Protein and Peptide Letters最新文献

{"title":"The Role of TGFBR3 in the Development of Lung Cancer.","authors":"Xin Deng, Nuoya Ma, Junyu He, Fei Xu, Guoying Zou","doi":"10.2174/0109298665315841240731060636","DOIUrl":"10.2174/0109298665315841240731060636","url":null,"abstract":"<p><p>The Transforming Growth Factor-β (TGF-β) mediates embryonic development, maintains cellular homeostasis, regulates immune function, and is involved in a wide range of other biological processes. TGF-β superfamily signaling pathways play an important role in cancer development and can promote or inhibit tumorigenesis. Type III TGF-β receptor (TGFBR3) is a co-receptor in the TGF-β signaling pathway, which often occurs with reduced or complete loss of expression in many cancer patients and can act as a tumor suppressor gene. The reduction or deletion of TGFBR3 is more pronounced compared to other elements in the TGF-β signaling pathway. In recent years, lung cancer is one of the major malignant tumors that endanger human health, and its prognosis is poor. Recent studies have reported that TGFBR3 expression decreases to varying degrees in different types of lung cancer, both at the tissue level and at the cellular level. The invasion, metastasis, angiogenesis, and apoptosis of lung cancer cells are closely related to the expression of TGFBR3, which strengthens the inhibitory function of TGFBR3 in the evolution of lung cancer. This article reviews the mechanism of TGFBR3 in lung cancer and the influencing factors associated with TGFBR3. Clarifying the physiological function of TGFBR3 and its molecular mechanism in lung cancer is conducive to the diagnosis and treatment of lung cancer.</p>","PeriodicalId":20736,"journal":{"name":"Protein and Peptide Letters","volume":" ","pages":"491-503"},"PeriodicalIF":1.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141875779","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":"Characterization of Heat-labile Uracil-DNA Glycosylase from <i>Oncorhynchus mykiss</i> and its Application for Carry-over Contamination Control in RT-qPCR.","authors":"Qingyuan Huang, Yaqi Zhang, Wenhao Hu, Keqi Chen, Jian Zhang, Zhidan Luo, Chen Lu","doi":"10.2174/0109298665283737240122105923","DOIUrl":"10.2174/0109298665283737240122105923","url":null,"abstract":"<p><strong>Background: </strong>Heat-labile uracil-DNA glycosylase (HL-UDG) is commonly employed to eliminate carry-over contamination in DNA amplifications. However, the prevailing HL-UDG is markedly inactivated at 50°C, rendering it unsuitable for specific one-step RT-qPCR protocols utilizing reverse transcriptase at an optimal temperature of 42°C.</p><p><strong>Objective: </strong>This study aimed to explore novel HL-UDG with lower inactivation temperature and for recombinant expression.</p><p><strong>Methods: </strong>The gene encoding an HL-UDG was cloned from the cold-water fish rainbow trout <i>(Oncorhynchus mykiss)</i> and expressed in <i>Escherichia coli</i> with high yield. The thermostability of this enzyme and other enzymatic characteristics were thoroughly examined. The novel HL-UDG was then applied for controlling carry-over contamination in one-step RT-qPCR.</p><p><strong>Results: </strong>This recombinantly expressed truncated HL-UDG of rainbow trout (OmUDG) exhibited high amino acids similarity (84.1% identity) to recombinant Atlantic cod UDG (rcUDG) and was easily denatured at 40°C. The optimal pH of OmUDG was 8.0, and the optimal concentrations of both Na⁺ and K⁺ were 10 mM. Since its inactivation temperature was lower than that of rcUDG, the OmUDG could be used to eliminate carry-over contamination in one-step RT-qPCR with moderate reverse transcription temperature.</p><p><strong>Conclusion: </strong>We successfully identified and recombinantly expressed a novel HL-UDG with an inactivation temperature of 40°C. It is suitable for eliminating carry-over contamination in one-step RT-qPCR.</p>","PeriodicalId":20736,"journal":{"name":"Protein and Peptide Letters","volume":" ","pages":"169-177"},"PeriodicalIF":1.