Journal of Receptors and Signal Transduction最新文献

{"title":"Transmembrane protein 88 inhibits transforming growth factor-β1-induced-extracellular matrix accumulation and epithelial-mesenchymal transition program in human pleural mesothelial cells through modulating TGF-β1/Smad pathway.","authors":"Zhongmin Sun,&nbsp;Qian Ning,&nbsp;Hong Li,&nbsp;Tinghua Hu,&nbsp;Ling Tang,&nbsp;Qing Wen,&nbsp;Liangrong Shen","doi":"10.1080/10799893.2020.1843493","DOIUrl":"https://doi.org/10.1080/10799893.2020.1843493","url":null,"abstract":"<p><p>Pleural fibrosis is an irreversible pathological process occurred in the development of several lung diseases. TMEM88 is a member of transmembrane (TMEM) family and has been found to be involved in the regulation of fibrogenesis. However, the role of TMEM88 in pleural fibrosis remains unknown. In this study, we aimed to explore the role of TMEM88 in pleural fibrosis <i>in vitro</i> using transforming growth factor-β1 (TGF-β1)-induced human pleural mesothelial cell line MeT-5A cells. Our results showed that the expression levels of TMEM88 were downregulated in pleural fibrosis tissues and TGF-β1-treated Met-5A cells. Overexpression of TMEM88 inhibited the proliferation of Met-5A cells under TGF-β1 stimulation. In addition, TMEM88 overexpression prevented TGF-β1-induced extracellular matrix (ECM) accumulation and epithelial-mesenchymal transition (EMT) in Met-5A cells with decreased expression levels of Col I and fibronectin, increased levels of cytokeratin-8 and E-cadherin, as well as decreased levels of vimentin and α-SMA. Furthermore, overexpression of TMEM88 inhibited the expression of TGF-β receptor I (TβRI) and TβRII and suppressed the phosphorylation of Smad2 and Smad3 in Met-5A cells. In conclusion, these results indicated that TMEM88 exhibited an anti-fibrotic activity in pleural fibrosis <i>via</i> inhibiting the activation of TGF-β1/Smad signaling pathway.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 1","pages":"60-66"},"PeriodicalIF":2.8,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1843493","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38678584","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}

{"title":"The stimulative function of long noncoding RNA CDKN2B-AS1 in osteosarcoma by targeting the microRNA-122/CCNG1 axis.","authors":"Abulaiti Abula,&nbsp;Guliayixiamu Saimaiti,&nbsp;Xayimardan Maimaiti,&nbsp;Wumitijiang Wuqikun,&nbsp;Alimujiang Abulaiti,&nbsp;Peng Ren,&nbsp;Aihemaitijiang Yusufu","doi":"10.1080/10799893.2020.1850784","DOIUrl":"https://doi.org/10.1080/10799893.2020.1850784","url":null,"abstract":"<p><p>Osteosarcoma (OS), a prevalent aggressive malignancy in the bone, has limited therapeutic targets and diagnostic biomarkers. In the current investigation, RT-qPCR showed that CDKN2B-AS1 was enhanced in OS samples and cells. This research was set to examine the modulation of CDKN2B-AS1 in OS. The expression of CDKN2B-AS1 and downstream molecules was analyzed by RT-qPCR method. CCK8, EdU staining along with Transwell assays were applied to evaluate cell proliferation and invasion. Those <i>in vitro</i> investigations specified that silencing of CDKN2B-AS1 with shRNAs obviously impeded the proliferation and invasion of MG63 cells. To authenticate the relationships between CDKN2B-AS1 and microRNA-122-5p (miR-122-5p) or cyclin G1 (CCNG1) and miR-122-5p, we next employed luciferase reporter assay. We displayed that CDKN2B-AS1 repressed miR-122-5p to restore CCNG1 expression. All in all, our findings substantiated the indispensable function of CDKN2B-AS1 in OS progression and the possible molecular mechanism.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 1","pages":"71-79"},"PeriodicalIF":2.8,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1850784","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38341969","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}

