Molecular and Cellular Biology最新文献

Hsp70/Hsp90 Organizing Protein (HOP) Maintains CRAF Kinase Activity and Regulates MAPK Signaling by Enhancing Hsp90-CRAF Association. Hsp70/Hsp90组织蛋白（HOP）通过增强Hsp90-CRAF关联维持CRAF激酶活性并调控MAPK信号传导。

IF 2.7 2区生物学

Molecular and Cellular Biology Pub Date : 2026-04-14 DOI: 10.1080/10985549.2026.2647809

Nilanjan Gayen, Sahana Mitra, Somesh Roy, Atin K Mandal

{"title":"Hsp70/Hsp90 Organizing Protein (HOP) Maintains CRAF Kinase Activity and Regulates MAPK Signaling by Enhancing Hsp90-CRAF Association.","authors":"Nilanjan Gayen, Sahana Mitra, Somesh Roy, Atin K Mandal","doi":"10.1080/10985549.2026.2647809","DOIUrl":"https://doi.org/10.1080/10985549.2026.2647809","url":null,"abstract":"The stability and activity of CRAF/Raf1 kinase are stringently regulated by heat shock protein 90 (Hsp90). Hsp90-mediated client folding and maturation are governed by its co-chaperones, but their functionality in chaperoning CRAF kinase to support signaling under physiological conditions remains poorly understood. Here, we show that Hsp70/Hsp90 organizing protein (HOP) associates with CRAF kinase tomaintain its activity and facilitates MAPK pathway activation. This activation is mediated by TPR2A-2B-DP2 domain of HOP and requires efficient binding to Hsp90. Although Cdc37 recruits Hsp90, it cannot compensate for HOP function. Downregulation of HOP/Sti1 in yeast and mammalian cell culture significantly reduces the CRAF signaling. Our data suggest that Hsp90 is recruited to CRAF in two distinct steps: first during folding/maturation via HOP and Cdc37, and later during activation mediated by HOP. Therefore, HOP is a regulator of CRAF kinase during activation of MAPK pathway and serves as a modulator of growth signaling beyond its client folding and maturation function.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"1-20"},"PeriodicalIF":2.7,"publicationDate":"2026-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147691097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Paeonol Ameliorates Gastric Mucosal Enterosis and Dysplasia Associated with Chronic Atrophic Gastritis by Modulating the JAK2/STAT3 Pathway. 丹皮酚通过调节JAK2/STAT3通路改善慢性萎缩性胃炎相关的胃黏膜肠病和发育不良

IF 2.7 2区生物学

Molecular and Cellular Biology Pub Date : 2026-03-19 DOI: 10.1080/10985549.2026.2638205

Lei Zhang, Lei Zou

{"title":"Paeonol Ameliorates Gastric Mucosal Enterosis and Dysplasia Associated with Chronic Atrophic Gastritis by Modulating the JAK2/STAT3 Pathway.","authors":"Lei Zhang, Lei Zou","doi":"10.1080/10985549.2026.2638205","DOIUrl":"https://doi.org/10.1080/10985549.2026.2638205","url":null,"abstract":"Paeonol (Pae) exhibits potent anti-inflammatory and antitumor effects. Chronic atrophic gastritis (CAG) is considered a gastric precancerous lesion, and the JAK2/STAT3 pathway plays a key role in gastrointestinal inflammation and tumorigenesis. Whether Pae ameliorates CAG by regulating this pathway remains unclear. A 1-methyl-3-nitro-1-nitrosoguanidine (MNNG)-induced malignant transformed cell (MC) model and a CAG rat model were established. The malignant biological behaviors of MC cells were assessed using the Cell Counting Kit-8 (CCK-8) assay, clone formation, and Transwell assays. Gastric histopathological changes were examined by pathological staining, inflammatory factors and gastric mucosa-associated factors were detected via enzyme-linked immunosorbent assay (ELISA). Inflammation, proliferation, epithelial-mesenchymal transition (EMT), and the JAK2/STAT3 pathway-related protein expression was analyzed by Western blotting. MC cells exhibited enhanced proliferation, migration, invasion, and EMT, all of which were significantly suppressed by Pae treatment. CAG rats showed severe gastric mucosal damage, intestinal metaplasia, collagen fiber disorganization, and increased Ki-67 expression. Pae treatment alleviated histopathological injury, reduced inflammatory factor levels, and promoted gastric mucosa-associated factor synthesis. Furthermore, Pae markedly inhibited the JAK2/STAT3 pathway in MC cells and gastric tissues. In conclusion, Pae suppresses malignant transformation and alleviates gastric histopathological injury in CAG by modulating the JAK2/STAT3 pathway.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"1-18"},"PeriodicalIF":2.7,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147481032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Chaihu Shugan Powder Attenuates Ferroptosis-Associated Injury in Acute Pancreatitis by Activating PGC-1α/Nrf2/HO-1 Pathway. 柴胡疏肝散通过激活PGC-1α/Nrf2/HO-1通路减轻急性胰腺炎铁中毒相关损伤

