Journal of Receptors and Signal Transduction最新文献_第9页

JAK2/STAT3 inhibitor reduced 5-FU resistance and autophagy through ATF6-mediated ER stress. JAK2/STAT3抑制剂通过atf6介导的内质网应激降低5-FU耐药和自噬。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-04-01 Epub Date: 2021-02-18 DOI: 10.1080/10799893.2021.1887219

Lijuan Ma, Youhui Wang

{"title":"JAK2/STAT3 inhibitor reduced 5-FU resistance and autophagy through ATF6-mediated ER stress.","authors":"Lijuan Ma, Youhui Wang","doi":"10.1080/10799893.2021.1887219","DOIUrl":"https://doi.org/10.1080/10799893.2021.1887219","url":null,"abstract":"Drug resistance seriously limits the efficacy of chemotherapy drugs and hinders successful treatment in patients with gastric cancer. Endoplasmic reticulum (ER) and autophagy are recognized to be one of the mechanisms involving the drug resistance of gastric cancer. The mechanisms of action of JAK2/STAT3 pathway were investigated in AGS cells with drug resistance of 5-fluorouracil (5-FU) by corresponding inhibitors. We firstly analyzed the effects of JAK2/STAT3 inhibitor on the expression of drug resistance genes, autophagy markers, and ER stress-related markers on AGS/5-FU cells by Western blot. Whether JAK2/STAT3 pathway regulated the transcription of ATF6 was investigated through luciferase reporter assay. The expression of LC3B was detected by immunofluorescence assay. Next, ER stress inhibitor and ATF6 overexpression plasmid were respectively used to treat AGS/5-FU cells for analyzing whether JAK2/STAT3 pathway regulated ER stress. The results showed that JAK2 inhibitor or STAT3 inhibitor significantly altered the expression of these proteins and suppressed the activities of ATF6 promoter. Intriguingly, ATP6 overexpression could markedly reverse their effects. Moreover, similar effects to JAK2 inhibitor or STAT3 inhibitor appeared in ER stress inhibitor-treated group. These findings indicated that the involvement of JAK2/STAT3 pathway in regulating ER stress affected the 5-FU resistance of AGS cells and autophagy, which was mediated by ATF6. Targeting JAK2/STAT3 pathway could be a potential approach to decrease the 5-FU resistance of gastric cancer and enhance the sensitivity of gastric cancer to 5-FU. Additionally, our study offers new insights into the molecular mechanisms underlying the resistance of gastric cancer to 5-FU.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 2","pages":"206-213"},"PeriodicalIF":2.8,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1887219","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25378962","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: 6

Inhibition of TGF-β1 on Gli2 expression was promoted by TNF-α in primary leukemia cells. TNF-α可促进原发性白血病细胞TGF-β1对Gli2表达的抑制作用。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-04-01 Epub Date: 2021-02-22 DOI: 10.1080/10799893.2021.1881555

Zhe Li, Shudan Mao, Ning Zhang

引用次数: 0

The protective effects of simvastatin in Cadmium-Induced preosteoblast injury through Nox4. 辛伐他汀对镉诱导的成骨前细胞损伤的保护作用。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-04-01 Epub Date: 2020-12-22 DOI: 10.1080/10799893.2020.1859533