{"title":"Molecular characterization of solitary pulmonary nodules in dual-energy CT nonlinear image fusion technology.","authors":"Qian Li,&nbsp;Huan Tan,&nbsp;Furong Lv","doi":"10.1080/10799893.2020.1853158","DOIUrl":"https://doi.org/10.1080/10799893.2020.1853158","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the feasibility and to optimize the parameters of nonlinear blending technique in dual-energy CT on solitary pulmonary nodules (SPN).</p><p><strong>Methods: </strong>The simulated enhanced SPN were used the mixture of nonionic iodinated contrast agent (Iopromide 370mgI/100 ml) and normal saline and then randomly placed inside an anthropomorphic chest phantom. The phantom was examined on SOMATOM definition flash with dual mode (80/140 kV) and single energy mode (120 kV) (the same CTDIvol). Nonlinear blending images and linear blending images with a weighting factor of 0.3 were generated and the image qualities were analyzed.</p><p><strong>Results: </strong>For different simulated density SPN, when 0 HU was chosen as the Blending Center (BC) and 0 to 30 HU were chosen as the Blending width (BW), the nonlinear blending images yielded a higher contrast-to-noise (CNR). There were significant differences in the image noise and signal-to-noise (SNR) of different simulated density SPN at non-linear blending images, linear blending images and 120 kV images (<i>p</i> < .05); But the differences of CNR between the three groups were not statistically significant (<i>p</i> > .05). The SNR of different simulated density SPN at non-linear blending images was significantly increased compared with it at linear blending images and 120 kV images (<i>p</i> < .05); And the image noise at non-linear blending was lower than it at linear blending images (<i>p</i> < .05).</p><p><strong>Conclusion: </strong>Nonlinear blending technique in dual-energy CT can increase the SNR of enhanced SPN, and it is helpful in diagnosis of SPN.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 1","pages":"95-99"},"PeriodicalIF":2.8,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1853158","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38658792","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}

{"title":"CACNA1B facilitates breast cancer cell growth and migration by regulating cyclin D1 and EMT: the implication of CACNA1B in breast cancer.","authors":"Yong-Mei Jin,&nbsp;Ying Ye,&nbsp;Wen-Qing Bao,&nbsp;Yang Tong,&nbsp;Shu-Bin Ni,&nbsp;Jian-Ping Liu,&nbsp;Bin Zhao","doi":"10.1080/10799893.2020.1837871","DOIUrl":"https://doi.org/10.1080/10799893.2020.1837871","url":null,"abstract":"<p><strong>Purpose: </strong>This study mainly aimed to explore the influences of Calcium Voltage-Gated Channel Subunit Alpha1 B (CACNA1B) on the development of breast cancer and the related mechanism.</p><p><strong>Materials and methods: </strong>The information of patients with breast cancer from TCGA database was used for analyses of CACNA1B expression and its prognostic value. Loss- and gain- of functions of CACNA1B were conducted in MCF7 and Bcap-37 cells, respectively. CCK-8, colony formation and transwell assays were applied for evaluating the cell viability and motility. Western blot was used for protein expression detection.</p><p><strong>Results: </strong>We revealed that highly expressed CACNA1B in breast cancer tissues was related to poor prognosis according to the data gained from TCGA database. The outcomes of functional assays showed that depletion of CACNA1B restrained MCF7 cell growth, invasion and migration and high-expression of CACNA1B fortified the growth, invasion and migration in Bcap-37 cells. Finally, we manifested that silencing CACNA1B obviously raised the protein expression level of E-cadherin and reduced the protein levels of Cyclin D1, N-cadherin and Snail in MCF7 cells, whilst, over-expression of CACNA1B reduced the level of E-cadherin and increased the expression of Cyclin D1, N-cadherin and Snail in Bcap-37 cells.</p><p><strong>Conclusions: </strong>These results identified CACNA1B as a forwarder of the growth, invasion and migration in breast cancer cells.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 1","pages":"1-8"},"PeriodicalIF":2.8,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1837871","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38525591","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}

