Journal of Receptors and Signal Transduction最新文献

{"title":"Bortezomib suppresses TGF-β1-mediated LOXL4 reduction through the inhibition of MEK/ERK pathways in MDA-MB-231 cells.","authors":"Tetsuro Kamiya, Kana Ishii, Kiyomi Ozawa, Hirokazu Hara","doi":"10.1080/10799893.2025.2455594","DOIUrl":"10.1080/10799893.2025.2455594","url":null,"abstract":"<p><p>Lysyl oxidase (LOX), a copper-containing secretory oxidase, plays a key role in the regulation of extracellular stiffness through cross-linking with collagen and elastin. Among the LOX family of enzymes, LOX-like 4 (LOXL4) exhibits pro-tumor and anti-tumor properties; therefore, the functional role of LOXL4 in tumor progression is still under investigation. Here, we first determined that transforming growth factor-β1 (TGF-β1) significantly decreased LOXL4 expression in human breast cancer MDA-MB-231 cells, which suggested that decreased LOXL4 may participate in tumor progression. In this study, we also investigated how TGF-β1 decreases LOXL4 expression. TGF-β1-induced intracellular reactive oxygen species (ROS) played a role in LOXL4 protein expression but had no effect on LOXL4 mRNA levels. The proteasomal inhibitor, bortezomib, significantly suppressed TGF-β1-mediated LOXL4 reduction, which indicated that TGF-β1 facilitates LOXL4 proteasomal degradation. Furthermore, bortezomib inhibited TGF-β1-induced MEK/ERK pathways which are involved in LOXL4 reduction and TGF-β1-mediated cell migration. Finally, we also determined the potential role of N-glycosylation in LOXL4 secretion. We found that the dysregulation of N-glycosylation may be involved in the reduction in LOXL4 secretion. Overall, bortezomib is expected to inhibit TNBC progression by inhibiting both the MEK/ERK and proteasomal degradation pathways, which regulate LOXL4 expression.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":" ","pages":"73-82"},"PeriodicalIF":2.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143039386","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":"Novel therapeutic approaches targeting 5-HT7 receptors outside the central nervous system.","authors":"Melis Kilic, Zeynep Karakoy, Hamza Halici, Elif Cadirci, Zekai Halici","doi":"10.1080/10799893.2024.2446401","DOIUrl":"10.1080/10799893.2024.2446401","url":null,"abstract":"<p><p>Serotonin (5-HT) is a neurotransmitter found throughout the human body that regulates many physiological events arising from the brain and central nervous system (CNS), such as sleep and appetite. However, it has many other functions in systems outside. In addition to the routine expression of 5-HT7 receptors in CNS regions, such as the pituitary gland, spinal cord, and hippocampus, many studies have reported the expression of these receptors in pathological conditions outside. The role of 5-HT7 receptors outside the CNS has been attracting increased attention in recent years. This review highlights the fact that 5-HT7 receptors are associated with diseases and systems beyond the CNS increasing or decreasing in response to cellular changes. Clinical, basic, <i>in vivo</i> and <i>in vitro</i> studies to date are described, but more research is needed to better understand the role of 5-HT7 receptors outside the CNS.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":" ","pages":"55-60"},"PeriodicalIF":2.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927271","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":"Evaluation of the effect of <i>Helicobacter pylori</i> -derived OMVs and released exosomes from stomach cells treated with OMVs on the expression of genes related to the TGF-β/SMAD signaling pathway in hepatocellular carcinoma.","authors":"Zohreh Mohammadi Azad, Mehrdad Moosazadeh Moghaddam, Mahdi Fasihi-Ramandi, Setareh Haghighat, Reza Mirnejad","doi":"10.1080/10799893.2024.2436461","DOIUrl":"10.1080/10799893.2024.2436461","url":null,"abstract":"<p><p>OMVs derived from <i>Helicobacter pylori</i> can lead to cell transformation in gastric epithelium and cancer. Additionally, exosomes (Exos) released by host cells infected with <i>H. pylori</i> can significantly contribute to the development of diseases such as cancer. In this study, the effects of both Exos from AGS cells treated with <i>H. pylori</i>-derived OMVs on the expression of genes related to the TGF-β/SMAD signaling pathway in hepatocellular carcinoma (HCC) cells were investigated. The TGF-β/SMAD pathway is one of the most important pathways that regulate the development and progression of HCC. For this purpose, after treating HepG2 cells with <i>H. pylori</i>-derived OMVs (directly) and Exos from AGS cells treated with <i>H. pylori</i>-derived OMVs (indirectly), the expression levels of <i>TGF</i>-<i>β</i>, <i>SMAD2</i>, <i>SMAD3</i>, <i>SMAD4</i>, and <i>ERK</i> genes were analyzed using Real-time PCR. The findings showed that OMVs derived from <i>H. pylori</i> can significantly increase the expression of genes involved in the TGF-β signaling pathway, which can affect the aggressive behavior of HepG2 cells. Additionally, exosomes secreted from AGS cells or AGS cells treated with OMVs had no effect on changing the expression of the studied genes. Therefore, only the OMVs released from H. pylori can affect the TGF-β/SMAD signaling pathway in HCC cells.