin-1-EGFP were generated using CRISPR-Cas9. We observed that Coronin-1 localizes at the reconnecting junction during cell rearrangement, which is dependent on actin interacting protein 1 (AIP1) and cofilin, actin disassemblers and known regulators of wing cell rearrangement. Loss of Coronin-1 function reduces cell rearrangement directionality and hexagonal cell fraction. These results suggest that Coronin-1 promotes directional cell rearrangement via its interaction with AIP1 and cofilin, highlighting the role of ABPs in the complex process of morphogenesis.Key words: morphogenesis, cell rearrangement, actin binding proteins (ABPs).","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":" ","pages":"251-257"},"PeriodicalIF":2.0,"publicationDate":"2023-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11496784/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138458219","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

Lysosomal membrane integrity in fibroblasts derived from patients with Gaucher disease 戈谢病患者成纤维细胞溶酶体膜的完整性

IF 1.5 4区生物学

Cell structure and function Pub Date : 2023-12-09 DOI: 10.1247/csf.23066

Asuka Hamamoto, Natsuki Kita, Siddabasave Gowda B Gowda, Hiroyuki Takatsu, Kazuhisa Nakayama, Makoto Arita, Shu-Ping Hui, Hye-Won Shin

引用次数: 0

Visual quantification of prostaglandin E₂ discharge from a single cell. 单个细胞前列腺素E2放电的视觉定量。

IF 2 4区生物学

Cell structure and function Pub Date : 2023-12-07 Epub Date: 2023-10-07 DOI: 10.1247/csf.23047

Tetsuya Watabe, Shinya Yamahira, Michiyuki Matsuda, Kenta Terai

{"title":"Visual quantification of prostaglandin E2 discharge from a single cell.","authors":"Tetsuya Watabe, Shinya Yamahira, Michiyuki Matsuda, Kenta Terai","doi":"10.1247/csf.23047","DOIUrl":"10.1247/csf.23047","url":null,"abstract":"Calcium transients drive cells to discharge prostaglandin E2 (PGE2). We visualized PGE2-induced protein kinase A (PKA) activation and quantitated PGE2 secreted from a single cell by combining fluorescence microscopy and a simulation model. For this purpose, we first prepared PGE2-producer cells that express either an optogenetic or a chemogenetic calcium channel stimulator: OptoSTIM1 or Gq-DREADD, respectively. Second, we prepared reporter cells expressing the Gs-coupled PGE2 reporter EP2 and the PKA biosensor Booster-PKA, which is based on the principle of Förster resonance energy transfer (FRET). Upon the stimulation-induced triggering of calcium transients, a single producer cell discharges PGE2 to stimulate PKA in the surrounding reporter cells. Due to the flow of the medium, the PKA-activated area exhibited a comet-like smear when HeLa cells were used. In contrast, radial PKA activation was observed when confluent MDCK cells were used, indicating that PGE2 diffusion was restricted to the basolateral space. By fitting the radius of the PKA-activated area to a simulation model based on simple diffusion, we estimated that a single HeLa cell secretes 0.25 fmol PGE2 upon a single calcium transient to activate PKA in more than 1000 neighboring cells. This model also predicts that the PGE2 discharge rate is comparable to the diffusion rate. Thus, our method quantitatively envisions that a single calcium transient affects more than 1000 neighboring cells via PGE2.Key words: prostaglandin E2, imaging, intercellular communication, biosensor, quantification.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":" ","pages":"241-249"},"PeriodicalIF":2.0,"publicationDate":"2023-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11496778/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41182095","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

Rab32 and Rab38 maintain bone homeostasis by regulating intracellular traffic in osteoclasts. Rab32和Rab38通过调节破骨细胞中的细胞内交通来维持骨稳态。

IF 2 4区生物学

Cell structure and function Pub Date : 2023-11-17 Epub Date: 2023-11-10 DOI: 10.1247/csf.23061

