Biochemical and biophysical research communications最新文献

{"title":"Role of CXCR4/SDF1 signaling in the initial migration of cardiac neural crest cells","authors":"Saori Tani-Matsuhana,&nbsp;Yumi Unozu,&nbsp;Kunio Inoue","doi":"10.1016/j.bbrc.2025.151914","DOIUrl":"10.1016/j.bbrc.2025.151914","url":null,"abstract":"<div><div>Neural crest cells are migratory and multipotent cell populations that give rise to various derivatives during the development of vertebrate embryos. The cells are specified in the neural folds and undergo epithelial mesenchymal transition (EMT) to delaminate and then migrate within the embryo. Cardiac neural crest cells originate from the caudal hindbrain and migrate through the pharyngeal arches to the heart. It has been shown that CXCR4/SDF1 signaling control cardiac neural crest cells migration toward pharyngeal arches in chicken embryos. Here, we investigated the effect of disruption of CXCR4/SDF1 signaling on cardiac neural crest cell migration by implanting beads into the lumen of the closing neural tube. We first observed that a CXCR4 antagonist inhibited initial cardiac neural crest migration. We also found that an ectopic source of SDF1 caused the accumulation of cardiac neural crest cells in the dorsal neural tube and the invasion of cardiac neural crest cells into the neural tube. Furthermore, disruption of signaling led to disorganization of the neural tube basement membrane but did not affect neural crest EMT. Overall, our data indicate that CXCR4/SDF1 signaling is critical for as early as the onset of cardiac neural crest cell migration after the delamination.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"767 ","pages":"Article 151914"},"PeriodicalIF":2.5,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143899551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Different temporal dynamics of primary cilia formation and elongation during adipocyte differentiation in umbilical cord- and bone marrow-derived mesenchymal stem cells","authors":"Masako Hirai ,&nbsp;Naokazu Inoue ,&nbsp;Tomoaki Nagai ,&nbsp;Michiru Nishita","doi":"10.1016/j.bbrc.2025.151918","DOIUrl":"10.1016/j.bbrc.2025.151918","url":null,"abstract":"<div><div>Umbilical cord-derived mesenchymal stem cells (UC-MSCs) are considered a promising alternative to bone marrow-derived MSCs (BM-MSCs) due to their high proliferative capacity and non-invasive accessibility. While UC-MSCs exhibit osteogenic, chondrogenic, and myogenic differentiation potential comparable to BM-MSCs, their adipogenic differentiation is significantly delayed. To investigate the underlying mechanisms, we focused on primary cilia, sensory organelles that regulate key adipogenic signaling pathways, including the insulin-Akt axis. Under serum-starved, growth-arrest conditions, both UC-MSCs and BM-MSCs formed primary cilia at similar frequencies and lengths; however, under serum-fed, proliferative conditions, UC-MSCs showed a significantly lower frequency of ciliation. During adipogenesis, BM-MSCs exhibited early ciliogenesis and stable cilium length, whereas UC-MSCs displayed delayed ciliogenesis and developed significantly longer cilia after repeated induction cycles. Despite comparable ciliation frequency and longer cilia in UC-MSCs at later stages, insulin-induced Akt activation was reduced compared to BM-MSCs, suggesting that primary cilia in UC-MSCs may be less efficient in sensing insulin. These alterations in insulin signaling may contribute to the reduced adipogenic capacity observed in UC-MSCs.