Chongxia Huang, Du Liang, Chongbo Huang, Baolin Li, Jiandong He, Ximou Huang

{"title":"The protective effects of simvastatin in Cadmium-Induced preosteoblast injury through Nox4.","authors":"Chongxia Huang, Du Liang, Chongbo Huang, Baolin Li, Jiandong He, Ximou Huang","doi":"10.1080/10799893.2020.1859533","DOIUrl":"https://doi.org/10.1080/10799893.2020.1859533","url":null,"abstract":"Cadmium (Cd) has a direct toxic effect on bones. Statins such as simvastatin have protective effects on various diseases, including on tissue injury. The current study revealed the efficacy of simvastatin on Cd-induced preosteoblast injury. Preosteoblast MC3T3-E1 cells were incubated with various doses of CdCl2 for 12 h, 24 h and 48 h, and then the cell cytotoxicity was assessed using MTT assay and flow cytometry, respectively. The expression level of Nox4 was assessed by Western blot and qRT-PCR. The morphological appearance of MC3T3-E1 cells was observed under a microscope. Cells exposed to CdCl2 (5 µM) were further treated by simvastatin at various doses, subsequently cell viability, apoptosis and the expression of Nox4 were measured. Furthermore, to confirm the protective effects of simvastatin on Cd-induced pre-osteoblast injury, functional rescue assays were performed after corresponding cell treatment by simvastatin (10-8 M), CdCl2 (5 µM), and overexpression of Nox4. Expressions of cell apoptosis-related markers were measured by Western blot and qRT-PCR. The results revealed that CdCl2 caused MC3T3-E1 cell injury because the cell viability was decreased and the apoptosis was increased. Nox4 expression was up-regulated with the increase of CdCl2 concentrations. Simvastatin increased the cell viability, relieved the cell apoptosis and Nox4 expression previously increased by CdCl2. The effects of CdCl2 on MC3T3-E1 cells and Nox4 expression could be attenuated by simvastatin, and promoted by Nox4 overexpression. The current study found that simvastatin protects Cd-induced preosteoblast injury via Nox4, thus, it can be used as a potential drug for treating cadmium-induced bone injury.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 2","pages":"117-124"},"PeriodicalIF":2.8,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1859533","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39087751","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: 2

Sauchinone inhibits hypoxia-induced invasion and epithelial-mesenchymal transition in osteosarcoma cells via inactivation of the sonic hedgehog pathway. 苏奇诺酮通过灭活sonic hedgehog通路抑制缺氧诱导的骨肉瘤细胞侵袭和上皮-间质转化。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-04-01 Epub Date: 2021-02-09 DOI: 10.1080/10799893.2021.1881556

Dan Zhou, Ling He

{"title":"Sauchinone inhibits hypoxia-induced invasion and epithelial-mesenchymal transition in osteosarcoma cells via inactivation of the sonic hedgehog pathway.","authors":"Dan Zhou, Ling He","doi":"10.1080/10799893.2021.1881556","DOIUrl":"https://doi.org/10.1080/10799893.2021.1881556","url":null,"abstract":"Hypoxia is a typical feature of solid tumors and is closely associated with tumor progression. Sauchinone, a biologically diastereomeric lignan, is isolated from the root of Saururus chinensis and has been widely used for the treatment of various diseases. Recently, sauchinone has been reported to play an anti-cancer role in cancer development under normoxia or hypoxia. However, the specific effects of sauchinone on osteosarcoma (OS) remain unclear. The aim of the present study was to investigate the role of sauchinone in OS progression under hypoxic conditions. The human OS cell lines U2OS and MG-63 were exposed to hypoxia followed by treatment with sauchinone. Cell viability was assessed by the CCK-8 assay. Cell migration and invasion were detected by transwell assays. The expression levels of VEGF, HIF-1α, E-cadherin and N-cadherin were examined by the western blot analysis. Our study showed that OS cell migration and invasion were significantly enhanced by hypoxia. Besides, hypoxic conditions resulted in a remarkable change in the expression of EMT markers. All these effects induced by hypoxia were abrogated by sauchinone treatment. Moreover, sauchinone inhibited hypoxia-induced activation of the sonic hedgehog (Shh) pathway. Additionally, the Shh agonist reversed the inhibitory effect of sauchinone on hypoxia-induced invasion and EMT of OS cells. In conclusion, these findings demonstrated that sauchinone inhibits hypoxia-induced invasion and EMT in OS cells via inactivation of the Shh pathway. We provided a novel insight for understanding the mechanisms underlying the anti-cancer effect of sauchinone and suggested sauchinone as a promising agent for OS treatment.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 2","pages":"173-179"},"PeriodicalIF":2.8,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1881556","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25350353","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: 4

