Journal of Receptors and Signal Transduction最新文献

{"title":"Deciphering the involvement of norepinephrine and β-adrenergic receptor subtypes in glucose induced insulin secretion: an integrated <i>in silico</i> and <i>in vitro</i> exploration using isolated pancreatic islets of C57BL/6J mice.","authors":"Vijayalakshmi Gangadhara, Asha Abraham","doi":"10.1080/10799893.2024.2446393","DOIUrl":"https://doi.org/10.1080/10799893.2024.2446393","url":null,"abstract":"<p><p>Regulating insulin production by pancreatic beta cells is crucial for maintaining metabolic balance. Previous studies observed elevated neurotransmitter levels, like norepinephrine (NE), in metabolic syndrome mice with impaired insulin secretion. Given the therapeutic potential of β-adrenergic receptors (β-ARs) for diabetes and obesity, and the lack of structural data on murine β-ARs, we aimed to construct and validate 3D models to investigate their roles in insulin secretion regulation. We constructed high-quality 3D models for murine β1-AR, β2-AR, and β3-AR using Phyre2 and Ramachandran plot analysis. Molecular docking revealed NE's strong binding affinity for all three β-AR subtypes through favorable docking scores and hydrogen bond formations. We evaluated the physiological impact of NE on glucose-induced insulin secretion <i>via</i> β-ARs under physiological and elevated glucose conditions using pancreatic islets from C57BL/6J mice. At physiological glucose levels, NE did not significantly increase insulin secretion. However, higher NE concentrations suppressed insulin release at elevated glucose. The β3-AR agonist CL316243 significantly increased (<i>p</i> < 0.01), insulin secretion under normal and hyperglycemic conditions, while the β3-AR antagonist L748337 substantially decreased (<i>p</i> < 0.01)insulin release under normal glucose, confirming their interactions through docking studies. The nonselective β-AR antagonist propranolol significantly decreased (<i>p</i> < 0.01)insulin secretion, suggesting alternative interactions with β1-AR and β2-AR despite lacking hydrogen bonds. Our study enhances the understanding of NE's role in modulating insulin secretion and underscores the significance of β-ARs, especially β3-AR, in its regulation, providing valuable insights for potential therapeutic interventions targeting these receptors in metabolic disorders.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":" ","pages":"1-13"},"PeriodicalIF":2.6,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142895580","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":"Computational insights into potent USP5 inhibitors based on multistep virtual screening and molecular dynamics simulation.","authors":"Qian Xie, Linan Zhao, Dong Hu, Jing Fu, Zhengping Chen, Xia Yang, Le Fu","doi":"10.1080/10799893.2024.2443682","DOIUrl":"https://doi.org/10.1080/10799893.2024.2443682","url":null,"abstract":"<p><p>USP5 is widely distributed in various malignant tumors and can regulate the stability and promoting tumor progression of many tumor-related proteins. However, there is still a lack of highly active USP5 inhibitors. Therefore, effective inhibitors were screened in the TCMIO database in this study. Three hit compounds, CHEMBL3645368, CHEMBL3689818, and CHEMBL2070208, were finally obtained by molecular docking, molecular fingerprint, quantum chemistry, and molecular dynamics simulation. Molecular docking results showed hit compounds had similar binding mode comparing with positive compound. Quantum chemistry and molecular dynamics results showed hit compounds had better binding energy and higher affinity than the positive compound. ADMET predicted hit compounds had low toxicity. These results all suggest CHEMBL3645368, CHEMBL3689818, and CHEMBL2070208 may inhibit USP5 and could be candidates for further exploration.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":" ","pages":"1-12"},"PeriodicalIF":2.6,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864480","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":"Quest for discovering novel CDK12 inhibitor.","authors":"Abhijit Debnath, Rajesh Kumar Singh, Rupa Mazumder, Avijit Mazumder, Shikha Srivastava, Hema Chaudhary, Saloni Mangal, Jahanvi Sanchitra, Pankaj Kumar Tyagi, Sachin Kumar Singh, Anil Kumar Singh","doi":"10.1080/10799893.2024.2441185","DOIUrl":"https://doi.org/10.1080/10799893.2024.2441185","url":null,"abstract":"<p><p>CDK12 is essential for cellular processes like RNA processing, transcription, and cell cycle regulation, inhibiting cancer cell growth and facilitating macrophage invasion. CDK12 is a significant oncogenic factor in various cancers, including HER2-positive breast cancer, Anaplastic thyroid carcinoma, Hepatocellular carcinoma, prostate cancer, and Ewing sarcoma. It is also regarded as a potential biomarker, emphasizing its broader significance in oncology. Targeting CDK12 offers a promising strategy to develop therapy. Various monoclonal antibodies have drawn wide attention, but they are expensive compared to small-molecule inhibitors, limiting their accessibility and affordability for patients. Consequently, this research aims to identify effective CDK12 inhibitors using comprehensive high-throughput virtual screening. RASPD protocol has been employed to screen three different databases against the target followed by drug-likeness, molecular docking, ADME, toxicity, Consensus molecular docking, MD Simulation, and <i>in-vitro</i> studies MTT assay. The research conducted yielded one compound ZINC11784547 has demonstrated robust binding affinity, favorable ADME features, less toxicity, remarkable stability, and cytotoxic effect. The identified compound holds promise for promoting cancer cell death through CDK12 inhibition.