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"768 ","pages":"Article 151918"},"PeriodicalIF":2.5,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143906970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Restoration of gut integrity by Bacteroides acidifaciens in water-deprived conditions","authors":"Siyuan Fan ,&nbsp;Xinyue Cai ,&nbsp;Wenbo Cui ,&nbsp;Peisen Ma ,&nbsp;Meiling Wu ,&nbsp;Jing Guo ,&nbsp;Yipeng Zhang ,&nbsp;Kun Xuan ,&nbsp;Zihan Li","doi":"10.1016/j.bbrc.2025.151917","DOIUrl":"10.1016/j.bbrc.2025.151917","url":null,"abstract":"<div><div>Water scarcity exerts profound physiological impacts, yet its effects on intestinal microbiota-barrier crosstalk remain poorly understood. This study investigates water-deprivation-induced gut dysbiosis and identifies <em>Bacteroides acidifaciens</em> (<em>B.acidifaciens</em>) as a critical mediator of epithelial barrier resilience. Using a murine model of graded water restriction, we observed colon shortening, villus atrophy, goblet cell loss, and barrier disruption correlated with water-deprivation severity. Oral supplementation of <em>B.acidifaciens</em> restored colonic architecture, enhanced mucin secretion, and ameliorated barrier dysfunction in water-deprived mice. Mechanistically, <em>B.acidifaciens</em> maintained barrier homeostasis by directly stimulating mucus production in intestinal epithelial cells and upregulating the expression of tight junction proteins. These findings establish <em>B.acidifaciens</em> as a critical species in mitigating water-deprivation-induced colon injury and advance our understanding of microbiota-directed interventions for dehydration-associated gastrointestinal disorders.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"767 ","pages":"Article 151917"},"PeriodicalIF":2.5,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143895703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selenium corrects dysregulated mitophagy and lipophagy in obesity-related acute pancreatitis through the GPX1-Mfn2-PLIN2 axis","authors":"Peiyu Han ,&nbsp;Xiaoyu Ma ,&nbsp;Yuqiu Ge ,&nbsp;Hongbo Ren ,&nbsp;Yu Wu","doi":"10.1016/j.bbrc.2025.151916","DOIUrl":"10.1016/j.bbrc.2025.151916","url":null,"abstract":"<div><div>The incidence of acute pancreatitis (AP) has been on the rise in recent years. Obesity, a significant contributor to AP, increases the risk of AP and promotes disease progression, leading to adverse outcomes. Mitophagy and lipophagy are two main types of selective autophagy in AP and obesity, but their contribution to comorbidity in obesity-related AP (OB-AP) remains unknown. This study demonstrated that OB-AP exhibited more severe pancreatic injury than AP <em>in vivo</em> and <em>in vitro</em>. We found that the balance between mitophagy and lipophagy was disrupted, with a significant increase in mitophagy and a corresponding significant decrease in lipophagy. Mechanistically, overexpression of selenoprotein glutathione peroxidase 1 (GPX1) stabilized mitofusin 2 (Mfn2) protein, promoting the interaction between Mfn2 and perilipin 2 (PLIN2), and thereby attenuating excessive mitophagy and increasing lipophagy. Selenium supplementation improved pancreatic autophagy homeostasis in OB-AP through increasing GPX1 expression, thereby reducing disease severity. Notably, OB-AP patients exhibited lower selenium levels than healthy individuals. In conclusion, selenium supplementation enhanced GPX1 expression, corrected the imbalance between mitophagy and lipophagy, and mitigated disease severity in OB-AP through the GPX1-Mfn2-PLIN2 axis, and therefore has therapeutic potential in OB-AP.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"768 ","pages":"Article 151916"},"PeriodicalIF":2.5,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143903278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nature's nano-factories: Pistacia khinjuk-mediated FeNPs with improved biomedical and environmental capabilities","authors":"Ali Raza Kashif ,&nbsp;Saima Naz ,&nbsp;Muhammad Naveed Rasheed ,&nbsp;Ambreen Ghani ,&nbsp;Muhammad Usama Younas ,&nbsp;Farooq Ahmad ,&nbsp;Zafar Muhammad Shahzad","doi":"10.1016/j.bbrc.2025.151884","DOIUrl":"10.1016/j.bbrc.2025.151884","url":null,"abstract":"<div><div>Iron oxide nanoparticles (FeNPs) hold immense promise in diverse fields, including medicine and environmental