Journal of cellular signaling最新文献

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A Computational Investigation on Rho-related GTP-binding Protein RhoB through Molecular Modeling and Molecular Dynamics Simulation Study rho相关gtp结合蛋白RhoB的分子建模和分子动力学模拟研究
Journal of cellular signaling Pub Date : 2023-04-24 DOI: 10.33696/signaling.4.089
Shamrat Kumar Paul, Chowdhury Lutfun Nahar Metu, Sunita Kumari Sutihar, Md. Saddam, Bristi Paul, Md. Lutful Kabir, Md. Mostofa Uddin Helal
{"title":"A Computational Investigation on Rho-related GTP-binding Protein RhoB through Molecular Modeling and Molecular Dynamics Simulation Study","authors":"Shamrat Kumar Paul, Chowdhury Lutfun Nahar Metu, Sunita Kumari Sutihar, Md. Saddam, Bristi Paul, Md. Lutful Kabir, Md. Mostofa Uddin Helal","doi":"10.33696/signaling.4.089","DOIUrl":"https://doi.org/10.33696/signaling.4.089","url":null,"abstract":"Background: An indispensable member of the Rho family, RhoB is an isoprenylated small GTPases that modulate the cellular cytoskeletal organization. While DNA gets damaged, it takes part in the neoplastic apoptotic mechanism. In this study, we evaluated the structure of Rho-related GTP-binding protein RhoB due to the unavailability of 3D structure in the protein data bank database. Results: The expected pI value of RhoB was 5.10 (acidic). The target–template alignment was computed using the GMQE value meanwhile 6hxu.1.A from Homo sapiens was selected as the template structure. The Swiss model was exploited to complete the model construction task. The structural compatibility and stability were revealed after a 100ns molecular dynamics simulation using GROMACA employing the OPLS-AA force field. Based on their fluctuating activity and their location between 100 and 110 and 140 and 150, PCA analysis discovered relevant residues. Conclusion: By providing an insight into the biophysical phenomenon of Rho-related GTP-binding protein RhoB inhibitors, this study will assist future investigations addressing the relationship between gene mutation and abnormalities produced by protein Rho-related GTP-binding protein RhoB in apoptotic events.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"95 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135278556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Purinergic P2X7 Receptor as a Potential Targeted Therapy for COVID-19-associated Lung Cancer Progression 嘌呤能P2X7受体作为covid -19相关肺癌进展的潜在靶向治疗
Journal of cellular signaling Pub Date : 2023-03-07 DOI: 10.33696/signaling.4.087
Hamidreza Zalpoor, A. Akbari, M. Nabi-Afjadi, Ali Norouzi, F. Seif, M. Pornour
{"title":"Purinergic P2X7 Receptor as a Potential Targeted Therapy for COVID-19-associated Lung Cancer Progression","authors":"Hamidreza Zalpoor, A. Akbari, M. Nabi-Afjadi, Ali Norouzi, F. Seif, M. Pornour","doi":"10.33696/signaling.4.087","DOIUrl":"https://doi.org/10.33696/signaling.4.087","url":null,"abstract":"Severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2) infection is a serious threat to lung cancer patients. Hereby, we hypothesize that Coronavirus disease 2019 (COVID-19) may contribute to lung cancer progression by increasing extracellular adenosine triphosphate (ATP) levels and hyperactivating the purinergic P2X purinoceptor 7 receptor (P2X7R). Hyperactivation of P2X7R by increased extracellular ATP may stimulate multiple signaling pathways and factors such as NLRP3 inflammasome; as a result, interleukin (IL)-1β, and IL-18 pro-inflammatory cytokines are released, JNK, Rho kinase, HMGB1-RAGE, PI3K/AKT, hypoxia-inducible factor-1 alpha (HIF-1α), and ERK. NLRP3 activation may play a pivotal role in fatal cytokine storm in critically ill patients with COVID-19 and tumor progression in patients with lung cancer. Consequently, inhibiting these signaling pathways may deviate immune responses toward anti-tumoral responses, and suppress lung cancer progression and cytokine storms. Therefore, targeting P2X7R by means of oxidized ATP and anti-P2X7 monoclonal antibodies may provide promising therapeutic approaches to prevent lung cancer progression in COVID-19 patients; however, no clinical trials have yet been conducted, and their clinical efficacy remains to be elucidated.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"69 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90714182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Targeting SCUBE3 in Hepatocellular Carcinoma 靶向SCUBE3治疗肝细胞癌
Journal of cellular signaling Pub Date : 2023-03-07 DOI: 10.33696/signaling.4.088
Teng Liu, Xia Yang, Ke Wang, Q. Luo
