{"title":"Investigation of neuroprotective effects of newly synthesized benzimidazolium salt against neurotoxicity in differentiated SH-SY5Y neuronal cells","authors":"Fatma Yıldız","doi":"10.1016/j.bbrc.2025.152255","DOIUrl":"10.1016/j.bbrc.2025.152255","url":null,"abstract":"<div><div>Neurodegenerative diseases (ND) are a group of neurological disorders characterized by various pathological features such as selective neuronal loss, chronic inflammation, and aggregation of specific proteins. This study aimed to investigate the possible protective effects of newly synthesized benzimidazolium salt (BS) against H<sub>2</sub>O<sub>2</sub>-induced oxidative stress in differentiated SH-SY5Y cells. Firstly, retinoic acid was applied to SH-SY5Y cells to obtain mature neurons. Then, a toxicity model was created by H<sub>2</sub>O<sub>2</sub> treatment of neuron-like differentiated SH-SY5Y (d- SH-SY5Y) cells. Survival rates of d–SH–SY5Y cells were determined using the 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) method. In addition, pro-inflammatory cytokine (tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), interleukin-6 (IL-6) levels were determined by ELISA method, while gene expression levels of apoptotic markers (Bax, Bcl-2, caspase-3 and caspase-8) were determined by RT-QPCR method. In addition, the effect of BS on neurite length in these cell groups was evaluated through morphological observations. According to our results, BS showed neuroprotective effect by increasing cell viability against H<sub>2</sub>O<sub>2</sub>-induced neurotoxicity in d–SH–SY5Y cells (<em>p</em> < 0.01). BS pretreatment provided H<sub>2</sub>O<sub>2</sub>-induced Bcl-2 up-regulation, Bax down-regulation, caspase-3 activation and caspase-8 inhibition. In addition, BS supported the decrease in TNF-α, IL-1β and IL-6 protein levels. This study demonstrated for the first time that BS exhibited potential neuroprotective effects on H<sub>2</sub>O<sub>2</sub>-induced neuronal damage by attenuating inflammation and apoptosis. These findings suggest that BS may be considered a promising candidate in preventing and treating oxidative stress-mediated neurodegenerative diseases.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"777 ","pages":"Article 152255"},"PeriodicalIF":2.5,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144489799","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}
Xue Chen , Anna Mazur , Wei Xu , W. Christopher Risher , Krista L. Denning , Yongke Lu
{"title":"PPARα regulates acyl-CoA oxidase 1 (ACOX1) but not catalase","authors":"Xue Chen , Anna Mazur , Wei Xu , W. Christopher Risher , Krista L. Denning , Yongke Lu","doi":"10.1016/j.bbrc.2025.152247","DOIUrl":"10.1016/j.bbrc.2025.152247","url":null,"abstract":"<div><div>Peroxisomes are membranous organelles, and peroxisomal membrane protein 70 (PMP70), a peroxisome transporter, is used as a marker of peroxisomes. Like mitochondria, peroxisomes can also oxidize fatty acids and its rate limiting enzyme is acyl-CoA oxidase 1 (ACOX1). But unlike mitochondria, peroxisomes generate hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) by ACOX1, and the generated H<sub>2</sub>O<sub>2</sub> is locally detoxified by catalase. PPARα agonist WY-14,643 induces peroxisome proliferation as indicated by the induction of PMP70, ACOX1 and catalase were also induced. However, ACOX1 was induced to a greater extent than catalase. After WY-14,643 withdrawal, the induced ACOX1 started to decrease after 2 days; but catalase remained at higher levels up to10 days. While mRNA levels of ACOX1 were also induced by WY-14,643, mRNA levels of catalase were not induced by WY-14,643. In the livers collected from liver-specific PEX16 knockout (<em>Pex16</em><sup><em>Alb-Cre</em></sup>) mice, peroxisomes are absent but catalase and ACOX1 were somehow upregulated. The mRNA of ACOX1 was also spontaneously elevated, but the catalase mRNA was not changed. When PPARα was abrogated through crossing the <em>Pex16</em><sup><em>Alb-Cre</em></sup> mice with <em>Pparα</em><sup><em>−/−</em></sup> mice to create the <em>Pparα</em><sup><em>−/−</em></sup>/<em>Pex16</em><sup><em>Alb-Cre</em></sup> mice, the upregulated ACOX1 protein was suppressed in the <em>Pparα</em><sup><em>−/−</em></sup>/<em>Pex16</em><sup><em>Alb-Cre</em></sup> mice, but catalase protein remained elevated. These results suggest that ACOX1 but not catalase is regulated by PPARα.