IF 2.7 2区生物学

Molecular and Cellular Biology Pub Date : 2026-03-16 DOI: 10.1080/10985549.2026.2638200

Yutao Chen, Dapeng Zhang, Quan Li, Yingqing Xing

{"title":"Chaihu Shugan Powder Attenuates Ferroptosis-Associated Injury in Acute Pancreatitis by Activating PGC-1α/Nrf2/HO-1 Pathway.","authors":"Yutao Chen, Dapeng Zhang, Quan Li, Yingqing Xing","doi":"10.1080/10985549.2026.2638200","DOIUrl":"https://doi.org/10.1080/10985549.2026.2638200","url":null,"abstract":"Acute pancreatitis (AP) is a life-threatening condition driven by premature pancreatic enzyme activation, leading to systemic complications and multi-organ dysfunction. Chaihu Shugan Powder (CSP) has been reported to mitigate pancreatic injury associated with AP, but the detailed regulatory mechanism was unclear. In our study, we investigated the fundamental mechanism of how CSP attenuated AP injury. The AP models were constructed by applying cerulein in AR42J cells and rats. Individual CSP interventions did not affect normal cell function. CSP partially reversed cerulein-induced cell damage, as reflected by increased cell viability, the level of glutathione (GSH), and ferroptosis protein markers but decreased the contents of inflammatory factor, reactive oxygen species (ROS), malondialdehyde (MDA), Fe2+ and iron. CSP activated the peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α)/nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway, which in turn reduced ferroptosis in cerulein-exposed AR42J cells. Silencing the PGC-1α gene could partially inhibit the activation of the PGC-1α/Nrf2/HO-1 pathway by CSP in cerulein-induced AR42J cells. In AP rats, CSP alleviated AP-related pathomorphological changes and ferroptosis in rats by activating PGC-1α/Nrf2/HO-1 pathway. Altogether, the mechanism by which CSP alleviated AP injury in rats may be correlated with the activation of PGC-1α/Nrf2/HO-1 pathway.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"1-14"},"PeriodicalIF":2.7,"publicationDate":"2026-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147468545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Loss of Splicing Homeostasis as a Hallmark of Aging. 剪接稳态丧失是衰老的标志。

IF 2.7 2区生物学

Molecular and Cellular Biology Pub Date : 2026-03-02 DOI: 10.1080/10985549.2026.2627235

