Current protein & peptide science最新文献

{"title":"Antimicrobial Peptides: Structure, Mechanisms, and Therapeutic Potential in Combating Infectious Diseases.","authors":"Shivendra Verma, Ranu Singh, Manoj Kumawat","doi":"10.2174/0113892037412027251205075307","DOIUrl":"https://doi.org/10.2174/0113892037412027251205075307","url":null,"abstract":"<p><p>Antimicrobial peptides (AMPs) are small, naturally occurring molecules that play a key role in the immune defense of multicellular organisms. They show strong and broad activity against many harmful agents, including bacteria, viruses, fungi, and even cancer cells. Because of their unique ability to target pathogens in multiple ways, AMPs are being studied as promising alternatives to traditional antibiotics-especially important given the growing problem of antibiotic resistance. AMPs can be grouped based on their structure, such as α-helical, β-sheet, loop, or extended forms, and by their source or biological activity. Their main ways of fighting microbes include damaging microbial membranes, disrupting essential processes inside cells, and helping regulate the host's immune system. These mechanisms make it difficult for pathogens to develop resistance, increasing their value in modern medicine. Therapeutically, AMPs are under investigation for a range of applications, including treatment of skin infections, respiratory diseases, sepsis, and some viral and cancer-related conditions. Several AMP-based drugs are in clinical trials, and a few have already reached the market. However, challenges remain, such as poor stability in the body, vulnerability to breakdown by enzymes, potential toxicity, and high production costs. Current research is focusing on improving their effectiveness through chemical modifications, smart design, and advanced delivery systems like nanoparticles. AMPs hold great potential in the search for nextgeneration anti-infective therapies.</p>","PeriodicalId":10859,"journal":{"name":"Current protein & peptide science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147493701","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":"TEAD4 Identified as a Potential Biomarker for Gastric Cancer Via Genes Associated with Liquid-Liquid Phase Separation.","authors":"Jianzhong Liu, Jingwen Zhang, Aixia Gong","doi":"10.2174/0113892037408980251201111913","DOIUrl":"https://doi.org/10.2174/0113892037408980251201111913","url":null,"abstract":"<p><strong>Introduction: </strong>Liquid-liquid phase separation (LLPS) has emerged as a critical mechanism in tumor progression, and its relevance to gastric cancer (GC) is increasingly recognized. However, the mechanisms linking LLPS to GC remain unclear. Preliminary studies suggest that the TEA domain transcription factor 4 (TEAD4) may contribute to tumorigenesis, yet its specific role in GC has not been fully elucidated. This study aims to investigate the potential influence of TEAD4 on GC and to uncover the underlying mechanisms.</p><p><strong>Methods: </strong>TEAD4 was identified as a key gene in GC by intersecting LLPS-related genes with differentially expressed genes from the TCGA-STAD dataset. TEAD4 mRNA and protein expression in GC were analyzed using TCGA, GEO, and HPA databases. Associations with clinical features, diagnostic and prognostic value, immune checkpoints, methylation, microsatellite instability (MSI), tumor mutation burden (TMB), and drug sensitivity were explored. TEAD4 expression was validated in vitro in GC cell lines via RT-qPCR and Western blot. Functional assays were performed by silencing TEAD4 in MKN45 cells to assess its effects on GC cell proliferation, migration, and invasion.</p><p><strong>Results: </strong>TEAD4, identified through LLPS-related genes, was found to be abnormally overexpressed in GC at both mRNA and protein levels (P < 0.05). High TEAD4 expression showed strong diagnostic accuracy (AUC > 0.9), correlated with tumor stage and location, and was associated with poorer overall survival (P = 5.02e-05). In GC, low TEAD4 expression was linked to increased immune cell infiltration, higher immune phenotype scores, and elevated expression of immune checkpoints. TEAD4 expression also correlated with methylation status, TMB, MSI, mutational allelic tumor heterogeneity (MATH), and chemosensitivity. In vitro, TEAD4 knockdown reduced proliferation, migration, and invasion of GC cells.