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":" ","pages":"1-21"},"PeriodicalIF":2.6,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142854582","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":"The combined use of thymoquinone and metformin provides more effective neuroprotection in a mouse model of MPTP-induced Parkinson's disease.","authors":"Oguzhan Kavrik, Nurhan Gumral, Ozlem Ozmen, Rahime Aslankoc, Mustafa Saygin, Arzu Yalcin","doi":"10.1080/10799893.2024.2434112","DOIUrl":"10.1080/10799893.2024.2434112","url":null,"abstract":"<p><p>Thymoquinone (TQ) is known for its antioxidant properties, and although metformin (MM) is known as an antidiabetic drug, it is suggested that it reduces neurodegeneration. The study aimed to investigate the neuroprotective effects of TQ and MM, particularly when used together, in relation to Parkinson's disease (PD). In the study, sixty-eight male C57BL/6 mice weighing 25-30 g were divided into five groups as follows: control, MPTP, MPTP+TQ, MPTP+MM, and MPTP+TQ+MM. MM (500 mg/kg, orally) and TQ (5 mg/kg, i.p.) were administered for 21 days. Motor coordination and locomotor activities were evaluated by the pole test. TOS and TAS analyses were conducted to determine oxidative stress levels in the substantia nigra. Dopaminergic degeneration in the substantia nigra was evaluated by analyzing Tyrosine hydroxylase (TH). To evaluate the apoptotic pathway, the expression levels of iNOS, BDNF, Complex 1, Bax, Bcl-2, Cytochrome C, AIF, and Caspase-3 were examined immunohistochemically. Compared to the MPTP-treated group, TQ, MM and MM+TQ treatment provided significant improvement in locomotor activity in mice, significantly increased antioxidant activity, significantly reduced the expression levels of iNOS, Bax, Cytochrome C, Caspase-3, and AIF, significantly increased BDNF, Bcl-2, and Complex 1 expressions, and significantly increased the number of TH positive cells. The separate use of TQ and MM exhibits neuroprotective activity, however, we showed that using TQ and MM in combination may be more effective. This may provide preclinical evidence supporting the therapeutic potential of their combined use for treating PD.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":" ","pages":"161-173"},"PeriodicalIF":2.6,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142716412","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":"Effect of dapagliflozin on pulmonary vascular remodeling in rats with chronic hypoxic pulmonary arterial hypertension.","authors":"Yi Xu, Wenxue Liang, Juan Huo, Ting Zhang, Tianpu Feng, Man Li, Zhemin Zhu, Ping Zhou, Shasha Zhu, Yingzhi Lu, Lei Wang","doi":"10.1080/10799893.2024.2433083","DOIUrl":"10.1080/10799893.2024.2433083","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the effects of sodium-glucose co-transporter 2 inhibitor dapagliflozin on pulmonary vascular remodeling in a rat model of chronic hypoxic pulmonary arterial hypertension.</p><p><strong>Methods: </strong>Eighteen female Sprague-Dawley rats were divided into three groups: control (CON), chronic hypoxia (HYP), and chronic hypoxia + dapagliflozin. The HYP and dapagliflozin groups were subjected to hypoxia and received saline or dapagliflozin. The CON group was normoxic and received saline. Body weight and fasting blood glucose were measured, and after 21 days, lung and heart tissues were analyzed for pulmonary artery reconstruction and right ventricular hypertrophy. Western blotting assessed Bax and Bcl-2 protein levels.</p><p><strong>Results: </strong>Chronic hypoxia increased pulmonary artery wall thickness and lung fibrosis and caused right ventricular hypertrophy. Dapagliflozin reduced these changes, decreasing artery wall thickness, fibrosis, and hypertrophy while increasing the Bax/Bcl-2 ratio.</p><p><strong>Conclusion: </strong>Dapagliflozin alleviates chronic hypoxia-induced pulmonary artery wall thickening and lung tissue fibrosis in rats, potentially through proapoptotic effects.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":" ","pages":"174-180"},"PeriodicalIF":2.6,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142823834","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":"Investigating the inhibitory potential of natural bioactive compounds against cyclin-dependent kinase 13: virtual high throughput screening and MD simulation studies to target CDK signaling.","authors":"Zehra, Farah Anjum, Talha Jawaid, Romana Ishrat, Md Imtaiyaz Hassan","doi":"10.1080/10799893.2024.2430495","DOIUrl":"10.1080/10799893.2024.2430495","url":null,"abstract":"<p><p>Cyclin-dependent kinase 13 (CDK13) belongs to the cyclin-dependent kinase (CDK) family that is actively involved in transcription regulation and RNA splicing. CDK13 binds with its partner, cyclin K, to regulate several biological processes. CDK13 and cyclin K complex