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139723769","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":"Enhancement of Oral Bioavailability of Protein and Peptide by Polysaccharide-based Nanoparticles.","authors":"Md Moidul Islam, Sarjana Raikwar","doi":"10.2174/0109298665292469240228064739","DOIUrl":"10.2174/0109298665292469240228064739","url":null,"abstract":"<p><p>Oral drug delivery is a prevalent and cost-effective method due to its advantages, such as increased drug absorption surface area and improved patient compliance. However, delivering proteins and peptides orally remains a challenge due to their vulnerability to degradation by digestive enzymes, stomach acids, and limited intestinal membrane permeability, resulting in poor bioavailability. The use of nanotechnology has emerged as a promising solution to enhance the bioavailability of these vital therapeutic agents. Polymeric NPs, made from natural or synthetic polymers, are commonly used. Natural polysaccharides, such as alginate, chitosan, dextran, starch, pectin, etc., have gained preference due to their biodegradability, biocompatibility, and versatility in encapsulating various drug types. Their hydrophobic-hydrophilic properties can be tailored to suit different drug molecules.</p>","PeriodicalId":20736,"journal":{"name":"Protein and Peptide Letters","volume":" ","pages":"209-228"},"PeriodicalIF":1.6,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140176131","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":"Participation of <i>CWINV</i> and <i>SUS</i> Genes in Sucrose Utilization in the Disruption of Cambium Derivatives Differentiation of Silver Birch.","authors":"Yulia Leonidovna Moshchenskaya, Natalia Alekseevna Galibina, Aleksandra Aleksandrovna Serkova, Tatyana Vladimirovna Tarelkina, Ksenia Michailovna Nikerova, Maksim Anatol'evich Korzhenevsky, Irina Nikolaevna Sofronova, Ludmila Igorevna Semenova","doi":"10.2174/0109298665309207240621094227","DOIUrl":"10.2174/0109298665309207240621094227","url":null,"abstract":"<p><strong>Background: </strong>The mechanisms that control the accumulation of woody biomass are of great interest to the study. Invertase and sucrose synthase are enzymes that are vital for distributing carbon in various biosynthetic pathways. Karelian birch (<i>Betula pendula</i> var. <i>carelica</i>) is a form of silver birch (<i>B. pendula</i> Roth) and is characterized by disruption of the differentiation of cambium derivatives towards both the xylem and phloem, which leads to a change in the proportion of the conducting tissues' structural elements and the figured wood formation. We researched the expression profiles of genes encoding sucrose-cleaving enzymes (<i>CWINV</i> and <i>SUS</i> gene families) and genes encoding CVIF protein, which is responsible for the post-translational regulation of the cell wall invertase activity.</p><p><strong>Objective: </strong>In our study, 16-year-old common silver birch (<i>Betula pendula</i> var. <i>pendula</i>) and Karelian birch were used for sampling non-figured and figured trunk section tissues, respectively. Samples were selected for the research based on the radial vector: non-conductive, conductive phloem, cambial zone - differentiating xylem - mature xylem.</p><p><strong>Methods: </strong>The enzyme's activity was investigated by biochemical methods. RT-PCR method was used to determine the level of gene expression. Anatomical and morphological methods were used to determine the stage of differentiation of xylem cambial derivatives.</p><p><strong>Results: </strong>Our research revealed a shift in the composition of xylem components in figured Karelian birch, characterized by increased parenchymatization and reduced vessel quantity. In all studied trunk tissues of Karelian birch, compared with common silver birch, an increase in the expression of the <i>CWINV</i> gene family and the <i>SUS3</i> gene and a decrease in the expression of SUS4 were shown.