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":" ","pages":"181-190"},"PeriodicalIF":2.6,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142769957","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":"An <i>in-silico</i> approach - molecular docking analysis of flavonoids against GSK-3β and TNF-α targets in Alzheimer's disease.","authors":"Sittarthan Viswanathan, Rengaraj Sivaraj, A Hannah Rachel Vasanthi, Kavimani Subramanian, Vimalavathini Ramesh","doi":"10.1080/10799893.2024.2396430","DOIUrl":"10.1080/10799893.2024.2396430","url":null,"abstract":"<p><strong>Introduction: </strong>Drug development for Alzheimer's disease has one of the greatest failure rates of any therapeutic field and AD is still incurable. Glycogen synthase kinase-3β is a critical enzyme implicated in the pathogenesis of AD, particularly in the hyperphosphorylation of tau protein, which leads to the formation of neurofibrillary tangles. TNF-α also plays a significant role in the pathogenesis of Alzheimer's disease by promoting neuroinflammation, contributing to the formation of amyloid plaques and neurofibrillary tangles, impairing synaptic function, and disrupting the balance of neurotrophic factors. Phytomedicine has numerous advantages over synthetic medications, acting multiple mode of action, including being less toxic and having fewer adverse effects. Flavonoids act as a promising therapeutic target for treating Alzheimer's disease. The present work investigates the anti-AD potentials of 35 flavonoids for the inhibition of GSK-3β and TNF-α.</p><p><strong>Methods: </strong>The physicochemical, pharmacokinetic parameters, toxicity profile and drug-likeliness of the selected 35 flavonoids were predicted using SwissADME & OSIRIS data Warrier property explorer web tool. All flavonoids were selected for docking studies on GSK-3β and TNF-α protein using Autodock 4.2.1.</p><p><strong>Results: </strong>The predictions of this study suggested that among the selected 35 flavonoids, Top 3 flavonoids, such as Epicatechin gallate -10.93 kcal/mol, Fisetin -9.44 kcal/mol and Eriodictyol -8.54 kcal/mol for GSK-3β targets. TNF-α Fisetin -11.52 kcal/mol, Sterubin -10.87 kcal/mol, Biochainin A -10.69 kcal/mol were compared with standard drug donepezil.</p><p><strong>Conclusion: </strong>Therefore, these flavonoids could be utilized as possible leads for the structure-based design in the advancement of new, strong Anti-Alzheimer's agents. However, more <i>invitro</i> and <i>invivo</i> analyses are required to finally confirm the outcomes of this research.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":" ","pages":"73-81"},"PeriodicalIF":2.6,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142073131","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":"UBE2C, targeted by miR-140-3p, promotes the progression of osteosarcoma via PI3K/AKT signaling pathway.","authors":"Wenze Huang, Yan Zhou, Jing Ren, Chunfa Chen","doi":"10.1080/10799893.2024.2423100","DOIUrl":"10.1080/10799893.2024.2423100","url":null,"abstract":"<p><strong>Background: </strong>UBE2C was reported to play carcinogenic effects in diverse cancers. However, the role of UBE2C in osteosarcoma was poorly understood, and its functional mechanisms were not fully clarified.</p><p><strong>Methods: </strong>RT-qPCR was used to assess the expression of UBE2C mRNA and miR-140-3p, and western blot technique was used to examine the UBE2C protein and PI3K/AKT pathway-associated proteins. CCK-8 test was applied to measure cell proliferation, and wound healing assay were used to measure migration. Using animal studies, the function of UBE2C <i>in vivo</i> was evaluated. Dual-luciferase reporter assay was used to confirm the potential interaction among UBE2C and miR-140-3p.</p><p><strong>Results: </strong>In osteosarcoma cells as well as tumor samples, UBE2C was strongly expressed. Osteosarcoma cell proliferation as well as cell migration were inhibited by UBE2C knockdown, and PI3K/AKT signaling activity was diminished. In addition, UBE2C knockdown impeded tumor growth in animal models. UBE2C expression was lessened by miR-140-3p as miR-140-3p targets it. UBE2C is overexpressed which promote osteosarcoma proliferation as well as migration, and strengthened the PI3K/AKT signaling activity, while forced miR-140-3p expression partially abolished these effects.</p><p><strong>Conclusion: </strong>UBE2C, targeted by miR-140-3p, drove carcinogenic effects in osteosarcoma through activating the PI3K/AKT pathway.