Glaucocalyxin a prevents hypoxia-induced epithelial-mesenchymal transition in human gastric cancer cells through the PI3K/Akt signaling pathway. 青萼藻素a通过PI3K/Akt信号通路阻止缺氧诱导的人胃癌细胞上皮-间质转化。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-04-01 Epub Date: 2020-12-13 DOI: 10.1080/10799893.2020.1853160

Xihan Zhou, Weijin Ma, Xiaohui Li, Jiali Xu

{"title":"Glaucocalyxin a prevents hypoxia-induced epithelial-mesenchymal transition in human gastric cancer cells through the PI3K/Akt signaling pathway.","authors":"Xihan Zhou, Weijin Ma, Xiaohui Li, Jiali Xu","doi":"10.1080/10799893.2020.1853160","DOIUrl":"https://doi.org/10.1080/10799893.2020.1853160","url":null,"abstract":"Abstract Hypoxia is a frequent occurrence in most solid tumors and associated with multiple cancer progression. Glaucocalyxin A (GLA) has been found to exhibit anti-tumor effect in several types of cancer, except gastric cancer (GC). The present study aimed to evaluate the function of GLA in GC and explore the underlying mechanism under hypoxia condition. Our results showed that GLA suppressed cell viability of MGC-803 cells in both normoxic or hypoxic conditions. MGC-803 cells were more sensitive to GLA in hypoxic condition. GLA attenuated hypoxia-induced migration and invasion of GC cells. Western blot assay proved that GLA elevated E-cadherin expression, as well reduced N-cadherin and vimentin expressions in hypoxia-induced GC cells. Moreover, we also found that GLA suppressed the expression of HIF-1α in both mRNA and protein levels. Furthermore, GLA blocked hypoxia-induced activation of PI3K/Akt pathway in GC cells. Notably, insulin like growth factor 1 (IGF-1), an activator of PI3K/Akt pathway, reversed the effects of GLA on cell migration, invasion and EMT in hypoxia-treated MGC-803 cells. In conclusion, these findings demonstrated that GLA exerted inhibitory effects on cell migration, invasion and epithelial to mesenchymal transition (EMT) via the PI3K/Akt signaling pathway in GC cells.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 2","pages":"109-116"},"PeriodicalIF":2.8,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1853160","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38702955","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: 7

Inhibition of TRIM14 protects cerebral ischemia/reperfusion injury through regulating NF-κB/NLRP3 pathway-mediated inflammation and apoptosis. 抑制TRIM14通过调节NF-κB/NLRP3通路介导的炎症和凋亡来保护脑缺血/再灌注损伤。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-04-01 Epub Date: 2021-03-10 DOI: 10.1080/10799893.2021.1887218

Xianlong Xie, Fan Wang, Xiujuan Li

{"title":"Inhibition of TRIM14 protects cerebral ischemia/reperfusion injury through regulating NF-κB/NLRP3 pathway-mediated inflammation and apoptosis.","authors":"Xianlong Xie, Fan Wang, Xiujuan Li","doi":"10.1080/10799893.2021.1887218","DOIUrl":"https://doi.org/10.1080/10799893.2021.1887218","url":null,"abstract":"Purpose: Many proteins in tripartite motif (TRIM) family have been reported to play an important role in cerebral ischemia/reperfusion (I/R) injury. This study was designed to investigate the effect of TRIM14 on the cerebral I/R injury in rats.Methods: The rat model was constructed through inserting thread into the middle cerebral artery. The expression of TRIM14 was measured by qRT-PCR, immunoblotting, and immunofluorescence. The hippocampal sections were stained with 2,3,5-triphenyltetrazolium chloride (TTC) to determine infarct volume and used for measuring the neurologic deficit score and brain water content. The H&E staining was used for immunohistochemical (IHC) staining. The number of apoptotic cells was measured by fluorescence microscopy. The levels of IL-6, IL-1β, and TNFα were detected by qRT-PCR and ELISA. The swimming speed, latency time, and number of platform crossings were measured by the water maze test.Results: TRIM14 was significantly enhanced in rats with cerebral I/R injury compared to Sham rats, showing its highest level at 24 h after I/R. TRIM14 inhibition reduced ischemic brain injury, suppressed neuron apoptosis, suppressed inflammation, and improved cognitive dysfunction in rats with cerebral I/R injury. TRIM14 inhibition also suppressed the activation of NF-κB/NLRP3 pathway in rats with cerebral I/R injury.Conclusion: In conclusion, the expression of TRIM14 was increased in rats with cerebral I/R injury, the protective effect of TRIM14 inhibitor on cerebral I/R injury in rats depends on its anti-apoptotic and anti-inflammatory effect. The underlying mechanism was, at least partially, through regulating NF-κB/NLRP3 pathway.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 2","pages":"197-205"},"PeriodicalIF":2.8,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1887218","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25454060","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: 7