</p><p><strong>Conclusion: </strong>Therefore, the increase in parenchymatization in figured Karelian birch is linked to a shift in sucrose metabolism towards the apoplastic pathway, indicated by a higher cell wall invertase activity and gene expression. The expression of the <i>SUS4</i> gene correlates with the decrease in xylem increments and vessel proportion. The research findings will enhance our understanding of how sucrose breaking enzymes regulate secondary growth in woody plants and aid in developing practical timber cultivation methods.</p>","PeriodicalId":20736,"journal":{"name":"Protein and Peptide Letters","volume":" ","pages":"479-489"},"PeriodicalIF":1.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141498758","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":"A Functional Human Glycogen Debranching Enzyme Encoded by a Synthetic Gene: Its Implications for Glycogen Storage Disease Type III Management.","authors":"Doriana Triggiani, Olivia C Demurtas, Elena Illiano, Silvia Massa, Alessandra Pasquo, Carlo Dionisi-Vici, Carmela Marino, Giovanni Giuliano, Rosella Franconi","doi":"10.2174/0109298665307430240628063339","DOIUrl":"10.2174/0109298665307430240628063339","url":null,"abstract":"<p><strong>Background: </strong>Glycogen Storage Disease type III (GSD III) is a metabolic disorder resulting from a deficiency of the Glycogen Debranching Enzyme (GDE), a large monomeric protein (approximately 170 kDa) with cytoplasmic localization and two distinct enzymatic activities: 4-α-glucantransferase and amylo-α-1,6-glucosidase. Mutations in the Agl gene, with consequent deficiency in GDE, lead to the accumulation of abnormal/toxic glycogen with shorter chains (phosphorylase limit dextrin, PLD) in skeletal and/or heart muscle and/or in the liver. Currently, there is no targeted therapy, and available treatments are symptomatic, relying on specific diets.</p><p><strong>Methods: </strong>Enzyme Replacement Therapy (ERT) might represent a potential therapeutic strategy for GSD III. Moreover, the single-gene nature of GSD III, the subcellular localization of GDE, and the type of affected tissues represent ideal conditions for exploring gene therapy approaches. Toward this direction, we designed a synthetic, codon-optimized cDNA encoding the human GDE.</p><p><strong>Results: </strong>This gene yielded high amounts of soluble, enzymatically active protein in Escherichia coli. Moreover, when transfected in Human Embryonic Kidney cells (HEK-293), it successfully encoded a functional GDE.</p><p><strong>Conclusion: </strong>These results suggest that our gene or protein might complement the missing function in GSD III patients, opening the door to further exploration of therapeutic approaches for this disease.</p>","PeriodicalId":20736,"journal":{"name":"Protein and Peptide Letters","volume":" ","pages":"519-531"},"PeriodicalIF":1.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141634344","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":"MicroRNA-605-3p Inhibited the Growth and Chemoresistance of Osteosarcoma Cells via Negatively Modulating RAF1.","authors":"Mao Wang, Weina Li, Guohui Han, Xiangdong Bai, Jun Xie","doi":"10.2174/0109298665314658240712051206","DOIUrl":"10.2174/0109298665314658240712051206","url":null,"abstract":"<p><strong>Background: </strong>Osteosarcoma (OS) is the leading cancer-associated mortality in childhood and adolescence. Increasing evidence has demonstrated the key function of microRNAs (miRNAs) in OS development and chemoresistance. Among them, miRNA-605-3p acted as an important tumor suppressor and was frequently down-regulated in multiple cancers. However, the function of miR-650-3p in OS has not been reported.</p><p><strong>Objective: </strong>The aim of this work is to explore the novel role of miR-605-3p in osteosarcoma and its possible involvement in OS chemotherapy resistance.</p><p><strong>Methods: </strong>The expression levels of miR-605-3p in OS tissues and cells were assessed by reverse transcription quantitative PCR (RT-qPCR). The relevance of miR-605-3p with the prognosis of OS patients was determined by the Kaplan-Meier analysis. Additionally, the influence of miR-605-3p on OS cell growth was analyzed using the cell counting kit-8, colony formation assay, and flow cytometry. The mRNA and protein expression of RAF1 were detected by RT-qPCR and western blot. The binding of miR-605-3p with the 3'-UTR of RAF1 was confirmed by dual-luciferase reporter assay.