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":" ","pages":"107-114"},"PeriodicalIF":2.6,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142582882","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":"Acetylcholinesterase - glucose-regulated protein 78 binding site prediction, a hope to cure neurological disorders such as Alzheimer's disease.","authors":"Ahmed M Ali, Ahmed A Mohamed, Ahmed N Ibrahim, Abdo A Elfiky","doi":"10.1080/10799893.2024.2426523","DOIUrl":"10.1080/10799893.2024.2426523","url":null,"abstract":"<p><p>Cerebral amyloid plaques in the brain define the elderly neuralgic disorder, Alzheimer's disease (AD). The enzyme Acetylcholinesterase (AChE) was reported to play a vital role in AD. It was shown that AChE induces amyloid fibril formation forming highly toxic AChE-Amyloid-β (Aβ) complexes. AChE can accelerate amyloid formation, and its inhibition could prevent such alterations to the enzyme. Understanding the proteostasis of AChE and its binding site to cellular chaperone GRP78 (Glucose-regulated protein 78) would help find a treatment for AD. In this study, the state of the art computational tools were utilized to predict the binding location of AChE that can stably associate with the cellular chaperone, GRP78. Sequence comparison along with molecular docking predicts two binding locations on AChE (C69-C96 and C257-C272) that could bind to GRP78 substrate binding domain β (SBDβ). The analysis of the docking data suggests that the former location has the best average binding affinity value (-12.16 kcal/mol) and average interaction pattern (13.9 ± 3.5 H-bonds, 5.5 ± 1.4 hydrophobic contacts, and 1.4 ± 1.2 salt bridges).</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":" ","pages":"122-128"},"PeriodicalIF":2.6,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142622685","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":"Virtual screening, molecular docking and dynamics simulation studies to identify potential agonists of orphan receptor GPR78 targeting CNS disorders.","authors":"Vasavi Garisetti, Roslin Elsa Varughese, Arthikasree Anandamurthy, Jebiti Haribabu, Claudio Allard Garrote, Gayathri Dasararaju","doi":"10.1080/10799893.2024.2405488","DOIUrl":"10.1080/10799893.2024.2405488","url":null,"abstract":"<p><p>G protein-coupled receptors (GPCRs) are important targets in drug discovery because of their roles in physiological and pathological processes. Orphan GPCRs are GPCR proteins for which endogenous ligands have not yet been identified and they present interesting avenues for therapeutic intervention. This study focuses on GPR78, an orphan GPCR that is expressed in the central nervous system and linked to neurological disorders. GPR78 has no reported crystal structure and there is limited research. In this study, we have predicted the three dimensional model of GPR78 and its probable binding pocket. Structure-based virtual screening was carried out using the ChemDiv and Enamine REAL databases, followed by induced-fit docking studies to identify potential lead compounds with favorable interactions. These lead compounds were then embedded into a POPC lipid bilayer for a 200 ns molecular dynamics simulation. Free energy landscapes and MM-PBSA analyses were performed to assess the binding energies and conformational dynamics. The results highlight the dynamic nature of GPR78 in the presence of lead compounds and show favorable binding interactions. This study aims to predict a reliable three dimensional model of GPR78 and identify novel lead compounds through a comprehensive <i>in silico</i> approach. The identification of these potential GPR78 agonists represents a significant step in the development of new therapeutics for neurological disorders, highlighting the therapeutic potential of orphan GPR78 in CNS disorders.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":" ","pages":"82-96"},"PeriodicalIF":2.6,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142307993","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":"Allosteric covalent inhibition of TOE1 as potential unexplored anti-cancer target: structure-based virtual screening and covalent molecular dynamics analysis.","authors":"Ibrahim Oluwatobi Kehinde, Ernest Oduro-Kwateng, Mahmoud E S Soliman","doi":"10.1080/10799893.2024.2411690","DOIUrl":"10.1080/10799893.2024.2411690","url":null,"abstract":"<p><p>Cancer remains a formidable challenge in therapeutic development owing to its complex molecular mechanisms and resistance to conventional treatments. Recent evidence suggests that TOE1 may play a role in cancer progression, making it an attractive target for therapeutic interventions, nevertheless, very limited research in literature has explored the potential of TOE1 inhibitors as anti-cancer. Herein, by exploring a library of 13,900 cysteine-targeted covalent inhibitors <i>via</i> a comprehensive virtual screening process, we sought to identify potential compounds that could be developed into effective cancer therapies against TOE1. The compounds were first screened based on their binding affinity, followed by their compliance with drug-like properties, and finally, by their effective covalent modeling to a reactive cysteine (Cys80). A total of 66 compounds, 28 compounds, and 3 compounds were found to have higher binding affinities, optimum drug-likeness, and higher covalent docking scores, respectively, than the reference compound. The top three screened compounds, 0462, 2204, and 7034, demonstrated favorable interaction profiles, covalent binding dynamics, free binding energetics, and per-residue energy contributions as compared to the reference compound. Notably, compound 0462 contributed to the highest free binding energy and significantly enhanced the stability and rigidity of TOE1, while restricting residue flexibility. This study provides an account of the molecular mechanics underpinning the covalent inhibition of TOE1, while providing a compelling case for further investigation and translation of the screened TOE1 inhibitors, particularly compound 0462, as novel therapeutics against cancer.