{"title":"miR-362-3p suppresses sinonasal squamous cell carcinoma progression via directly targeting pituitary tumor-transforming gene 1.","authors":"Zhaolun Meng,&nbsp;Shu Zhu,&nbsp;Na Liu,&nbsp;Jie Tian","doi":"10.1080/10799893.2020.1839766","DOIUrl":"https://doi.org/10.1080/10799893.2020.1839766","url":null,"abstract":"<p><strong>Background: </strong>Sinonasal squamous cell carcinoma (SNSCC) is a main subtype of sinonasal malignancy with unclear pathogenesis. microRNAs (miRNAs) are involved in SNSCC progression. Nevertheless, the role and mechanism of miR-362-3p in SNSCC development are unclear.</p><p><strong>Methods: </strong>The SNSCC tissues (<i>n</i> = 23) and normal sinonasal samples (<i>n</i> = 13) were harvested. SNSCC cell line RPMI-2650 cells were transfected using Lipofectamine 3000. miR-362-3p and pituitary tumor-transforming gene 1 (PTTG1) were determined by quantitative reverse transcription polymerase chain reaction and western blot. Cell proliferation was analyzed <i>via</i> Cell Counting Kit-8 and 5-ethynyl-2'-deoxyuridine assays. Cell migration and invasion was assessed using wound healing assay and transwell assay. Epithelial-mesenchymal transition (EMT)-associated protein (E-cadherin, N-cadherin and Vimentin) levels were measured <i>via</i> western blot. The binding relationship was analyzed <i>via</i> bioinformatic analysis and dual-luciferase reporter assay.</p><p><strong>Results: </strong>miR-362-3p abundance was decreased in SNSCC samples. miR-362-3p addition constrained cell proliferation, migration, invasion and EMT, but miR-362-3p knockdown played an opposite effect. PTTG1 was targeted and negatively modulated by miR-362-3p. PTTG1 abundance was elevated in SNSCC samples. PTTG1 overexpression mitigated miR-362-3p-modulated suppression of cell proliferation, migration, invasion and EMT in SNSCC cells.</p><p><strong>Conclusion: </strong>miR-362-3p repressed cell proliferation, migration, invasion and EMT in SNSCC <i>via</i> targeting PTTG1.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 1","pages":"43-51"},"PeriodicalIF":2.8,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1839766","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38573658","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}

{"title":"Isoflurane activates AMP-activated protein kinase to inhibit proliferation, and promote apoptosis and autophagy in cervical carcinoma both <i>in vitro</i> and <i>in vivo</i>.","authors":"Hongfang Wei,&nbsp;Tianze Sun,&nbsp;Jie Liu,&nbsp;Xiaowei Wang,&nbsp;Guangping Zhao,&nbsp;Jiong Shi,&nbsp;Yongxue Chen","doi":"10.1080/10799893.2020.1831535","DOIUrl":"https://doi.org/10.1080/10799893.2020.1831535","url":null,"abstract":"<p><strong>Objective: </strong>Isoflurane is an extensively used inhalational anesthesia, and its carcinogenic or anti-cancerous effect has been identified recently. However, the specific role of isoflurane in cervical cancer remains unclear.</p><p><strong>Aim: </strong>This study aimed to investigate the function of isoflurane in cervical cancer as well as the underlying mechanism.</p><p><strong>Methods: </strong>After isoflurane treatment, HeLa cell viability, percentage of apoptotic cells, expression of active caspase-3/9 were examined by CCK-8 assay, Annexin V-FITC/PI double staining, and Western blot analysis, respectively. ROS generation, ratio of NAD⁺/NADH, and ATP level after isoflurane stimulation were determined using commercial assay kits. Afterwards, activation of AMPK and autophagy was assessed through Western blot analysis and immunofluorescence. Whether AMPK mediated the isoflurane-induced apoptosis and autophagy was explored by adding an AMPK inhibitor (Compound C). The <i>in vivo</i> function of isoflurane was finally investigated on a HeLa cell <i>xenograft</i> model.</p><p><strong>Results: </strong>Isoflurane inhibited cell viability and induced apoptosis evidenced by upregulation of active caspase-3/9 in HeLa cells. Oxidative stress was triggered by isoflurane, as isoflurane elevated ROS level, and lowered ratio of NAD⁺/NADH and ATP level. Further results showed isoflurane activated the AMPK/mTOR pathway and induced autophagy. In addition, inhibition of AMPK led to ameliorated effects of isoflurane on apoptosis and autophagy. <i>In vivo</i> experiments proved isoflurane could repress tumorigenesis, activate AMPK, and induce autophagy in <i>Xenograft</i> mouse.</p><p><strong>Conclusions: </strong>Isoflurane activated AMPK to inhibit proliferation and promote apoptosis and autophagy both <i>in vitro</i> and <i>in vivo</i>.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"41 6","pages":"538-545"},"PeriodicalIF":2.8,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1831535","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38574206","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}