{"title":"Targeting SCUBE3 in Hepatocellular Carcinoma","authors":"Teng Liu, Xia Yang, Ke Wang, Q. Luo","doi":"10.33696/signaling.4.088","DOIUrl":"https://doi.org/10.33696/signaling.4.088","url":null,"abstract":"HCC is one of the most common malignant tumors. The life and health of humans are gravely threatened by HCC because of its hidden onset, high recurrence rate, poor therapeutic effect, and high mortality. It is essential to explore the particular pathological mechanisms of HCC in order to increase the rate of early diagnosis and enhance patient therapy outcomes. Recent research has demonstrated that SCUBE3 can influence HCC cell proliferation by regulating the TGFβ/PI3K/AKT/GSK3β pathway. The molecular regulatory network of HCC proliferation is improved by this research, which also offers a solid theoretical and experimental foundation for SCUBE3 as a potential new therapeutic target for HCC.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"33 14 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82549516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Radiation-induced Bystander Effect and Its Possible Countermeasures 辐射诱发的旁观者效应及其可能的对策
Journal of cellular signaling Pub Date : 2023-03-07 DOI: 10.33696/signaling.4.086
G. Ghosh
{"title":"Radiation-induced Bystander Effect and Its Possible Countermeasures","authors":"G. Ghosh","doi":"10.33696/signaling.4.086","DOIUrl":"https://doi.org/10.33696/signaling.4.086","url":null,"abstract":"Ionizing radiation has been indispensable to medical diagnosis. In cancer, radiation therapy or radiotherapy (RT) offers patients a better chance of survival. It destroys cancer by depositing high-energy radiation on the cancer tissues, though it may directly damage a few normal cells. Therefore, the total radiation dose is administered in fractionated modalities over weeks or months. However, experimental evidence indicates that the irradiated cancer cells subsequently release cytokines in the blood that enter into nearby unirradiated nuclei/cells through several signaling pathways and cause radiation-induced bystander effects (RIBEs) such as DNA damage, chromosomal instability, mutation, and apoptosis in them as side effects of RT. Recently, many combined therapeutic protocols consisting of a few natural and synthetic products have been proposed to minimize RIBEs. This article reviews the present understanding of RIBEs and their possible countermeasures. Besides, a new protocol of combined therapy of nanoparticle-based ion treatment (NIT) and RT to minimize RIBEs has been proposed.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"30 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82769332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Augmenting Venetoclax Activity Through Signal Transduction in AML. 在AML中通过信号转导增强Venetoclax活性。
Journal of cellular signaling Pub Date : 2023-01-01 DOI: 10.33696/signaling.4.085
Ian Michael Bouligny, Keri Renee Maher, Steven Grant
{"title":"Augmenting Venetoclax Activity Through Signal Transduction in AML.","authors":"Ian Michael Bouligny,&nbsp;Keri Renee Maher,&nbsp;Steven Grant","doi":"10.33696/signaling.4.085","DOIUrl":"https://doi.org/10.33696/signaling.4.085","url":null,"abstract":"<p><p>Venetoclax, a small-molecule B-cell lymphoma 2 (BCL-2) inhibitor, selectively eradicates leukemic stem cells (LSCs). While venetoclax has revolutionized the treatment of acute myeloid leukemia (AML), treatment failure and disease relapse are common. Mechanisms underlying venetoclax resistance are surprisingly heterogeneous. Venetoclax resistance encompasses a spectrum of genetic and epigenetic changes, with numerous pathways contributing to the upregulation of additional anti-apoptotic proteins. In this review, we address the mechanisms of venetoclax resistance in the context of signal transduction. We emphasize how aberrant cell signaling impairs apoptosis and predisposes to venetoclax failure. Commonly activated pathways, such as FLT3, PI3K/AKT/mTOR, and RAS, contribute to upregulated anti-apoptotic mediators and are frequently responsible for refractory disease or disease relapse. We highlight novel combination strategies aimed at disabling constitutively active signal transduction to augment response and overcome venetoclax resistance.</p>","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"4 1","pages":"1-12"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9997087/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9465260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
Optogenetics Sheds Light on Brown and Beige Adipocytes. 光遗传学揭示棕色和米色脂肪细胞。
Journal of cellular signaling Pub Date : 2023-01-01 DOI: 10.33696/signaling.4.105
Aaron Clifford Brown
{"title":"Optogenetics Sheds Light on Brown and Beige Adipocytes.","authors":"Aaron Clifford Brown","doi":"10.33696/signaling.4.105","DOIUrl":"10.33696/signaling.4.105","url":null,"abstract":"<p><p>Excessive food intake leads to lipid accumulation in white adipose tissue, triggering inflammation, cellular stress, insulin resistance, and metabolic syndrome. In contrast, the dynamic energy expenditure and heat generation of brown and beige adipose tissue, driven by specialized mitochondria, render it an appealing candidate for therapeutic strategies aimed at addressing metabolic disorders. This review examines the therapeutic potential of brown and beige adipocytes for obesity and metabolic disorders, focusing on recent studies that employ optogenetics for thermogenesis control in these cells. The findings delve into the mechanisms underlying UCP1-dependent and UCP1-independent thermogenesis and how optogenetic approaches can be used to precisely modulate energy expenditure and induce thermogenesis. The convergence of adipocyte biology and optogenetics presents an exciting frontier in combating metabolic disorders and advancing our understanding of cellular regulation and energy balance.