</p><p><strong>Discussion: </strong>TEAD4 is associated with epigenetic modifications, immune regulation, tumor heterogeneity, and therapeutic response in GC, highlighting its potential mechanistic role in disease progression.</p><p><strong>Conclusion: </strong>TEAD4 contributes to GC progression and may serve as a biomarker for diagnosis, prognosis, and immune infiltration, providing insights for potential therapeutic strategies.</p>","PeriodicalId":10859,"journal":{"name":"Current protein & peptide science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147321266","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":"Protocatechuic Acid Alleviates Neurodemyelination by Modulating PKCα-p38/MAPK Pathways in an LPC-Induced Model of Neurodegeneration.","authors":"Sonia Siddiqui, Priya Tufail, Faisal Khan, Muhammad Farooq Khalid, Farhia Khalid","doi":"10.2174/0113892037385148251207081917","DOIUrl":"https://doi.org/10.2174/0113892037385148251207081917","url":null,"abstract":"<p><strong>Introduction: </strong>Neuroinflammation, axonal damage, and alterations in extracellular matrix (ECM) protein expression are hallmarks of neurodegenerative diseases. Therapies that enhance recovery from brain injury are of significant clinical value. Therefore, this study investigated the antiinflammatory properties of protocatechuic acid (PCA).</p><p><strong>Methods: </strong>Neuroglial cocultures were prepared from P0-P1 rats. Demyelination was induced using LPC (0.003%). The effects of PCA (10 and 25 μg) on neurite outgrowth were assessed using morphometry software. Expression of COX-2, NF-κβ, PKC-α, and p38/MAPK was examined through immunostaining, SDS-PAGE, and Western blotting. Expression intensities were quantified using ImageJ software. Sustained repetitive neuronal firing was evaluated using the patch-clamp technique.</p><p><strong>Results: </strong>PCA increased neurite outgrowth in LPC-treated cultures after 72 hours in vitro. LPCinduced upregulation of ECM proteins TN-C, LN, and CSPGs was significantly reduced by PCA treatment compared with LPC controls. Similarly, PCA decreased the expression intensities of the pro-inflammatory markers NF-κβ and COX-2 relative to LPC controls. Furthermore, PCA reversed the sustained neuronal firing pattern observed in untreated LPC-exposed neurons.</p><p><strong>Discussion: </strong>Purified bioactive compounds commonly present in everyday foods show therapeutic potential for Parkinson's and Alzheimer's diseases due to their lower toxicity compared with conventional drugs. Artificial intelligence tools, such as AlphaFold and RoseTTAFold, further support drug development by predicting PCA binding modes with PKCα and P38/MAPK, thereby contributing to the design of personalized therapeutics and advancing neuroscience research.</p><p><strong>Conclusion: </strong>PCA alleviated neuroinflammation by reducing phosphorylation of PKCα and p38/MAPK.</p>","PeriodicalId":10859,"journal":{"name":"Current protein & peptide science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146149531","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":"Multi-omics Analysis Reveals the Role of lncRNAs and Peptides in the Age-related Hearing Loss.","authors":"Cong Li, Danyang Liu, Kunyan He, Song Shi, Xinwei Chen","doi":"10.2174/0113892037423330251019171447","DOIUrl":"https://doi.org/10.2174/0113892037423330251019171447","url":null,"abstract":"<p><strong>Introduction: </strong>The pathogenesis of age-related hearing loss (ARHL), especially the role of long non-coding RNAs (lncRNAs) and their encoded peptides, remains incompletely understood. This study aimed to characterize expression changes in lncRNAs and peptides in the cochleae of ARHL mice and explore the potential functions of lncRNA-encoded peptides via multi- -omics analysis.</p><p><strong>Methods: </strong>C57BL/6J mice were used to establish the ARHL model. The molecular expression profiles of cochlear tissues from normal and ARHL mice were synthesized by lncRNA sequencing, peptidomics, and bioinformatics.