Stefano Donega, Myriam Gorospe, Lorna W Harries, Luigi Ferrucci

{"title":"Loss of Splicing Homeostasis as a Hallmark of Aging.","authors":"Stefano Donega, Myriam Gorospe, Lorna W Harries, Luigi Ferrucci","doi":"10.1080/10985549.2026.2627235","DOIUrl":"https://doi.org/10.1080/10985549.2026.2627235","url":null,"abstract":"Alternative splicing is a fundamental mechanism that ensures accurate gene expression, supports cellular adaptability, and expands protein diversity beyond the limits of a fixed gene pool. With aging, splicing fidelity weakens, contributing to decline in RNA homeostasis and disrupting essential cellular functions, including mitochondrial oxidative phosphorylation, genome stability, and immune regulation, and in turn accelerating tissue and organ dysfunction. Evidence from senescent cells, aged tissues, and model organisms shows that altered levels of splicing factors and increased RNA polymerase II elongation rates impair co-transcriptional splicing and promote mis-spliced isoforms that reinforce senescence and drive pathology. Dysfunction of RNA-binding proteins further contributes to aberrant splicing, linking splicing defects to age-related diseases such as atherosclerosis, osteoarthritis, sarcopenia, and neurodegenerative disorders like Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. Therapeutic strategies to correct splicing defects, such as antisense oligonucleotides, RNA interference, CRISPR-Cas systems, ADAR-mediated editing, and RNA aptamers, can restore a homeostatic balance of mRNA isoforms. However, major challenges remain, including distinguishing adaptive physiological from pathological splicing 'noise' and achieving targeted delivery to tissues. Despite these obstacles, RNA splicing dysregulation represents a promising avenue to extend health span by reestablishing homeostatic RNA programs, and reinforces the idea that \"transcriptomic instability\" is a hallmark of aging.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"1-19"},"PeriodicalIF":2.7,"publicationDate":"2026-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147343635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

TRF-1 Mediates PRC2 Function at Ectopic Telomere Repeats in Neurospora crassa. TRF-1介导粗神经孢子虫异位端粒重复PRC2功能。

IF 2.7 2区生物学

Molecular and Cellular Biology Pub Date : 2026-02-17 DOI: 10.1080/10985549.2026.2627225

Colleen C Mumford, Peregrine D Painter, Kevin J McNaught, Hideki Tanizawa, Nolan J Smith, Shinji Honda, Osamu Iwasaki, Sanki Tashiro, Ken-Ichi Noma, Eric U Selker

{"title":"TRF-1 Mediates PRC2 Function at Ectopic Telomere Repeats in Neurospora crassa.","authors":"Colleen C Mumford, Peregrine D Painter, Kevin J McNaught, Hideki Tanizawa, Nolan J Smith, Shinji Honda, Osamu Iwasaki, Sanki Tashiro, Ken-Ichi Noma, Eric U Selker","doi":"10.1080/10985549.2026.2627225","DOIUrl":"https://doi.org/10.1080/10985549.2026.2627225","url":null,"abstract":"Telomeres are crucial for maintaining chromosomal integrity and are characterized by repetitive DNA sequences, which may be stabilized by the shelterin protein complex or by formation of secondary structures, such as G-quadruplexes (G4 DNA). Frequently, subtelomeric regions are decorated with di- and tri-methylated lysine 27 on histone H3 (H3K27me), repressive marks catalyzed by Polycomb Repressive Complex 2 that are associated with facultative heterochromatin in many eukaryotes. Our previous work with the filamentous fungus Neurospora crassa demonstrated that native telomere repeats induce H3K27me at ectopic loci. Here we report investigations into the mechanism of this and demonstrate that some non-native telomere repeats can also induce H3K27me. Hi-C analyses demonstrated that ectopic telomeric repeats can interact with native telomeres. Chromatin immunoprecipitation (ChIP) experiments with an anti-G4-DNA antibody showed that establishment of H3K27me was not correlated with the presence of G4 DNA. Other ChIP experiments demonstrated that the telomere repeat-binding protein TRF-1, which has been demonstrated to be a member of the shelterin complex in other systems, binds to interstitial telomere repeats that induce H3K27me. Tethering experiments revealed that TRF-1 binding is sufficient to induce H3K27me. Together these results suggest that TRF-1 plays a crucial role in establishment of H3K27me, and thus repression, at telomere sequences.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"1-15"},"PeriodicalIF":2.7,"publicationDate":"2026-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146207331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Molecular Mechanisms of Transcription Factors with Dual Activator and Repressor Functions. 具有双重激活和抑制功能的转录因子的分子机制。

IF 2.7 2区生物学

Molecular and Cellular Biology Pub Date : 2026-01-28 DOI: 10.1080/10985549.2026.2619741

Jinhong Dong, Michael J Guertin

引用次数: 0

Importance of E3 Ligases for Preserving Genome Integrity: Progress and Challenges. E3连接酶对保持基因组完整性的重要性：进展和挑战。