</p><p><strong>Results: </strong>Our results showed that miR-605-3p was markedly decreased in OS tissues and cells. A lower level of miR-605-3p was strongly correlated with lymph node metastasis and poor 5-year overall survival rate of OS patients. <i>In vitro</i> assay found that miR-605-3p suppressed OS cell proliferation and promoted cell apoptosis. Mechanistically, the proto-oncogene RAF1 was seen as a target of miR-605-3p and strongly suppressed by miR-605-3p in OS cells. Restoration of RAF1 markedly eliminated the inhibitory effect of miR-605-3p on OS progression, suggesting RAF1 as a key mediator of miR-605-3p. Consistent with the decreased level of RAF1, miR-605-3p suppressed the activation of both MEK and ERK in OS cells, which are the targets of RAF1. Moreover, lower levels of miR-605-3p were found in chemoresistant OS patients, and downregulated miR-605-3p increased the resistance of OS cells to therapeutic agents.</p><p><strong>Conclusion: </strong>Our data revealed that miR-605-3p serves as a tumor suppressor gene by regulating RAF1 and increasing the chemosensitivity of OS cells, which provided the novel working mechanism of miR-605-3p in OS. Engineering stable nanovesicles that could efficiently deliver miR-605-3p with therapeutic activity into tumors could be a promising therapeutic approach for the treatment of OS.</p>","PeriodicalId":20736,"journal":{"name":"Protein and Peptide Letters","volume":" ","pages":"559-568"},"PeriodicalIF":1.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11497142/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141793186","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":"Interleukin 6 Antagonists in Severe COVID-19 Disease: Cardiovascular and Respiratory Outcomes.","authors":"Shahzad Khan","doi":"10.2174/0109298665266730240118054023","DOIUrl":"10.2174/0109298665266730240118054023","url":null,"abstract":"<p><strong>Background: </strong>Inhibitors of interleukin 6 [IL-6] have been utilized to treat severe COVID-19 disease. Their immunosuppressive or immunomodulating impact may be beneficial in COVID-19.</p><p><strong>Objectives: </strong>To discuss the role of IL-6 inhibitors and assess various trials conducted to evaluate the efficacy of IL-6 inhibitors in COVID-19 disease.</p><p><strong>Summary: </strong>Two of the most common causes of mortality in COVID-19-infected critically ill individuals are acute respiratory distress syndrome (ARDS) and multiorgan failure. Increased levels of inflammatory cytokines suggest that a cytokine storm, also known as cytokine release syndrome (CRS), is involved in the etiology of COVID-19. Most tissue damage, sepsis, and pulmonary and cardiovascular problems are caused mainly by the host defense system. Therefore, regulating this inflammatory cascade using immunomodulators is a prudent strategy. Although corticosteroids, as immunomodulators, are routinely used in COVID-19 management, interleukin (IL) inhibitors, especially IL-6 inhibitors, are also tested in many trials. Many studies have demonstrated that IL-6 inhibitors improve disease outcomes and decrease mortality, whereas others have shown that they are ineffective. In this paper, we briefly examined the role of IL-6 in COVID-19 pathogenesis and trials that support or refute the use of IL-6 inhibitors in treating COVID-19 disease.</p><p><strong>Results: </strong>Though mixed results are coming from trials regarding the adjuvant use of IL-6 inhibitors and standard anti-viral therapy with dexamethasone, a consensus favors using IL-6 inhibitors in severely ill COVID-19 patients regardless of the outcome.