remediation. This study aims to develop a sustainable, biogenic synthesis of FeNPs using <em>Pistacia khinjuk</em> leaf extract and evaluate their multifunctional applications. The biogenically synthesized FeNPs were rigorously analyzed to confirm their properties - UV–Vis spectroscopy verified nanoparticle formation through characteristic absorption, XRD revealed the crystalline phase structure, PSA quantified the size distribution profile, and FTIR detected organic functional groups responsible for stabilization, while SEM visualized the surface morphology and aggregation behavior. More precisely, the UV–Vis spectroscopy confirmed FeNPs formation (peak at ʎ = 365 nm), while XRD and PSA revealed a cubic crystalline structure with average sizes of ∼17.41 and ∼21 nm. The FeNPs exhibited significant antioxidant (72.3 μg/mL DPPH scavenging at 100 μg/mL) and enhanced antibacterial activity against <em>Xanthomonas oryzae</em> and <em>Pseudomonas</em> sp., surpassing the extract alone. Selective cytotoxicity against HeLa cells (vs. normal fibroblasts) and photocatalytic degradation of Reactive Black-5 dye (71 % removal in 180 min under UV) were also demonstrated. These findings highlight the potential of P. khinjuk-derived FeNPs for biomedical and environmental applications.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"766 ","pages":"Article 151884"},"PeriodicalIF":2.5,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143881437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From cause to relief: Vitamin D plays a crucial role in overactive bladder via the RhoA/ROCK signaling pathway","authors":"Chong Wang ,&nbsp;Jiaxin Zhou ,&nbsp;Qiang Zhang ,&nbsp;Hongsong Chen ,&nbsp;Xingguo Luo ,&nbsp;Zhenmin Liu ,&nbsp;Zihan Ye ,&nbsp;Zhicheng Zhang ,&nbsp;Guanghui Wei ,&nbsp;Xing Liu","doi":"10.1016/j.bbrc.2025.151919","DOIUrl":"10.1016/j.bbrc.2025.151919","url":null,"abstract":"<div><div>Overactive bladder (OAB) is a common urological disorder, characterized by urinary urgency and frequency. However, the etiology and pathogenesis of OAB remain unclear. The objective of this study was to construct a Vitamin D-deficient rat model with the aim of clarifying the relationship between Vitamin D deficiency and the development of OAB, as well as investigating the potential mechanisms involved. The findings revealed that rats with vitamin D deficiency exhibited indications of OAB, including increased urinary frequency and urgency, as evidenced by void spot assay and cystometry. Furthermore, supplementation with vitamin D proved to be an effective intervention in alleviating these symptoms. The activation of RhoA/ROCK pathway was found in the bladder tissues and urine of rats with vitamin D deficiency. Moreover, supplementation with vitamin D led to a significant decrease in the expression levels of RhoA/ROCK pathway in both bladder tissue and urine. In conclusion, our study was the first to demonstrate that vitamin D deficiency is one of the etiological factors of OAB through the activation of the RhoA/ROCK signaling pathway, and that vitamin D supplementation has been shown to effectively alleviate OAB symptoms by inhibiting this pathway. Meanwhile, urinary RhoA may be a biomarker of OAB. Our present work makes a significant contribution to the clarification of the etiology and mechanism of OAB, as well as to the refinement of OAB treatment strategies.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"766 ","pages":"Article 151919"},"PeriodicalIF":2.5,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143887560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of molecular subtypes and a prognostic risk model based on mitochondrial dynamic related genes in clear cell renal cell carcinoma","authors":"Kaibo Yang ,&nbsp;Kun Yang ,&nbsp;Zitong Lei ,&nbsp;Kunjin Wu ,&nbsp;Jing Li ,&nbsp;Qiuting Peng ,&nbsp;Chang Liu ,&nbsp;Kai Qu ,&nbsp;Ting Lin","doi":"10.1016/j.bbrc.2025.151911","DOIUrl":"10.1016/j.bbrc.2025.151911","url":null,"abstract":"<div><h3>Background</h3><div>Clear cell renal cell carcinoma (ccRCC) represents the most prevalent histological subtype and primary contributor to unfavorable prognosis in renal cancer. While mitochondrial dynamics serve as a critical quality control mechanism linked to tumor malignancy, their clinical significance and specific mechanisms in ccRCC remain poorly understood.