IF 2.7 2区生物学

Molecular and Cellular Biology Pub Date : 2026-01-01 Epub Date: 2026-03-17 DOI: 10.1080/10985549.2026.2638203

Rumpa Mahata, Manas Kumar Santra

引用次数: 0

Silybin Improves Acute Kidney Injury by Regulating HDAC6/NF-κB/NLRP3 Signaling to Reduce Inflammation and Ferroptosis. 水飞蓟宾通过调节HDAC6/NF-κB/NLRP3信号减少炎症和铁下垂改善急性肾损伤。

IF 2.7 2区生物学

Molecular and Cellular Biology Pub Date : 2026-01-01 Epub Date: 2025-12-08 DOI: 10.1080/10985549.2025.2594183

Ying Wei, Mingjing Yin, Guojiang Chen, Menghua Chen

{"title":"Silybin Improves Acute Kidney Injury by Regulating HDAC6/NF-κB/NLRP3 Signaling to Reduce Inflammation and Ferroptosis.","authors":"Ying Wei, Mingjing Yin, Guojiang Chen, Menghua Chen","doi":"10.1080/10985549.2025.2594183","DOIUrl":"10.1080/10985549.2025.2594183","url":null,"abstract":"Inflammation and ferroptosis play a crucial role in cisplatin (CP)-induced acute kidney injury (AKI). Silybin (SYB), a polyphenolic flavonoid, has shown renal protective effects, but its underlying mechanisms remain unclear. CP-induced HK-2 cell and mouse AKI models were used to explore the role of SYB. CCK-8, lactate dehydrogenase release, flow cytometry, and calcein/PI staining, were performed to evaluate cell viability, proliferation, and apoptosis. Oxidative stress and ferroptosis markers were measured, while renal function was assessed by serum creatinine and urea nitrogen. Mitochondrial ultrastructure was examined, and histological staining was conducted to analyze renal pathology and iron deposition. Western blotting detected HDAC6, NF-κB, NLRP3, and ferroptosis-related proteins expression. SYB treatment alleviated CP-induced mitochondrial damage, reduced lactate dehydrogenase release, inflammatory cytokines, oxidative stress, and ferroptosis, and improved proliferation and viability in HK-2 cells. In mice, 100 mg/kg SYB decreased serum creatinine, urea nitrogen, and cytokine levels, while ameliorating renal tissue injury. Mechanistically, SYB downregulated HDAC6 and inhibited NF-κB/NLRP3 activation, thereby suppressing ferroptosis. Notably, overexpression of HDAC6 restored NF-κB/NLRP3 activity and attenuated the protective effects of SYB. In conclusion, SYB mitigates CP-induced AKI by reducing inflammation and ferroptosis by modulating the HDAC6/NF-κB/NLRP3 pathway.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"546-565"},"PeriodicalIF":2.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145701035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Xiangpi Shengji Ointment Accelerates Anal Fistula Healing by Regulating Macrophage-Fibroblast Crosstalk Through the Nuclear Factor Kappa B/Hypoxia-Inducible Factor Alpha/Vascular Endothelial Growth Factor Signaling Axis. 香皮生脂膏通过核因子κ B/缺氧诱导因子α /血管内皮生长因子信号轴调节巨噬细胞-成纤维细胞串音促进肛瘘愈合。

IF 2.7 2区生物学

Molecular and Cellular Biology Pub Date : 2026-01-01 Epub Date: 2025-12-29 DOI: 10.1080/10985549.2025.2597464