</p>","PeriodicalId":20736,"journal":{"name":"Protein and Peptide Letters","volume":" ","pages":"178-191"},"PeriodicalIF":1.6,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139906301","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":"Neuropeptide Network of Polycystic Ovary Syndrome - A Review.","authors":"Dheepthi Jayamurali, Nivetha Ravishankar, Nivedita Manoharan, Rajeshwari Parasuraman, Sri Kameshwaran Jayashankar, Sathya Narayanan Govindarajulu","doi":"10.2174/0109298665309949240822105900","DOIUrl":"10.2174/0109298665309949240822105900","url":null,"abstract":"<p><strong>Background: </strong>Polycystic Ovary Syndrome (PCOS), the ubiquitous reproductive disorder, has been documented as highly prevalent (6-9%) in India. 10% of women globally are predicted to have the disease. The highly mutable endocrinopathy, with differential clinical criteria for each diagnosis of PCOS, can mask the severity of the syndrome by influencing the incidence and occurrence of PCOS.</p><p><strong>Area covered: </strong>When there is a solid theoretical hypothesis between the neuroendocrine origin and ovarian origin of PCOS, recent evidence supports the neuroendocrine derivation of the pathology. It is considered of neuroendocrine basis - as it controls the ovarian axis and acts as a delicate target because it possesses receptors for various gonadal hormones, neurotransmitters & neuropeptides. Can these neuroendocrine alterations, variations in central brain circuits, and neuropeptide dysregulation be the tie that would link the pathophysiology of the disorder, the occurrence of all the 1˚ and 2˚ symptoms like polycystic ovaries, hyperandrogenism, obesity, insulin resistance, etc., in PCOS?</p><p><strong>Conclusion: </strong>This review anticipates providing a comprehensive overview of how neuropeptides such as Kisspeptin, Neurokinin B, Dynorphin A, β-Endorphin, Nesfatin, Neuropeptide Y, Phoenixin, Leptin, Ghrelin, Orexin, and Neudesin influence PCOS, the understanding of which may help to establish potential drug candidates against precise targets in these central circuits.</p>","PeriodicalId":20736,"journal":{"name":"Protein and Peptide Letters","volume":" ","pages":"667-680"},"PeriodicalIF":1.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142308471","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":"Tribute to Prof. Ben M. Dunn: A Remarkable Biochemist and Editor-in-Chief of Protein & Peptide Letters and Current Protein & Peptide Science.","authors":"","doi":"10.2174/092986653101240120233748","DOIUrl":"10.2174/092986653101240120233748","url":null,"abstract":"","PeriodicalId":20736,"journal":{"name":"Protein and Peptide Letters","volume":"31 1","pages":"1"},"PeriodicalIF":1.6,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140040195","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":"Corrigendum to: Neuropeptide Network of Polycystic Ovary Syndrome - A Review.","authors":"Dheepthi Jayamurali, Nivetha Ravishankar, Nivedita Manoharan, Rajeshwari Parasuraman, Sri Kameshwaran Jayashankar, Sathya Narayanan Govindarajulu","doi":"10.2174/092986653111241230222032","DOIUrl":"https://doi.org/10.2174/092986653111241230222032","url":null,"abstract":"<p><p>An error was found in the affiliations of the author in the article titled 'Neuropeptide Network of Polycystic Ovary Syndrome - A Review'', published in Protein and Peptide Letters, 2024, 31(9), 667-680 [1]. Details of the error and a correction are provided here. Original: *Address correspondence Department of Physiology, Dr. ALM PG Institute of Basic Medical Sciences, University of Madras, Taramani, Chennai 600 113, India; E-mail: drgsathyanarayanan@gmail.com Corrected: *Address correspondence to this author at the Department of Physiology, Dr. ALM PG Institute of Basic Medical Sciences, University of Madras, Taramani, Chennai 600 113, India; E-mail: drgsathyanarayanan@gmail.com We regret the error and apologize to readers. The original article can be found online at: http://dx.doi.org/10.2174/0109298665309949240822105900 PMID: 39313871.</p>","PeriodicalId":20736,"journal":{"name":"Protein and Peptide Letters","volume":"31 11","pages":"907"},"PeriodicalIF":1.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142932483","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}