{"title":"Berberine modulates Keratin 17 to inhibit cervical cancer cell viability and metastasis.","authors":"Luping Liu,&nbsp;Li Sun,&nbsp;Jing Zheng,&nbsp;Li Cui","doi":"10.1080/10799893.2020.1830110","DOIUrl":"https://doi.org/10.1080/10799893.2020.1830110","url":null,"abstract":"<p><strong>Aim: </strong>Berberine (BBR) acts as a tumor suppressor in different cancer cells. Our paper exerted efforts to discover the effect of BBR on cervical cancer.</p><p><strong>Methods: </strong>Human cervical cancer cell lines SiHa and Ca Ski were treated with different concentrations of BBR. Cell viability, apoptosis, migration and invasion were detected by MTT assay, flow cytometry, wound healing assay, and Transwell assay, respectively. Expressions of Bcl-2-associated X protein (Bax), Bcl-2, cleaved (C) caspase-3 and epithelial-mesenchymal transition (EMT)-related proteins were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. Keratin 17 (KRT17) expression in cervical cancer was identified by GEPIA2 and qRT-PCR. Rescue assay was then performed to assess the functional interaction between BBR and KRT17.</p><p><strong>Results: </strong>Human cervical cancer cell viability, migration, and invasion were inhibited by BBR. BBR promoted cell apoptosis by increasing Bax and C caspase-3 expressions and decreasing Bcl-2 expression. Besides, BBR inhibited EMT in cells by decreasing the expressions of MMP-9, N-cadherin and Vimentin and increasing E-cadherin expression. Effects of BBR on cervical cancer cells were in a dose-dependent manner. Higher expression of KRT17 was found in cervical cancer SiHa and Ca Ski cells. BBR rescued the effects of KRT17 on promoting cell viability, metastasis, and the expressions of Bcl-2, MMP-9, N-cadherin and Vimentin, and suppressing apoptosis and the expressions of Bax, C-caspase-3 and E-cadherin.</p><p><strong>Conclusion: </strong>BBR inhibited cervical cancer cell viability, metastasis and EMT but promoted cell apoptosis <i>via</i> suppressing KRT 17 expression.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"41 6","pages":"521-531"},"PeriodicalIF":2.8,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1830110","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38482194","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}

