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p38 mitogen-activated protein kinase contributes to TNFα-induced endothelial tube formation of bone-marrow-derived mesenchymal stem cells by activating the JAK/STAT/TIE2 signaling axis. p38丝裂原活化蛋白激酶通过激活JAK/STAT/TIES2信号轴,参与TNFα诱导的骨髓间充质干细胞内皮管的形成。
IF 2.9 3区 生物学
BMB Reports Pub Date : 2024-05-01
Sukjin Ou, Tae Yoon Kim, Euitaek Jung, Soon Young Shin
{"title":"p38 mitogen-activated protein kinase contributes to TNFα-induced endothelial tube formation of bone-marrow-derived mesenchymal stem cells by activating the JAK/STAT/TIE2 signaling axis.","authors":"Sukjin Ou, Tae Yoon Kim, Euitaek Jung, Soon Young Shin","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Bone marrow-derived mesenchymal stem cells (BM-MSCs) can differentiate into endothelial cells in an inflammatory microenvironment. However, the regulatory mechanisms underlying this process are not entirely understood. Here, we found that TIE2 in BM-MSCs was upregulated at the transcriptional level after stimulation with tumor necrosis factor-alpha (TNFα), a major pro-inflammatory cytokine. Additionally, the STAT-binding sequence within the proximal region of TIE2 was necessary for TNFα-induced TIE2 promoter activation. TIE2 and STAT3 knockdown reduced TNFα-induced endothelial tube formation in BMMSCs. Among the major TNFα-activated MAP kinases (ERK1/2, JNK1/2, and p38 MAPK) in BM-MSCs, only inhibition of the p38 kinase abrogated TNFα-induced TIE2 upregulation by inhibiting the JAK-STAT signaling pathway. These findings suggest that p38 MAP contributes to the endothelial differentiation of BM-MSCs by activating the JAK-STAT-TIE2 signaling axis in the inflammatory microenvironment. [BMB Reports 2024; 57(5): 238-243].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"238-243"},"PeriodicalIF":2.9,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11139678/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71420405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The contribution of the nervous system in the cancer progression. 神经系统在癌症进展中的作用。
IF 2.9 3区 生物学
BMB Reports Pub Date : 2024-04-01
Hongryeol Park, Chan Hee Lee
{"title":"The contribution of the nervous system in the cancer progression.","authors":"Hongryeol Park, Chan Hee Lee","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Cancer progression is driven by genetic mutations, environmental factors, and intricate interactions within the tumor microenvironment (TME). The TME comprises of diverse cell types, such as cancer cells, immune cells, stromal cells, and neuronal cells. These cells mutually influence each other through various factors, including cytokines, vascular perfusion, and matrix stiffness. In the initial or developmental stage of cancer, neurotrophic factors such as nerve growth factor, brain-derived neurotrophic factor, and glial cell line-derived neurotrophic factor are associated with poor prognosis of various cancers by communicating with cancer cells, immune cells, and peripheral nerves within the TME. Over the past decade, research has been conducted to prevent cancer growth by controlling the activation of neurotrophic factors within tumors, exhibiting a novel attemt in cancer treatment with promising results. More recently, research focusing on controlling cancer growth through regulation of the autonomic nervous system, including the sympathetic and parasympathetic nervous systems, has gained significant attention. Sympathetic signaling predominantly promotes tumor progression, while the role of parasympathetic signaling varies among different cancer types. Neurotransmitters released from these signalings can directly or indirectly affect tumor cells or immune cells within the TME. Additionally, sensory nerve significantly promotes cancer progression. In the advanced stage of cancer, cancer-associated cachexia occurs, characterized by tissue wasting and reduced quality of life. This process involves the pathways via brainstem growth and differentiation factor 15-glial cell line-derived neurotrophic factor receptor alpha-like signaling and hypothalamic proopiomelanocortin neurons. Our review highlights the critical role of neurotrophic factors as well as central nervous system on the progression of cancer, offering promising avenues for targeted therapeutic strategies. [BMB Reports 2024; 57(4): 167-175].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"167-175"},"PeriodicalIF":2.9,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11058356/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140206330","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Triamcinolone acetonide alleviates benign biliary stricture by ameliorating biliary fibrosis and inflammation. 曲安奈德通过改善胆道纤维化和炎症,缓解良性胆道狭窄。
IF 2.9 3区 生物学
BMB Reports Pub Date : 2024-04-01
Seyeon Joo, See Young Lee, Su Yeon Lee, Yeseong Hwang, Minki Kim, Jae Woong Jeong, Sung Ill Jang, Sungsoon Fang