Kanako Tokuda, Shiou-Ling Lu, Zidi Zhang, Yumiko Kato, Siyu Chen, Kazuya Noda, Katsutoshi Hirose, Yu Usami, Narikazu Uzawa, Shinya Murakami, Satoru Toyosawa, Mitsunori Fukuda, Ge-Hong Sun-Wada, Yoh Wada, Takeshi Noda

{"title":"Rab32 and Rab38 maintain bone homeostasis by regulating intracellular traffic in osteoclasts.","authors":"Kanako Tokuda, Shiou-Ling Lu, Zidi Zhang, Yumiko Kato, Siyu Chen, Kazuya Noda, Katsutoshi Hirose, Yu Usami, Narikazu Uzawa, Shinya Murakami, Satoru Toyosawa, Mitsunori Fukuda, Ge-Hong Sun-Wada, Yoh Wada, Takeshi Noda","doi":"10.1247/csf.23061","DOIUrl":"10.1247/csf.23061","url":null,"abstract":"Osteoclasts play a crucial role in bone homeostasis by forming resorption pits on bone surfaces, resulting in bone resorption. The osteoclast expression of Rab38 protein is highly induced during differentiation from macrophages. Here we generated mice with double knockout (DKO) of Rab38 and its paralogue, Rab32, to investigate the roles of these proteins in osteoclasts. Bone marrow-derived macrophages from Rab32/38 DKO mice differentiated normally into osteoclasts in vitro. However, DKO osteoclasts showed reduced bone resorption activity. These osteoclasts also demonstrated defective secretion of tartrate-resistant acid phosphatase and cathepsin K into culture medium. Furthermore, the plasma membrane localization of a3, an osteoclast-specific a subunit of V-ATPase, was abrogated in DKO mice, substantiating the reduced resorption activity. In vivo, Rab32- and Rab38-positive cells were attached to the bone surface. Eight-week-old DKO mice showed significantly thickened trabecular bones in micro-CT and histomorphometry analysis, as well as reduced serum levels of cross-linked C-telopeptide of type I collagen, indicating diminished bone resorption in vivo. In DKO male mice over 10 weeks of age, hyperostosis appeared at the talofibular syndesmosis, the distal junction of the tibia and fibula. Furthermore, middle-aged mice (10 to 12 months of age) exhibited kyphosis, which is not usually observed in wild-type male mice until around 24 months of age. These results indicate that Rab32 and Rab38 contribute to osteoclast function by supporting intracellular traffic, thereby maintaining normal bone homeostasis.Key words: Rab32, Rab38, osteoclast, lysosome-related organelle, secretory lysosome.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":" ","pages":"223-239"},"PeriodicalIF":2.0,"publicationDate":"2023-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11496785/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41102656","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

Signal sequence-triage is activated by translocon obstruction sensed by an ER stress sensor IRE1α. 信号序列分诊由ER应力传感器IRE1α感测到的易位障碍激活。

IF 2 4区生物学

Cell structure and function Pub Date : 2023-11-03 Epub Date: 2023-09-28 DOI: 10.1247/csf.23072

Ashuei Sogawa, Ryota Komori, Kota Yanagitani, Miku Ohfurudono, Akio Tsuru, Koji Kadoi, Yukio Kimata, Hiderou Yoshida, Kenji Kohno