{"title":"Overexpression of NDRG2 promotes the therapeutic effect of pazopanib on ovarian cancer.","authors":"Ying Cui,&nbsp;Guihua Shen,&nbsp;Linlin Ma,&nbsp;Qiubo Lv","doi":"10.1080/10799893.2020.1831536","DOIUrl":"https://doi.org/10.1080/10799893.2020.1831536","url":null,"abstract":"<p><strong>Objectives: </strong>Ovarian cancer is the second commonly seen cancer in the US, patients with ovarian cancer are commonly diagnosed in the advanced stage. Pazopanib is an inhibitor of multiple tyrosine kinases and has been approved in treatment for carcinoma by FDA. N-myc downstream-regulated gene 2 (NDRG2) has been regarded as a cancer suppressor gene and presented an inhibition effect in cancer proliferation, invasion, and migration.</p><p><p><b>Design:</b> NDRG2 was overexpressed or inhibited in SKOV-3 cells, then experiments were performed to detect the apoptosis of cells. The expression or secretion of pro-cancer molecules was detected. And the expression of apoptosis-related proteins and the ASK1/JNK1 signaling pathway was detected.</p><p><strong>Methods: </strong>The NDRG2 overexpression and inhibition model was firstly constructed in SKOV-3 cells, the apoptotic cells were detected using flow cytometry. The expression of cellular metastasis genes was detected using the qPCR method. The angiogenesis factors was detected using the ELISA method. Expression of each target protein was detected using western blotting analysis.</p><p><strong>Results: </strong>NDRG2 overexpression and inhibition model were constructed in the SKOV-3 cell line, overexpression of NDRG2 enhanced the effect of pazopanib on inhibition of the expression of metastasis-related molecules and angiogenesis-related factors. The apoptosis process of cells was also enhanced after overexpression of NDRG2, and these effects were regulated by the activation of the ASK1/JNK1 signaling pathway.</p><p><p><b>Limitations:</b> The effect of NDRG2 in animal models and more cell lines needs to be explored in further study.</p><p><strong>Conclusions: </strong>NDRG2 might be a therapeutic target in treatment for ovarian cancer.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"41 6","pages":"546-552"},"PeriodicalIF":2.8,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1831536","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38484055","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}

{"title":"LncRNA SUMO1P3 regulates the invasion, migration and cell cycle of gastric cancer cells through Wnt/β-catenin signaling pathway.","authors":"Zhong Xu,&nbsp;Jing Ran,&nbsp;Kai Gong,&nbsp;Yihan Hou,&nbsp;Ji Li,&nbsp;Yijuan Guo","doi":"10.1080/10799893.2020.1836494","DOIUrl":"https://doi.org/10.1080/10799893.2020.1836494","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the regulatory effect of long non-coding RNA (lncRNA) SUMO1P3 on invasion, migration and cell cycle of gastric cancer (GC) cells through Wnt/β-catenin signaling pathway.</p><p><strong>Methods: </strong>Tumor tissues and adjacent normal tissues from the GC patients were collected, and human normal gastric epithelial cells GES1 and GC cells SGC-7901, MKN45, HGC-27 and AGS were selected for study. The expression of SUMO1P3 in GC tissues and cells were detected by RT-qPCR. The effects of SUMO1P3 on the proliferation, invasion and migration of SGC-7901 and MKN45 cells were detected by CCK-8, transwell and wound healing assay respectively, and the effects of SUMO1P3 on apoptosis and cycle progression of SGC-7901 and MKN45 cells were detected by flow cytometry. The expressions of Wnt/β-catenin pathway-related and cell cycle-related proteins were detected by Western blot.</p><p><strong>Results: </strong>The expression of SUMO1P3 was significantly upregulated in GC tissues and cell lines. Downregulation of SUMO1P3 significantly inhibited the SGC-7901 and MKN45 cell proliferation, invasion, migration, and cycle progression and promoted the cell apoptosis, while overexpression of SUMO1P3 showed the opposite effect. Further study showed that downregulation of SUMO1P3 significantly reduced the expressions of Wnt1, β-catenin, c-myc, and Cyclin D1 in SGC-7901 and MKN45 cells.</p><p><strong>Conclusion: </strong>SUMO1P3 may promote invasion, migration, and cycle progression of SGC-7901 and MKN45 cells by enhancing the Wnt/β-catenin pathway.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"41 6","pages":"574-581"},"PeriodicalIF":2.8,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1836494","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38593130","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}

{"title":"Correction.","authors":"","doi":"10.1080/10799893.2021.1924709","DOIUrl":"https://doi.org/10.1080/10799893.2021.1924709","url":null,"abstract":"","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"41 6","pages":"III"},"PeriodicalIF":2.8,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1924709","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39017821","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}