</div></div><div><h3>Methods</h3><div>Consnsuclusterplus was used to consensus clustering and molecular subtype screening, Kaplan-Meier analysis was used to analyze survival in different subtypes. PINK1 expression was detected by westernblot, and CCK8 is used to detect cell activity. Immunofluorescence staining of LC3 for evaluating mitochondrial autophagy levels.</div></div><div><h3>Results</h3><div>In this study, we classified 534 ccRCC samples, identified from the UCSC XENA database, into A and B clusters based on 42 mitochondrial dynamic related genes. Cluster A demonstrated superior survival outcomes compared to cluster B. Subsequent analysis revealed significant inter-cluster differences in gene expression profiles, mutational spectra, and immune infiltration patterns. We established a mitochondrial dynamics-related prognostic model incorporating PINK1, NIPSNAP1, and MTFR2, with mitophagy-associated genes represented by PINK1 showing particular prognostic significance in ccRCC. Gene Ontology (GO) analysis indicated significant enrichment of mitophagy pathways in cluster A. Functional investigations demonstrated that PINK1-overexpressing cells exhibited increased sensitivity to sunitinib (lower IC50 values), whereas PINK1 knockdown conferred therapeutic resistance. Western blot and immunofluorescence analyses confirmed elevated mitophagy levels in PINK1-overexpressing cells under sunitinib treatment, contrasting with diminished mitophagy in PINK1-deficient cells.</div></div><div><h3>Conclusions</h3><div>Our findings advance the understanding of mitochondrial dynamics in ccRCC progression, demonstrating that PINK1-mediated enhancement of mitophagy critically potentiates the anti-tumor effects of sunitinib in ccRCC.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"767 ","pages":"Article 151911"},"PeriodicalIF":2.5,"publicationDate":"2025-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143899552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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 “Bone mesenchymal stem cell-derived extracellular vesicles inhibit DAPK1-mediated inflammation by delivering miR-191 to macrophages” [Biochem. Biophys. Res. Commun. 598 (2022) 46981]","authors":"Hui Liu ,&nbsp;Luming Zhang ,&nbsp;Meilian Li ,&nbsp;Fengzhi Zhao ,&nbsp;Fan Lu ,&nbsp;Feng Zhang ,&nbsp;Sida Chen ,&nbsp;Juntao Guo ,&nbsp;Rui Zhang ,&nbsp;Haiyan Yin","doi":"10.1016/j.bbrc.2025.151791","DOIUrl":"10.1016/j.bbrc.2025.151791","url":null,"abstract":"","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"766 ","pages":"Article 151791"},"PeriodicalIF":2.5,"publicationDate":"2025-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143906951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mogroside V prevents ethanol-induced hangover and liver damage by reducing oxidative stress, steatosis and inflammation","authors":"Rui Ai ,&nbsp;Muzhao Tian ,&nbsp;Jiawang Sun ,&nbsp;Shuying He ,&nbsp;Zhi Cui ,&nbsp;Yizhuang Yang ,&nbsp;Xinyue Hou ,&nbsp;Yue Zhao ,&nbsp;Tong Dou ,&nbsp;Xu Chen ,&nbsp;Juan Wang","doi":"10.1016/j.bbrc.2025.151912","DOIUrl":"10.1016/j.bbrc.2025.151912","url":null,"abstract":"<div><div>Excessive alcohol consumption is a leading cause of alcohol-associated liver disease (ALD). Previous studies presented Mogroside V (MV) have protective effects on against nonalcoholic fatty liver disease. however, the effects of MV on ethanol-induced hangover and liver damage remains to be elucidated. Herein, we investigated the potential effects of MV in relieving