</p>","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"4 4","pages":"178-186"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10635576/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72016272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Targeting the Complex Protein Network of MYCN-amplified Anaplastic Ependymoma: A Case Report 靶向mycn扩增间变性室管膜瘤复杂蛋白网络1例
Journal of cellular signaling Pub Date : 2022-12-22 DOI: 10.33696/signaling.3.082
MD Michael P. Castro
{"title":"Targeting the Complex Protein Network of MYCN-amplified Anaplastic Ependymoma: A Case Report","authors":"MD Michael P. Castro","doi":"10.33696/signaling.3.082","DOIUrl":"https://doi.org/10.33696/signaling.3.082","url":null,"abstract":"The MYCN oncoprotein has been notoriously undruggable and is infamous for causing aggressive cancer with poor outcomes in children and adults. Following surgery, radiation, and chemotherapy, patients who develop progressive disease have few treatment options. An analysis of the dysregulated protein network caused by MYCN amplification suggested co-targeting PLK1, AURKA, CKS1, AKT, MTOR, and USP7 would be useful to take advantage of synthetic lethal vulnerabilities while overcoming redundancies and resistance mechanisms that stabilize N-Myc by preventing its proteasome degradation. Naturopathic compounds, (genistein, tanshinone, resveratrol, betulinic acid) and fluoxetine were re-purposed to target the complex protein network in a patient with MYCN -amplified and PTEN -deficient multifocal, relapsed anaplastic ependymoma following standard therapy. The patient achieved a clinically meaningful and durable response for 6 months prior to developing disease progression characterized by chromosome 11q ( YAP1, BIRC2/3 ) amplification. The experience suggests molecularly-informed integration of naturopathic compounds can have utility for disease control and survival. The success, although anecdotal, suggests that the previous failure of single agent strategies could be overcome with a network targeting approach that simultaneously precipitates cell cycle arrest, rescues FBXW7 ubiquitination, and enhances oxidative stress. As such, MYCN may no longer be strictly unactionable but appears amenable to co-targeting key nodes in its self-sustaining disease network.","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"201 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74888730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
New Insights into the Proteolytic Regulation of the Structural Protein Junctophilin-2 by Calpain Calpain对结构蛋白Junctophilin-2蛋白水解调控的新认识
Journal of cellular signaling Pub Date : 2022-12-22 DOI: 10.33696/signaling.3.081
G. Weninger, S. Lehnart
{"title":"New Insights into the Proteolytic Regulation of the Structural Protein Junctophilin-2 by Calpain","authors":"G. Weninger, S. Lehnart","doi":"10.33696/signaling.3.081","DOIUrl":"https://doi.org/10.33696/signaling.3.081","url":null,"abstract":"Citation","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"15 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75352320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Can Mono- or Combination Therapy of Metformin with Cimetidine and Ibuprofen be a Promising Potential Therapy for Breast Cancer? 二甲双胍与西咪替丁和布洛芬单独或联合治疗乳腺癌是一种有希望的潜在治疗方法吗?
Journal of cellular signaling Pub Date : 2022-12-22 DOI: 10.33696/signaling.3.080
S. Mostafavi, Hamidreza Zalpoor, Zuhair Mohammad Hassan
{"title":"Can Mono- or Combination Therapy of Metformin with Cimetidine and Ibuprofen be a Promising Potential Therapy for Breast Cancer?","authors":"S. Mostafavi, Hamidreza Zalpoor, Zuhair Mohammad Hassan","doi":"10.33696/signaling.3.080","DOIUrl":"https://doi.org/10.33696/signaling.3.080","url":null,"abstract":"and Ibuprofen be a Promising Potential Therapy for","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"7 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78318520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
New Aspects in the Mechanism of Action of ALDH1A1 and 1A3 Isoforms in Carcinogenesis ALDH1A1和1A3亚型在癌变中作用机制的新进展
Journal of cellular signaling Pub Date : 2022-09-12 DOI: 10.33696/signaling.3.078
{"title":"New Aspects in the Mechanism of Action of ALDH1A1 and 1A3 Isoforms in Carcinogenesis","authors":"","doi":"10.33696/signaling.3.078","DOIUrl":"https://doi.org/10.33696/signaling.3.078","url":null,"abstract":"","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"53 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75955435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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