phosphorylates RNA pol II carboxyl-terminal domain (CTD) at several serine residues, creating transcription elongation. The upregulation of the kinase contributes to tumor growth and cell proliferation, and is highly associated with various cancers, including skin, stomach, and ovarian. Thus, it can be considered an efficient therapeutic target for the development of drugs against cancer. In this work, a virtual high throughput screening (vHTS) of the ZINC library was carried out to elucidate the initial potent compounds. Further, filters were applied to identify the hit compounds among the ∼90,000 compound library. Based on the docking scores and binding affinity, the top 100 hits were elucidated, and they were further narrowed down to 50 compounds based on ADMET and Lipinski's RO5 filter. Finally, 10 compounds were chosen that showed appreciable biological activity. Among them, ZINC02136558 was selected as a potent lead compound that showed strong interaction with the amino acid residues of active and binding sites of CDK13. Furthermore, the all-atom molecular dynamic simulation was performed at 200 ns to explore the dynamic evolution of the system. Finally, the results showed that the ZINC02136558 may be considered as a potential lead molecule to inhibit CDK13 and implicated in therapeutic management of cancer and associated diseases.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":" ","pages":"140-150"},"PeriodicalIF":2.6,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142693161","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":"Effect of elastin on abnormal proliferation of pulmonary artery smooth muscle cells at an early stage of hypoxic exposure.","authors":"Hao Dong, Pengshuai Li, Xuefei Wang, Yuxin Zhang, Fei Han, Shan Gao, Weicao Hu, Xuewei Hao","doi":"10.1080/10799893.2024.2430489","DOIUrl":"10.1080/10799893.2024.2430489","url":null,"abstract":"<p><p>Elastin (Eln) is an extracellular matrix protein implicated in the proliferation of vascular smooth muscle cells. However, its potential role in hypoxic pulmonary hypertension (HPH) remains uncertain. This study is the first to demonstrate that elastin can promote the proliferation of mouse pulmonary artery smooth muscle cells (mPASMCs) and that hypoxia significantly induces Eln expression in cultured mPASMCs, thereby participating in the cell cycle. Interference with Eln expression <i>via</i> siRNA led to the downregulation of PCNA, Cyclin A, and Cyclin D, thus, the hypoxia-induced proliferation of mPASMCs was reversed. Furthermore, our study demonstrated that the hypoxia-induced expression of Eln and the proliferation of mPASMCs are associated with the proliferation-related phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway. In conclusion, these data suggest that Eln is a key regulatory factor in mPASMCs proliferation, potentially elucidating the mechanism underlying hypoxia-induced mPASMCs proliferation. This finding may offer valuable insights for the study of hypoxic pulmonary hypertension.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":" ","pages":"129-139"},"PeriodicalIF":2.6,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142716348","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 cannabinoid CB₂ receptor positive allosteric modulator EC21a exhibits complicated pharmacology <i>in vitro</i>.","authors":"Aidong Qi, Xueqing Han, Marc Quitalig, Jessica Wu, Plamen P Christov, KyuOk Jeon, Somnath Jana, Kwangho Kim, Darren W Engers, Craig W Lindsley, Alice L Rodriguez, Colleen M Niswender","doi":"10.1080/10799893.2024.2431986","DOIUrl":"10.1080/10799893.2024.2431986","url":null,"abstract":"<p><p>Schizophrenia is a complex disease involving the dysregulation of numerous brain circuits and patients exhibit positive symptoms (hallucinations, delusions), negative symptoms (anhedonia), and cognitive impairments. We have shown that the antipsychotic efficacy of positive allosteric modulators (PAMs) of both the M₄ muscarinic receptor and metabotropic glutamate receptor 1 (mGlu₁) involve the retrograde activation of the presynaptic cannabinoid type-2 (CB₂) receptor, indicating that CB₂ activation or potentiation could result in a novel therapeutic strategy for schizophrenia. We used two complementary assays, receptor-mediated phosphoinositide hydrolysis and GIRK channel activation, to characterize a CB₂ PAM scaffold, represented by the compound EC21a, to explore its potential as a starting point to optimize therapeutics for schizophrenia. These studies revealed that EC21a acts as an allosteric inverse agonist at CB₂ in both assays and exhibits a mixed allosteric agonist/negative allosteric modulator profile at CB₁ depending upon the assay used for profiling. A series of compounds related to EC21a also functioned as CB₂ inverse agonists. Overall, these results suggest that EC21a exhibits complicated and potentially assay-dependent pharmacology, which may impact interpretation of <i>in vivo</i> studies.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":" ","pages":"151-159"},"PeriodicalIF":2.6,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11636628/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142687251","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}

{"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}