A review of protein-protein interaction and signaling pathway of Vimentin in cell regulation, morphology and cell differentiation in normal cells Vimentin蛋白-蛋白相互作用及信号通路在正常细胞细胞调控、细胞形态和细胞分化中的研究进展

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-03-16 DOI: 10.1080/10799893.2022.2047199

Danial Hashemi Karoii, Hossein Azizi

{"title":"A review of protein-protein interaction and signaling pathway of Vimentin in cell regulation, morphology and cell differentiation in normal cells","authors":"Danial Hashemi Karoii, Hossein Azizi","doi":"10.1080/10799893.2022.2047199","DOIUrl":"https://doi.org/10.1080/10799893.2022.2047199","url":null,"abstract":"Abstract The Vimentin intermediate filament (VIF) is an essential cytoskeleton component. It shows dynamically changing expression patterns throughout various phases of the differentiation process, suggesting that the protein is physiologically important. Vimentin’s essential functions have recently been clear, so Vimentin-deficient of animals was described as a change of morphology and signaling pathway. Recent research has discovered many vital roles for Vimentin that were previously unknown. VIF emerges as an organizer of many essential proteins involved in movement and cell signaling. The highly dynamic and complicated phosphorylation of VIF seems to be a regulator mechanism for various activities. Changes in IF expression patterns are often linked with cancer progression, especially those leading to enhanced invasion and cellular migration. This review will discuss the function of Vimentin intermediate filaments in normal cell physiology, cell adhesion structures, cell shape, and signaling pathways. The genes interaction and gene network linked with Vimentin will be discussed in more studies. However, research aimed at understanding the function of Vimentin in different signaling cascades and gene interactions might offer novel methods for creating therapeutic medicines. Enrichr GEO datasets used gene ontology (GO) and pathway enrichment analyses. STRING online was used to predict the functional connections of proteins-proteins, followed by Cytoscape analysis to find the master genes. Cytoscape and STRING research revealed that eight genes, Fas, Casp8, Casp6, Fadd, Ripk1, Des, Tnnc2, and Tnnt3, were required for protein-protein interactions with Vimentin genes involved in cell differentiation.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"9 1","pages":"512 - 520"},"PeriodicalIF":2.8,"publicationDate":"2022-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84203337","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: 10

QSAR study of antituberculosis activity of oxadiazole derivatives using DFT calculations 用DFT计算恶二唑衍生物抗结核活性的QSAR研究

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-03-09 DOI: 10.1080/10799893.2022.2044860