{"title":"Triamcinolone acetonide alleviates benign biliary stricture by ameliorating biliary fibrosis and inflammation.","authors":"Seyeon Joo, See Young Lee, Su Yeon Lee, Yeseong Hwang, Minki Kim, Jae Woong Jeong, Sung Ill Jang, Sungsoon Fang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We conducted a comprehensive series of molecular biological studies aimed at unraveling the intricate mechanisms underlying the anti-fibrotic effects of triamcinolone acetonide (TA) when used in conjunction with fully covered self-expandable metal stents (FCSEMS) for the management of benign biliary strictures (BBS). To decipher the molecular mechanisms responsible for the anti-fibrotic effects of corticosteroids on gallbladder mucosa, we conducted a comprehensive analysis. This analysis included various methodologies such as immunohistochemistry, ELISA, real-time PCR, and transcriptome analysis, enabling us to examine alterations in factors related to fibrosis and inflammation at both the protein and RNA levels. Overall, our findings revealed a dose-dependent decrease in fibrosisrelated signaling with higher TA concentrations. The 15 mg of steroid treatment (1X) exhibited anti-fibrosis and anti-inflammatory effects after 4 weeks, whereas the 30 mg of steroid treatment (2X) rapidly reduced fibrosis and inflammation within 2 weeks in BBS. Transcriptomic analysis results consistently demonstrated significant downregulation of fibrosis- and inflammation-related pathways and genes in steroid-treated fibroblasts. Use of corticosteroids, specifically TA, together with FCSEMS was effective for the treatment of BBS, ameliorating fibrosis and inflammation. Our molecular biological analysis supports the potential development of steroid-eluted FCSEMS as a therapeutic option for BBS in humans resulting from various surgical procedures. [BMB Reports 2024; 57(4): 200-205].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"200-205"},"PeriodicalIF":2.9,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11058357/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140206331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Mitofusin-2 enhances cervical cancer progression through Wnt/β-catenin signaling. Mitofusin-2 通过 Wnt/β-catenin 信号增强宫颈癌的进展。
IF 2.9 3区 生物学
BMB Reports Pub Date : 2024-04-01
Sung Yong Ahn
{"title":"Mitofusin-2 enhances cervical cancer progression through Wnt/β-catenin signaling.","authors":"Sung Yong Ahn","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Overexpression of mitofusin-2 (MFN2), a mitochondrial fusion protein, is frequently associated with poor prognosis in cervical cancer patients. Here, I aimed to investigate the involvement of MFN2 in cervical cancer progression and determine the effect of MFN2 on prognosis in cervical cancer patients. After generating MFN2-knockdown SiHa cells derived from squamous cell carcinoma, I investigated the effect of MFN2 on SiHa cell proliferation using the Cell Counting Kit-8 assay and determined the mRNA levels of proliferation markers. Colony-forming ability and tumorigenesis were evaluated using a colonyformation assay and tumor xenograft mouse models. The migratory and invasive abilities associated with MFN2 were measured using wound-healing and invasion assays. Wnt/β-cateninmediated epithelial-mesenchymal transition (EMT) markers related to MFN2 were assessed through quantitative RT-PCR. MFN2-knockdown SiHa cells exhibited reduced proliferation, colony formation, migration, invasion, and tumor formation in vivo. The motility of SiHa cells with MFN2 knockdown was reduced through Wnt/β-catenin-mediated EMT inhibition. MFN2 promoted cancer progression and tumorigenesis in SiHa cells. Overall, MFN2 could serve as a therapeutic target and a novel biomarker for cervical cancer. [BMB Reports 2024; 57(4): 194-199].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"194-199"},"PeriodicalIF":2.9,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11058360/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140048753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","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 cell surface glucose-regulated protein 94 in gastric cancer with an anti-GRP94 human monoclonal antibody. 用抗 GRP94 人单克隆抗体靶向胃癌细胞表面葡萄糖调节蛋白 94。
IF 2.9 3区 生物学
BMB Reports Pub Date : 2024-04-01
Hyun Jung Kim, Yea Bin Cho, Kyun Heo, Ji Woong Kim, Ha Gyeong Shin, Eun-Bi Lee, Seong-Min Park, Jong Bae Park, Sukmook Lee