</p><p><strong>Results: </strong>Compared with the control group, a total of 789 differentially expressed lncRNAs and 466 differentially expressed peptides were identified in the ARHL group. Functional enrichment analysis revealed their association with key pathways, including ion transport, calcium signaling, the TCA cycle, and cytoskeleton regulation, indicating broad molecular dysregulation in the aging cochlea. Notably, 64 differentially expressed lncRNAs showed high translational potential, yielding 107 novel lncRNA-encoded peptides. These were mainly short peptides, some with stabilizing hydrophobic properties suited for membrane interactions, and enriched in domains like Pkinase and C2, suggesting involvement in signal transduction.</p><p><strong>Discussion: </strong>These results emphasized that lncRNA-encoded peptides were novel regulators of ARHL, potentially regulating calcium homeostasis and mitochondrial function. The overlap of pathways such as the cytoskeleton and fatty acid metabolism indicated that the lncRNA-peptide axis drove auditory decline, providing institutional insights into the epigenetic basis of ARHL.</p><p><strong>Conclusion: </strong>Our findings suggest that lncRNA-encoded peptides are a novel class of regulatory molecules involved in the complex pathogenesis of ARHL, highlighting them as promising targets for future therapeutic strategies.</p>","PeriodicalId":10859,"journal":{"name":"Current protein & peptide science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146050804","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 Role of Mitochondrial Ion Channels in the Evolution of Anticancer Drug Resistance.","authors":"Swaroop Kumar Pandey, Ayush Kulshreshtha, Anuja Mishra","doi":"10.2174/0113892037410334251021155546","DOIUrl":"https://doi.org/10.2174/0113892037410334251021155546","url":null,"abstract":"<p><p>Apoptosis, drug resistance, and cellular metabolism are all crucially regulated by mitochondria, especially through ion channels and translocases embedded in their membranes. The outer mitochondrial membrane (OMM) contains the voltage dependent anion channel (VDAC), which acts with proteins such as hexokinase II and BAX to regulate apoptosis and metabolic reprogramming in cancer while facilitating the flow of important metabolites and ions. Anti apoptotic proteins like Bcl2 and Mcl1 closely regulate the mitochondrial apoptosis induced channel (MAC), which is created by pro-apoptotic Bcl2 family members BAX and BAK and controls cytochrome c release when overexpressed, leading to drug resistance. Furthermore, the translocase of the outer membrane (TOM) complex, which regulates mitochondrial protein import, is frequently dysregulated in cancers. Numerous ion channels, such as potassium channels, the mitochondrial calcium uniporter (MCU), and the mitochondrial permeability transition pore (m-PTP), are found within the inner mitochondrial membrane (IMM) and regulate important functions like ATP synthesis, the control of reactive oxygen species (ROS), and apoptotic signaling. Cancer cells can avoid apoptosis, adapt to environmental stress, and become resistant to treatments like doxorubicin and cisplatin when these channels are dysregulated. Metabolic flexibility and antioxidant defense are improved by overexpressing or functionally modifying IMM potassium channels and calcium transporters. Additionally, drug resistance is facilitated by increased mitophagy and anti-apoptotic proteins that inhibit m-PTP opening. This review discusses the functions of mitochondrial ion channels.</p>","PeriodicalId":10859,"journal":{"name":"Current protein & peptide science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146050814","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":"Research Progress on the Intervention of Traditional Chinese Medicine Monomers on Signaling Pathways Related to Sarcopenia and Osteoporosis.","authors":"Zhuo-Xu Gu, Xian-Quan Zhang, Guang-Hui Zhou, Chu-Jia Huang, Gui-Hong Liang, Ling-Feng Zeng, Xiao Xiao","doi":"10.2174/0113892037388848251013135335","DOIUrl":"https://doi.org/10.2174/0113892037388848251013135335","url":null,"abstract":"<p><p>Sarcopenia and osteoporosis are conditions characterized by the synergistic effects of sarcopenia and osteoporosis, leading to the loss of muscle mass, muscle strength, bone density, and bone quality. This condition is marked by a high disability rate, limited diagnostic and therapeutic options, and significant clinical harm. The pathogenesis of sarcopenia and osteoporosis involves diminished differentiation of osteoblasts and myoblasts, as well as enhanced proliferation of osteoclasts. Signaling pathways such as Wnt/β-catenin, mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt), and nuclear factor-κB (NF-κB) play crucial roles in promoting the differentiation of osteoblasts and myoblasts while inhibiting osteoclast differentiation, thereby contributing to the treatment of sarcopenia and osteoporosis. Traditional Chinese medicine (TCM) has demonstrated significant efficacy in addressing \"muscle atrophy\" and \"bone depletion.