S. Hosseini, S. Ketabi, Golnar Hasheminasab

{"title":"QSAR study of antituberculosis activity of oxadiazole derivatives using DFT calculations","authors":"S. Hosseini, S. Ketabi, Golnar Hasheminasab","doi":"10.1080/10799893.2022.2044860","DOIUrl":"https://doi.org/10.1080/10799893.2022.2044860","url":null,"abstract":"Abstract Mycobacterium tuberculosis (Mtb) is the causative agent of infectious diseases worldwide. Oxadiazole derivatives have many biological activities and can be a good alternative to antimicrobial drugs. In this study, the quantitative structure–activity relationship (QSAR) of fifty-one novel oxadiazoles derivatives has been studied using the density functional theory (DFT) and statistical methods. Becke’s three-parameter hybrid method and the Lee-Yang-Parr B3LYP functional employing 6–31++G (d) basis set are used to calculated quantum chemical descriptors using Gaussian09 software. The other descriptors including Lipinski, physicochemistry, topological, etc. were calculated using Chembio3d software. Statistically, the best correlation between the independent variables and the PMIC as the dependent variable was a 6-variable equation for which the correlation coefficient were as follows R 2 = 0.86 and R = 0.93. Also, the values of MAE = 0.003 and Q 2 CV = 0.9 confirm the acceptability of the obtained model. The obtained equation shows that NRB, energy gap (ΔE), Henry’s law constant, O–C, and C–N bonds length, and the Free Gibbs energy have the highest correlation with the anti-Tb activity.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"21 1","pages":"503 - 511"},"PeriodicalIF":2.8,"publicationDate":"2022-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78285156","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: 4

MiR-370-5p inhibits the progression of breast cancer via targeting LUC7L3 MiR-370-5p通过靶向LUC7L3抑制乳腺癌的进展

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-03-04 DOI: 10.1080/10799893.2022.2054577

引用次数: 6

Morroniside protects HT-22 cells against oxygen-glucose deprivation/reperfusion through activating the Nrf2/HO-1 signaling pathway. Morroniside通过激活Nrf2/HO-1信号通路保护HT-22细胞免受氧糖剥夺/再灌注。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-02-01 Epub Date: 2020-10-26 DOI: 10.1080/10799893.2020.1837872

Lan Zhang, Huiping Wang, Yan Liu, Li Wang, Weikang Pan, Bo Yuan

{"title":"Morroniside protects HT-22 cells against oxygen-glucose deprivation/reperfusion through activating the Nrf2/HO-1 signaling pathway.","authors":"Lan Zhang, Huiping Wang, Yan Liu, Li Wang, Weikang Pan, Bo Yuan","doi":"10.1080/10799893.2020.1837872","DOIUrl":"https://doi.org/10.1080/10799893.2020.1837872","url":null,"abstract":"Neonatal hypoxic-ischemic encephalopathy (HIE) is a devastating condition that affects neurodevelopment and results in brain injury in infants. Morroniside (MOR), a natural secoiridoid glycoside, has been found to possess neuroprotective effect. However, the effects of MOR on neonatal HIE are unclear. An in vitro HIE model was established in murine hippocampal neurons HT-22 cells using oxygen-glucose deprivation/reoxygenation (OGD/R) stimulation. Our results showed that MOR improved OGD/R-caused cell viability reduction in HT-22 cells. MOR suppressed the production of reactive oxygen species (ROS) and malondialdehyde (MDA) in OGD/R-induced HT-22 cells in a dose-dependent manner. The activities of superoxide dismutase (SOD) and glutathione peroxidase (GPX) were significantly elevated by MOR. Moreover, MOR treatment caused a significant increase in bcl-2 expression, and obvious decreases in the expression levels of bax, cleaved caspase-3, and cleaved caspase-9 expression. Furthermore, MOR significantly upregulated the expression levels of nuclear Nrf2 and HO-1 in OGD/R-treated HT-22 cells. Additionally, knockdown of Nrf2 or HO-1 abrogated the effects of MOR on OGD/R-induced oxidative stress and apoptosis in HT-22 cells. In conclusion, these findings suggested that MOR protects HT-22 cells against OGD/R via regulating the Nrf2/HO-1 signaling pathway.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 1","pages":"9-15"},"PeriodicalIF":2.8,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1837872","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38621622","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: 4