{"title":"Signal sequence-triage is activated by translocon obstruction sensed by an ER stress sensor IRE1α.","authors":"Ashuei Sogawa, Ryota Komori, Kota Yanagitani, Miku Ohfurudono, Akio Tsuru, Koji Kadoi, Yukio Kimata, Hiderou Yoshida, Kenji Kohno","doi":"10.1247/csf.23072","DOIUrl":"10.1247/csf.23072","url":null,"abstract":"Secretory pathway proteins are cotranslationally translocated into the endoplasmic reticulum (ER) of metazoan cells through the protein channel, translocon. Given that there are far fewer translocons than ribosomes in a cell, it is essential that secretory protein-translating ribosomes only occupy translocons transiently. Therefore, if translocons are obstructed by ribosomes stalled or slowed in translational elongation, it possibly results in deleterious consequences to cellular function. Hence, we investigated how translocon clogging by stalled ribosomes affects mammalian cells. First, we constructed ER-destined translational arrest proteins (ER-TAP) as an artificial protein that clogged the translocon in the ER membrane. Here, we show that the translocon clogging by ER-TAP expression activates triage of signal sequences (SS) in which secretory pathway proteins harboring highly efficient SS are preferentially translocated into the ER lumen. Interestingly, the translocon obstructed status specifically activates inositol requiring enzyme 1α (IRE1α) but not protein kinase R-like ER kinase (PERK). Given that the IRE1α-XBP1 pathway mainly induces the translocon components, our discovery implies that lowered availability of translocon activates IRE1α, which induces translocon itself. This results in rebalance between protein influx into the ER and the cellular translocation capacity.Key words: endoplasmic reticulum, translocation capacity, translocon clogging, IRE1, signal sequence.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":" ","pages":"211-221"},"PeriodicalIF":2.0,"publicationDate":"2023-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11496779/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41121498","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

VAMP5 and distinct sets of cognate Q-SNAREs mediate exosome release. VAMP5和不同的同源Q-SNARE组介导外泌体释放。

IF 2 4区生物学

Cell structure and function Pub Date : 2023-10-27 Epub Date: 2023-09-14 DOI: 10.1247/csf.23067

Takahide Matsui, Yuriko Sakamaki, Shu Hiragi, Mitsunori Fukuda

{"title":"VAMP5 and distinct sets of cognate Q-SNAREs mediate exosome release.","authors":"Takahide Matsui, Yuriko Sakamaki, Shu Hiragi, Mitsunori Fukuda","doi":"10.1247/csf.23067","DOIUrl":"10.1247/csf.23067","url":null,"abstract":"Small extracellular vesicles (sEVs) are largely classified into two types, plasma-membrane derived sEVs and endomembrane-derived sEVs. The latter type (referred to as exosomes herein) is originated from late endosomes or multivesicular bodies (MVBs). In order to release exosomes extracellularly, MVBs must fuse with the plasma membrane, not with lysosomes. In contrast to the mechanism responsible for MVB-lysosome fusion, the mechanism underlying the MVB-plasma membrane fusion is poorly understood. Here, we systematically analyze soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) family proteins and identify VAMP5 as an MVB-localized SNARE protein required for exosome release. Depletion of VAMP5 in HeLa cells impairs exosome release. Mechanistically, VAMP5 mediates exosome release by interacting with SNAP47 and plasma membrane SNARE Syntaxin 1 (STX1) or STX4 to release exosomes. VAMP5 is also found to mediate asymmetric exosome release from polarized Madin-Darby canine kidney (MDCK) epithelial cells through interaction with the distinct sets of Q-SNAREs, suggesting that VAMP5 is a general exosome regulator in both polarized cells and non-polarized cells.Key words: exosome, small extracellular vesicle (sEV), multivesicular body, SNARE, VAMP5.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":" ","pages":"187-198"},"PeriodicalIF":2.0,"publicationDate":"2023-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11496780/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10231461","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

FilGAP, a GAP for Rac1, down-regulates invadopodia formation in breast cancer cells. FilGAP，Rac1的一种GAP，下调乳腺癌症细胞内隐泡形成。

IF 2 4区生物学

Cell structure and function Pub Date : 2023-09-23 Epub Date: 2023-07-22 DOI: 10.1247/csf.23032

Koji Saito, Sakino Ozawa, Yosuke Chiba, Ruri Takahashi, Ryoya Ogomori, Kojiro Mukai, Tomohiko Taguchi, Hiroyasu Hatakeyama, Yasutaka Ohta