Kui Li, Jiaqing Xiong, Sai Yang, Mintao Jian

{"title":"Xiangpi Shengji Ointment Accelerates Anal Fistula Healing by Regulating Macrophage-Fibroblast Crosstalk Through the Nuclear Factor Kappa B/Hypoxia-Inducible Factor Alpha/Vascular Endothelial Growth Factor Signaling Axis.","authors":"Kui Li, Jiaqing Xiong, Sai Yang, Mintao Jian","doi":"10.1080/10985549.2025.2597464","DOIUrl":"10.1080/10985549.2025.2597464","url":null,"abstract":"This study elucidates the molecular mechanism by which Xiangpi Shengji ointment (Xiangpi Shengji gao, XPSJG) promotes anal fistula wound healing. Integrated network pharmacology and transcriptomic analyses (GSE28914, GSE203244) revealed the involvement of the NF-κB/HIF-α/VEGF axis, with elevated expression of NF-κB, HIF1A, and VEGFA observed during the early healing phase (days 3 and 7). Single-cell RNA sequencing further indicated that activation of this signaling axis may drive early macrophage M1 polarization. In vitro experiments confirmed early treatment with the aqueous extract of XPSJG powder significantly enhanced macrophage M1 polarization and upregulated VEGF, COL1A1, and α-SMA, promoting fibroblast proliferation and migration (assessed via CCK-8, ELISA, WB, RT-qPCR). In vivo, using a murine anal fistula model, XPSJG accelerated wound closure, improved tissue architecture, and reduced inflammation and apoptosis through modulation of the NF-κB/HIF-α/VEGF axis. These effects were partially reversed by an NF-κB inhibitor, further verifying pathway involvement. Collectively, the findings demonstrate that early application of XPSJG facilitates anal fistula healing by inducing macrophage M1 polarization and enhancing fibroblast function via the NF-κB/HIF-α/VEGF signaling axis, thereby providing a mechanistic rationale for its clinical use in chronic wound management.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"336-360"},"PeriodicalIF":2.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145850367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Pharmacological Modulation of Autophagy Corrects Cellular Defects in Pediatric Crohn's Disease. 自噬的药理调节纠正儿童克罗恩病的细胞缺陷。

IF 2.7 2区生物学

Molecular and Cellular Biology Pub Date : 2026-01-01 Epub Date: 2025-11-13 DOI: 10.1080/10985549.2025.2583173

Mara Creoli, Pietro Buono, Sabrina Cenni, Marianna Casertano, Alessandra Vitale, Mariantonia Maglio, Roman Polishchuk, Elena Polishchuk, Laura Cinque, Erasmo Miele, Massimo Martinelli, Carmine Settembre, Annamaria Staiano, Pasquale Dolce, Caterina Strisciuglio

{"title":"Pharmacological Modulation of Autophagy Corrects Cellular Defects in Pediatric Crohn's Disease.","authors":"Mara Creoli, Pietro Buono, Sabrina Cenni, Marianna Casertano, Alessandra Vitale, Mariantonia Maglio, Roman Polishchuk, Elena Polishchuk, Laura Cinque, Erasmo Miele, Massimo Martinelli, Carmine Settembre, Annamaria Staiano, Pasquale Dolce, Caterina Strisciuglio","doi":"10.1080/10985549.2025.2583173","DOIUrl":"10.1080/10985549.2025.2583173","url":null,"abstract":"Crohn's disease (CD) is an inflammatory gastrointestinal disorder marked by impaired autophagy due to inefficient bacterial uptake. We studied the effects of autophagy modulation using Tat-beclin-1 and carbamazepine (CBZ) on dendritic cells (DCs) and Paneth cell functionality in pediatric CD patients. Twenty CD children genotyped for the ATG16L1 rs2241880 polymorphism and 10 healthy controls were enrolled. DCs were incubated with fluorochrome-conjugated particles of Escherichia coli or DQ-ovalbumin after pretreatment with CBZ or Tat-beclin-1 to evaluate antigen processing. Treated DCs were stained for P62, LAMP1, and LC3, and analyzed by confocal microscopy. Paneth cells from biopsies were pretreated with both drugs, stained for lysozyme, and analyzed by transmission electron microscopy. Antigen processing increased after Tat-beclin-1 and CBZ treatment in all groups. DCs expressed higher activation markers HLA-DR and CD86+, notably in high-risk patients, who also showed increased DQ-OVA processing. The number of lysozymes in Paneth cells from controls did not change after Tat-beclin-1 treatment, while in the CD group, it decreased significantly, suggesting increased exocytosis. CBZ treatment increased secretory granules only in CD inflamed tissue. Our results indicate that CBZ and Tat-beclin-1 enhance autophagic flux, representing a novel approach to treating pediatric CD patients.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"270-280"},"PeriodicalIF":2.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145505646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0