\" Both single herbs and compound formulas can achieve therapeutic effects on sarcopenia and osteoporosis by modulating the expression of these signaling pathways. By summarizing the current research on these signaling pathways and TCM interventions, we aim to provide new insights for the clinical prevention and treatment of sarcopenia and osteoporosis using TCM and offer a foundation for further in-depth studies.</p>","PeriodicalId":10859,"journal":{"name":"Current protein & peptide science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146050809","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":"Plant Protein Essentials: From Source to Production.","authors":"Bhawna Sharma, Iti Chauhan, Rohit Pandey, Gaurav Pratap Singh, Alok Pratap Singh","doi":"10.2174/0113892037416124251202091550","DOIUrl":"https://doi.org/10.2174/0113892037416124251202091550","url":null,"abstract":"<p><p>Plant-based proteins are receiving increasing attention as sustainable and healthconscious alternatives to animal-derived proteins, addressing both environmental concerns and growing consumer demand. This review explores key plant protein sources-including cereals, legumes, pseudocereals, nuts, and seeds-which often provide protein content comparable to or greater than that of milk and meat. The review highlights various production techniques such as extrusion processing for meat-like textures and traditional fermentation methods. Plant molecular farming, using microalgae, plant cells, and whole plants, has emerged as a promising strategy for recombinant protein production. Extraction methods-mechanical, solvent-based, and enzyme-assisted-are also discussed, along with recent innovations like ultrasound- and microwave-assisted extraction. By examining the nutritional quality, processing methods, and potential applications of plant proteins, this review underscores their significance in achieving global food security and promoting sustainable dietary practices.</p>","PeriodicalId":10859,"journal":{"name":"Current protein & peptide science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146046039","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":"Intricacies of PKB/Akt Activity after Sciatic Nerve Damage: A Comprehensive Review.","authors":"Rajesh Dabur","doi":"10.2174/0113892037393362251027073929","DOIUrl":"https://doi.org/10.2174/0113892037393362251027073929","url":null,"abstract":"<p><p>Sciatic nerve injury represents a prevalent and incapacitating condition characterized by denervation, muscular atrophy, and compromised functionality. The Protein Kinase B (PKB)/ Akt signaling cascade serves as a vital modulator of skeletal muscle hypertrophy, metabolic processes, and regenerative capabilities. Subsequent to sciatic nerve injury, the PI3K/Akt signaling pathway exhibits dysregulation, exacerbating muscle atrophy and hindering recovery processes due to feedback inhibition of PKB/Akt phosphorylation by mTORC1, which consequently increases the expression of E3 ubiquitin ligases and causes muscle atrophy. Additionally, a multitude of other variables, encompassing neurotrophic factors, intracellular calcium ion concentrations, carboxyl-terminal modulator proteins, connexins, and tumor necrosis factor-α, either exert regulatory influences on Akt or are subject to regulation by Akt in a multifaceted manner. Hence, this review discusses the complex role of the PI3K/Akt signaling pathway in skeletal muscle dynamics following sciatic nerve injury, emphasizing its regulatory mechanisms and downstream effectors, and highlights strategies to target this pathway to enhance muscle regeneration and restore functional capabilities.