{"title":"Targeting cell surface glucose-regulated protein 94 in gastric cancer with an anti-GRP94 human monoclonal antibody.","authors":"Hyun Jung Kim, Yea Bin Cho, Kyun Heo, Ji Woong Kim, Ha Gyeong Shin, Eun-Bi Lee, Seong-Min Park, Jong Bae Park, Sukmook Lee","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Gastric cancer (GC), a leading cause of cancer-related mortality, remains a significant challenge despite recent therapeutic advancements. In this study, we explore the potential of targeting cell surface glucose-regulated protein 94 (GRP94) with antibodies as a novel therapeutic approach for GC. Our comprehensive analysis of GRP94 expression across various cancer types, with a specific focus on GC, revealed a substantial overexpression of GRP94, highlighting its potential as a promising target. Through in vitro and in vivo efficacy assessments, as well as toxicological analyses, we found that K101.1, a fully human monoclonal antibody designed to specifically target cell surface GRP94, effectively inhibits GC growth and angiogenesis without causing in vivo toxicity. Furthermore, our findings indicate that K101.1 promotes the internalization and concurrent downregulation of cell surface GRP94 on GC cells. In conclusion, our study suggests that cell surface GRP94 may be a potential therapeutic target in GC, and that antibody-based targeting of cell surface GRP94 may be an effective strategy for inhibiting GRP94-mediated GC growth and angiogenesis. [BMB Reports 2024; 57(4): 188-193].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"188-193"},"PeriodicalIF":2.9,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11058359/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140048754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
ErbB3 binding protein 1 contributes to adult hippocampal neurogenesis by modulating Bmp4 and Ascl1 signaling. ErbB3结合蛋白1通过调节Bmp4和Ascl1信号传导促进成年海马神经发生。
IF 2.9 3区 生物学
BMB Reports Pub Date : 2024-04-01
Youngkwan Kim, Hyo Rim Ko, Inwoo Hwang, Jee-Yin Ahn
{"title":"ErbB3 binding protein 1 contributes to adult hippocampal neurogenesis by modulating Bmp4 and Ascl1 signaling.","authors":"Youngkwan Kim, Hyo Rim Ko, Inwoo Hwang, Jee-Yin Ahn","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Neural stem cells (NSCs) in the adult hippocampus divide infrequently; the endogenous molecules modulating adult hippocampal neurogenesis (AHN) remain largely unknown. Here, we show that ErbB3 binding protein 1 (Ebp1), which plays important roles in embryonic neurodevelopment, acts as an essential modulator of adult neurogenic factors. In vivo analysis of Ebp1 neuron depletion mice showed impaired AHN with a low number of hippocampal NSCs and neuroblasts. Ebp1 leads to transcriptional repression of Bmp4 and suppression of Ascl1 promoter methylation in the dentate gyrus of the adult hippocampus reflecting an unusually high level of Bmp4 and low Ascl1 level in neurons of Ebp1-deficient mice. Therefore, our findings suggests that Ebp1 could act as an endogenous modulator of the interplay between Bmp4 and Ascl1/Notch signaling, contributing to AHN. [BMB Reports 2024; 57(4): 182-187].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"182-187"},"PeriodicalIF":2.9,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11058358/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41190371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Memory allocation at the neuronal and synaptic levels. 神经元和突触水平的记忆分配。
IF 2.9 3区 生物学
BMB Reports Pub Date : 2024-04-01
HyoJin Park, Bong-Kiun Kaang
{"title":"Memory allocation at the neuronal and synaptic levels.","authors":"HyoJin Park, Bong-Kiun Kaang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Memory allocation, which determines where memories are stored in specific neurons or synapses, has consistently been demonstrated to occur via specific mechanisms. Neuronal allocation studies have focused on the activated population of neurons and have shown that increased excitability via cAMP response element-binding protein (CREB) induces a bias toward memoryencoding neurons. Synaptic allocation suggests that synaptic tagging enables memory to be mediated through different synaptic strengthening mechanisms, even within a single neuron. In this review, we summarize the fundamental concepts of memory allocation at the neuronal and synaptic levels and discuss their potential interrelationships. [BMB Reports 2024; 57(4): 176-181].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"176-181"},"PeriodicalIF":2.9,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11058361/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"107590066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Calnexin as a dual-role biomarker: antibody-based diagnosis and therapeutic targeting in lung cancer. 作为双重角色生物标记物的 Calnexin:基于抗体的肺癌诊断和治疗靶点。
IF 3.8 3区 生物学
BMB Reports Pub Date : 2024-03-01
Soyeon Lim, Youngeun Ha, Boram Lee, Junho Shin, Taiyoun Rhim