{"title":"FilGAP, a GAP for Rac1, down-regulates invadopodia formation in breast cancer cells.","authors":"Koji Saito, Sakino Ozawa, Yosuke Chiba, Ruri Takahashi, Ryoya Ogomori, Kojiro Mukai, Tomohiko Taguchi, Hiroyasu Hatakeyama, Yasutaka Ohta","doi":"10.1247/csf.23032","DOIUrl":"10.1247/csf.23032","url":null,"abstract":"Invadopodia are protrusive structures that mediate the extracellular matrix (ECM) degradation required for tumor invasion and metastasis. Rho small GTPases regulate invadopodia formation, but the molecular mechanisms of how Rho small GTPase activities are regulated at the invadopodia remain unclear. Here we have identified FilGAP, a GTPase-activating protein (GAP) for Rac1, as a negative regulator of invadopodia formation in tumor cells. Depletion of FilGAP in breast cancer cells increased ECM degradation and conversely, overexpression of FilGAP decreased it. FilGAP depletion promoted the formation of invadopodia with ECM degradation. In addition, FilGAP depletion and Rac1 overexpression increased the emergence of invadopodia induced by epidermal growth factor, whereas FilGAP overexpression suppressed it. Overexpression of GAP-deficient FilGAP mutant enhanced invadopodia emergence as well as FilGAP depletion. The pleckstrin-homology (PH) domain of FilGAP binds phosphatidylinositol 3,4-bisphosphate [PI(3,4)P2], which is distributed on membranes of the invadopodia. FilGAP localized to invadopodia in breast cancer cells on the ECM, but FilGAP mutant lacking PI(3,4)P2-binding showed low localization. Similarly, the decrease of PI(3,4)P2 production reduced the FilGAP localization. Our results suggest that FilGAP localizes to invadopodia through its PH domain binding to PI(3,4)P2 and down-regulates invadopodia formation by inactivating Rac1, inhibiting ECM degradation in invasive tumor cells.Key words: invadopodia, breast carcinoma, Rac1, FilGAP, PI(3,4)P2.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":" ","pages":"161-174"},"PeriodicalIF":2.0,"publicationDate":"2023-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11496788/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9860271","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

IC2 participates in the cooperative activation of outer arm dynein densely attached to microtubules. IC2参与紧密附着在微管上的外臂动力蛋白的协同激活。

IF 2 4区生物学

Cell structure and function Pub Date : 2023-09-23 Epub Date: 2023-07-28 DOI: 10.1247/csf.23044

Yusuke Kondo, Tomoka Ogawa, Emiri Kanno, Masafumi Hirono, Takako Kato-Minoura, Ritsu Kamiya, Toshiki Yagi

{"title":"IC2 participates in the cooperative activation of outer arm dynein densely attached to microtubules.","authors":"Yusuke Kondo, Tomoka Ogawa, Emiri Kanno, Masafumi Hirono, Takako Kato-Minoura, Ritsu Kamiya, Toshiki Yagi","doi":"10.1247/csf.23044","DOIUrl":"10.1247/csf.23044","url":null,"abstract":"Ciliary outer-arm dynein (OAD) consists of heavy chains (HCs), intermediate chains (ICs), and light chains (LCs), of which HCs are the motor proteins that produce force. Studies using the green alga Chlamydomonas have revealed that ICs and LCs form a complex (IC/LC tower) at the base of the OAD tail and play a crucial role in anchoring OAD to specific sites on the microtubule. In this study, we isolated a novel slow-swimming Chlamydomonas mutant deficient in the IC2 protein. This mutation, E279K, is in the third of the seven WD repeat domains. No apparent abnormality was observed in electron microscope observations of axonemes or in SDS-PAGE analyses of dynein subunits. To explore the reason for the lowered motility in this mutant, in vitro microtubule sliding experiments were performed, which revealed that the motor activity of the mutant OAD was lowered. In particular, a large difference was observed between wild type (WT) and the mutant in the microtubule sliding velocity in microtubule bundles formed with the addition of OAD: ~35.3 μm/sec (WT) and ~4.3 μm/sec (mutant). From this and other results, we propose that IC2 in an OAD interacts with the β HC of the adjacent OAD, and that an OAD-OAD interaction is important for efficient beating of cilia and flagella.Key words: cilia, axoneme, dynein heavy chain, cooperativity.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":" ","pages":"175-185"},"PeriodicalIF":2.0,"publicationDate":"2023-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11496786/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9899811","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