</p>","PeriodicalId":10859,"journal":{"name":"Current protein & peptide science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146046010","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Signaling and Biased Agonism of the CHEMR23 Receptor: Implications for Inflammation Resolution and Bone Remodeling.","authors":"Olga A Neprelyuk, Inessa G Romanenko, Oksana L Irza, Maxim A Kriventsov, Sergei Ya Neprelyuk","doi":"10.2174/0113892037430991251201141701","DOIUrl":"https://doi.org/10.2174/0113892037430991251201141701","url":null,"abstract":"<p><p>The chemerin chemokine-like receptor 1 (CHEMR23), a member of the G proteincoupled receptor (GPCR) family, has emerged as a key regulator of immune homeostasis and skeletal remodeling. Notably, CHEMR23 exhibits ligand-specific biased agonism, enabling divergent intracellular signaling pathways depending on the ligand involved. Pro-inflammatory ligands such as chemerin predominantly activate Gi/o protein-dependent cascades, promoting cytokine release, osteoclastogenesis, and tissue degradation. In contrast, the binding of specialized proresolving mediators (SPMs), such as resolvins, preferentially triggers β-arrestin-mediated signaling. This pathway suppresses NF-κB activation, promotes macrophage polarization toward a proresolving phenotype, and facilitates the resolution of inflammation. This signaling bifurcation is particularly relevant in chronic inflammatory diseases characterized by progressive bone loss, including periodontitis. Expression of CHEMR23 is dynamically modulated by inflammatory stimuli, metabolic stress, and genetic polymorphisms, underscoring its potential as a target for resolution- directed therapies. Emerging therapeutic strategies, ranging from lipid-derived SPMs to monoclonal antibodies, are under investigation for their ability to modulate CHEMR23 activity in a ligand- and context-specific manner. This review provides an integrated overview of molecular, cellular, and translational data on CHEMR23, emphasizing its dual functional roles and therapeutic potential in inflammation-associated pathologies.</p>","PeriodicalId":10859,"journal":{"name":"Current protein & peptide science","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145898756","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":"MmpS5-MmpL5 Transporters Deliver <i>M. tuberculosis</i> Resistance to Bedaquiline (BDQ) and Delamanid (DLM).","authors":"Khaoula Balgouthi, Emel Eker, Manaf AlMatar","doi":"10.2174/0113892037383330250807101618","DOIUrl":"10.2174/0113892037383330250807101618","url":null,"abstract":"<p><strong>Introduction: </strong>One of the earliest illnesses that has been identified is tuberculosis (TB). The largest challenge in managing tuberculosis today is the growing number of individuals infected with TB bacilli, particularly those that are Extensively drug resistant-tuberculosis (XDR-TB) and Multidrug-resistant tuberculosis (MDR-TB). However, by figuring out the resistance's molecular mechanism, Advanced molecular methods may be used to rapidly determine therapy plans. Combining Delamanid (DLM) with Bedaquiline (BDQ), one of the recently authorized medications, indicates that the therapy is effective.</p><p><strong>Methods: </strong>We aim to investigate efflux-mediated resistance mechanisms in M. Tuberculosis by using quantitative real-time PCR to assess the expression level of <i>mmpS5</i> and <i>mmpL5</i>.</p><p><strong>Results: </strong>The median (M) and interquartile range (Iqr) of <i>mmpL5</i> and <i>mmpS5</i> expression varied from 5.65 to 9.01 and 7.95 to 10.74, respectively, when resistant strains were compared with sensitive ones. M and Iqr of <i>mmpL5</i> and <i>mmpS5</i> expression, however, ranged from 0.08-3.04 and 0.05- 1.61 for sensitive strains, correspondingly.</p><p><strong>Discussion: </strong>Our findings have implications for the development of fast genotypic drug susceptibility testing (DST). Quantitative real-time PCR to measure the expression level of mmpS5 and mmpL5 of baseline and post-baseline isolates is important to track the development of BDQ and DLM resistance.</p><p><strong>Conclusion: </strong>Thus, when developing anti-tuberculosis drugs, mycobacterial MmpS5-MmpL5 transporters should be taken into consideration early on, as they are an MDR-efflux system.</p>","PeriodicalId":10859,"journal":{"name":"Current protein & peptide science","volume":" ","pages":"182-188"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145063375","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}