{"title":"Calnexin as a dual-role biomarker: antibody-based diagnosis and therapeutic targeting in lung cancer.","authors":"Soyeon Lim, Youngeun Ha, Boram Lee, Junho Shin, Taiyoun Rhim","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Lung cancer carries one of the highest mortality rates among all cancers. It is often diagnosed at more advanced stages with limited treatment options compared to other malignancies. This study focuses on calnexin as a potential biomarker for diagnosis and treatment of lung cancer. Calnexin, a molecular chaperone integral to N-linked glycoprotein synthesis, has shown some associations with cancer. However, targeted therapeutic or diagnostic methods using calnexin have been proposed. Through 1D-LCMSMS, we identified calnexin as a biomarker for lung cancer and substantiated its expression in human lung cancer cell membranes using Western blotting, flow cytometry, and immunocytochemistry. Anti-calnexin antibodies exhibited complement-dependent cytotoxicity to lung cancer cell lines, resulting in a notable reduction in tumor growth in a subcutaneous xenograft model. Additionally, we verified the feasibility of labeling tumors through in vivo imaging using antibodies against calnexin. Furthermore, exosomal detection of calnexin suggested the potential utility of liquid biopsy for diagnostic purposes. In conclusion, this study establishes calnexin as a promising target for antibody-based lung cancer diagnosis and therapy, unlocking novel avenues for early detection and treatment. [BMB Reports 2024; 57(3): 155-160].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"155-160"},"PeriodicalIF":3.8,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10979343/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139671249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Detecting DNA hydroxymethylation: exploring its role in genome regulation. 检测 DNA 羟甲基化:探索其在基因组调控中的作用。
IF 2.9 3区 生物学
BMB Reports Pub Date : 2024-03-01
Sun-Min Lee
{"title":"Detecting DNA hydroxymethylation: exploring its role in genome regulation.","authors":"Sun-Min Lee","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>DNA methylation is one of the most extensively studied epigenetic regulatory mechanisms, known to play crucial roles in various organisms. It has been implicated in the regulation of gene expression and chromatin changes, ranging from global alterations during cell state transitions to locus-specific modifications. 5-hydroxymethylcytosine (5hmC) is produced by a major oxidation, from 5-methylcytosine (5mC), catalyzed by the ten-eleven translocation (TET) enzymes, and is gradually being recognized for its significant role in genome regulation. With the development of state-of-the-art experimental techniques, it has become possible to detect and distinguish 5mC and 5hmC at base resolution. Various techniques have evolved, encompassing chemical and enzymatic approaches, as well as thirdgeneration sequencing techniques. These advancements have paved the way for a thorough exploration of the role of 5hmC across a diverse array of cell types, from embryonic stem cells (ESCs) to various differentiated cells. This review aims to comprehensively report on recent techniques and discuss the emerging roles of 5hmC. [BMB Reports 2024; 57(3): 135-142].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"135-142"},"PeriodicalIF":2.9,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10979348/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140048752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Whole-genome doubling is a double-edged sword: the heterogeneous role of whole-genome doubling in various cancer types. 全基因组加倍是一把双刃剑:全基因组加倍在不同癌症类型中的异质性作用。
IF 2.9 3区 生物学
BMB Reports Pub Date : 2024-03-01
Eunhyong Chang, Joon-Yong An
{"title":"Whole-genome doubling is a double-edged sword: the heterogeneous role of whole-genome doubling in various cancer types.","authors":"Eunhyong Chang, Joon-Yong An","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Whole-genome doubling (WGD), characterized by the duplication of an entire set of chromosomes, is commonly observed in various tumors, occurring in approximately 30-40% of patients with different cancer types. The effect of WGD on tumorigenesis varies depending on the context, either promoting or suppressing tumor progression. Recent advances in genomic technologies and large-scale clinical investigations have led to the identification of the complex patterns of genomic alterations underlying WGD and their functional consequences on tumorigenesis progression and prognosis. Our comprehensive review aims to summarize the causes and effects of WGD on tumorigenesis, highlighting its dualistic influence on cancer cells. We then introduce recent findings on WGD-associated molecular signatures and genetic aberrations and a novel subtype related to WGD. Finally, we discuss the clinical implications of WGD in cancer subtype classification and future therapeutic interventions. Overall, a comprehensive understanding of WGD in cancer biology is crucial to unraveling its complex role in tumorigenesis and identifying novel therapeutic strategies. [BMB Reports 2024; 57(3): 125-134].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"125-134"},"PeriodicalIF":2.9,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10979346/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140048755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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