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":" ","pages":"97-106"},"PeriodicalIF":2.6,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142391390","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":"Low pH modulates lipopolysaccharide-induced tumor necrosis factor-alpha expression and macropinocytotic activity in RAW264.7 cells.","authors":"Miku Otsugu, Ayumi Mine, Izumi Uchida, Yuta Miyake, Ryo Tachihara, Kurumi Fujiwara, Ayako Ichimura, Koichi Sato, Hideaki Tomura","doi":"10.1080/10799893.2024.2395310","DOIUrl":"10.1080/10799893.2024.2395310","url":null,"abstract":"<p><p>Inflammation triggers various types of diseases that need to be addressed. Macrophages play important roles in the inflammatory responses. As atherosclerosis progresses, macrophages transform into foam cells. Extracellular acidification is observed at and around bacterial infection and atherosclerotic sites. However, the effects of acidification on the inflammatory response of macrophages and the progression of atherosclerosis have not been fully understood. This study investigates the impact of extracellular acidification on lipopolysaccharide-induced tumor necrosis factor-alpha (TNF-α) expression and macropinocytotic activity in RAW264.7 cells. TNF-α expression is measured by real-time polymerase chain reaction (relative value to glyceraldehyde-3-phosphate dehydrogenase expression). Macropinocytotic activity is measured by neutral red uptake (absorbance at 540 nm). Results show that TNF-α expression increased with decreasing extracellular pH in both un-foamed and foamed cells. Macropinocytotic activity was upregulated at pH 6.8 in un-foamed cells, but downregulated in foamed cells stimulated at low pH. Proton-sensing G protein-coupled receptors (GPCRs) were involved in the expression of TNF-α and in the macropinocytotic activity of foamed cells. In conclusion, this study reveals that extracellular acidification differently affect various inflammatory responses such as LPS-induced TNF-α expression and macropinocytotic activity of RAW264.7 cells and different proton-sensing GPCRs are involved in the different inflammatory responses.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":" ","pages":"63-71"},"PeriodicalIF":2.6,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142036062","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":"Heat shock protein (Hsp27)-ceramide synthase (Cers1) protein-protein interactions provide a new avenue for unexplored anti-cancer mechanism and therapy.","authors":"Musab Ali, Zhichao Zhang, Mahmoud A A Ibrahim, Mahmoud E S Soliman","doi":"10.1080/10799893.2024.2392711","DOIUrl":"10.1080/10799893.2024.2392711","url":null,"abstract":"<p><p>Hsp27 is a member of the small heat-shock proteins (sHSPs) - the known cellular line of defence against abnormal protein folding behaviors. Nevertheless, its upregulation is linked to a variety of pathological disorders, including several types of cancers. The ceramide synthases (CerS) mediate the synthesis of ceramide, a critical structural and signaling lipid. Functionally, downstream ceramide metabolites are implicated in the apoptosis process and their abnormal functionality has been linked to anticancer resistance. Studies showed that CerS1 are possibly inhibited by Hsp27 leading to biochemical anticancer effects <i>in vitro</i>. Nevertheless, the nature of such protein-protein interaction (PPI) has not been considerably investigated in molecular terms, hence, we present the first description of the dynamics CerS1-Hsp27 interaction landscapes using molecular dynamics simulations. Time-scale molecular dynamics simulation analysis indicated a system-wide conformational events of decreased stability, increased flexibility, reduced compactness, and decreased folding of CerS1. Analysis of binding energy showed a favorable interaction entailing 56 residues at the interface and a total stabilizing energy of -158 KJ/mol. The CerS1 catalytic domain experienced an opposite trend compared to the protein backbone. Yet, these residues adopted a highly compact conformation as per DCCM and DSSP analysis. Furthermore, conserved residues (SER 212, ASP 213, ALA 240, GLY 243, ASP 319) comprising the substrate shuttling machinery showed notable rigidity implying a restrained ceramide precursor access and assembly; hence, a possible inhibitory mechanism. Findings from this report would streamline a better molecular understanding of CerS1-Hsp27 interactions and decipher its potential avenue toward unexplored anti-cancer mechanisms and therapy.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":" ","pages":"41-53"},"PeriodicalIF":2.6,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142073132","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}