hangover and mitigating liver injury induced by ethanol. MV significantly reduced blood ethanol, liver histological alterations and serum ALT, AST、TG levels in ethanol-treated mice. Moreover, MV accelerates alcohol metabolism by inhibiting the upregulation of CYP2E1 induced by ethanol, while enhancing the activity of ADH and ALDH, as well as upregulating the expression of ADH1 and ALDH2. MV mitigates oxidative stress by decreased hepatic malondialdehyde (MDA) levels, restored glutathione (GSH)、superoxide dismutase (SOD) and catalase (CAT) content in ethanol-induced mice. Mechanistically, MV activated the <em>p</em>-AMPK/SREBP-1/FASN pathway to decreased hepatic lipid accumulation and alleviated steatosis. Additionally, MV promoted nuclear translocation of Nrf-2 to attenuates oxidative stress and suppressed TLR4/MyD88/NF-κB signaling pathway to reduce Inflammatory responses triggered by ethanol in mice. In summary, this study highlights mogroside V's hangover relieving effect and its protective effects against ethanol-related liver damage through its lipid metabolism regulation, antioxidative action and anti-inflammatory properties. These results suggest that mogroside V could be developed as a potential therapeutic agent against ethanol-induced liver damage.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"766 ","pages":"Article 151912"},"PeriodicalIF":2.5,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143881866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pituitary folliculo-stellate cells modulate tumor vasculature and extracellular matrix composition in experimental lactosomatotropinomas","authors":"S.A. Valla ,&nbsp;A. Chimento ,&nbsp;G. Demarchi ,&nbsp;E.N. Prodan ,&nbsp;E. Werner ,&nbsp;D.L. Vitale ,&nbsp;M.L. Romano ,&nbsp;L.D. Alaniz ,&nbsp;D. Becú-Villalobos ,&nbsp;C. Cristina","doi":"10.1016/j.bbrc.2025.151876","DOIUrl":"10.1016/j.bbrc.2025.151876","url":null,"abstract":"<div><div>Folliculo-stellate cells (FSCs) constitute 5–10 % of the adenohypophysis and have been proposed as paracrine regulators of pituitary cells. However, their participation in pituitary tumor development remains unclear. We generated a lacto-somatotropic tumor model by subcutaneous injection of GH3 (lacto-somatotrophs) and the FSCs TtT/GF, isolated or combined, in immunodeficient mice, to study the role of the FSCs on tumor formation, hormone secretion, vascularization and extra-cellular matrix involvement. The co-culture of both cell lines let us gain insight into the proliferative and secretory action of FSC in pituitary tumor modulation. Our results showed that initially GH3:TtT/GF tumors had an earlier onset, but lately, TtT/GF cells restrained GH3:TtT/GF tumor growth and their <em>Prl</em> synthesis, although no differences were observed in the proliferative potential of tumor cells <em>in vivo</em>. Instead, TtT/GF cells exerted a direct mitogenic action on GH3 cells <em>in vitro.</em> Moreover, GH3 tumors had fewer irrigating vessels, lower vascular area and a higher VEGF/bFGF ratio that correlated with <em>Hif1a</em> expression, consistent with the tissue hypoxia and hemorrhage. These features were downregulated in their co-injected counterparts, which interestingly showed an increased deposition of collagens, glycoproteins and mucopolysaccharides extra-cellular matrix (EMC) components. Isolated TtT/GF injected cells did not generate tumors, but they developed fibrous masses characterized by collagen and high bFGF production. In conclusion, our results demonstrate that FSCs are dual regulators of pituitary tumor growth, with a mitogenic action on tumor cells but also a restrictive tumor effect on the cancer processes angiogenesis, hypoxia, and ECM remodeling.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"767 ","pages":"Article 151876"},"PeriodicalIF":2.5,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143891173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}