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"777 ","pages":"Article 152247"},"PeriodicalIF":2.5,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144489801","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":"Serotonin regulates nutrient-dependent food intake in Drosophila","authors":"Tae Hoon Ryu , Kweon Yu","doi":"10.1016/j.bbrc.2025.152250","DOIUrl":"10.1016/j.bbrc.2025.152250","url":null,"abstract":"<div><div>Serotonin is a key neurotransmitter in feeding behavior. However, its role in regulating food intake based on nutrient composition remains unclear. In this study, we utilized the Drosophila model to investigate the influence of serotonin on feeding behavior. By employing transient thermogenetic tools, we transiently manipulated the activity of serotonergic neurons while minimizing effects on other physiological processes, including sleep. By measuring the intake of sucrose, sucralose, yeast, and tryptone, we evaluated the role of serotonin signaling in nutrient-dependent food intake. Our findings demonstrate that distinct subsets of serotonergic neurons in the subesophageal zone (SEZ) independently regulate the intake of sucrose and protein. Additionally, we identified serotonin receptors <em>5-HT2B</em> and <em>5-HT1A</em> in the mushroom body γ lobes as key modulators of sucrose and protein consumption, respectively. Taken together, our results highlight the role of serotonin in nutrient-specific feeding regulation and provide insights into the neural mechanisms underlying dietary choices.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"777 ","pages":"Article 152250"},"PeriodicalIF":2.5,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144501989","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":"Mitophagy: A double-edged sword in tumor cell death regulation and therapeutic response","authors":"Tong Chu , Zifeng Huang , Wenzhe Ma","doi":"10.1016/j.bbrc.2025.152254","DOIUrl":"10.1016/j.bbrc.2025.152254","url":null,"abstract":"<div><div>Mitophagy, a core mechanism governing cellular homeostasis, plays dual roles in tumorigenesis and therapeutic response by selectively eliminating damaged mitochondria. This review systematically summarizes the molecular mechanisms of mitophagy mediated by receptor-dependent ubiquitin-independent pathways and ubiquitin-dependent pathways, and explores their intricate crosstalk with tumor cell death modalities. Mitophagy dynamically regulates mitochondrial quality to modulate the progression of apoptosis, ferroptosis, necroptosis, immunogenic cell death (ICD), and pyroptosis. Notably, mitophagy exhibits context-dependent roles in tumors: moderate activation suppresses tumor growth by clearing carcinogen-damaged mitochondria, whereas excessive activation may directly induce cell death via functional mitochondrial depletion or synergize with chemotherapy to amplify tumor eradication. Furthermore, this review highlights the challenges in therapeutic strategies targeting the mitophagy-tumor death axis, emphasizing the potential of spatiotemporal-specific regulation and combinatorial interventions across distinct death pathways, thereby providing a theoretical framework for precision oncology.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"777 ","pages":"Article 152254"},"PeriodicalIF":2.5,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144489800","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}
Yanxin Xiang , Min Liang , Mengyao Feng , Yan Peng , Xiaowei Liu , Xingcheng Nie , Xiaoqian He , Luping Yu , Qiaoju Hu , Xiaofei Dong , Wenxing Liu , Changyou Gao
{"title":"Biosafety of hyperbranched polylysine and its regulatory effect on non-alcoholic fatty liver and gut microbiota","authors":"Yanxin Xiang , Min Liang , Mengyao Feng , Yan Peng , Xiaowei Liu , Xingcheng Nie , Xiaoqian He , Luping Yu , Qiaoju Hu , Xiaofei Dong , Wenxing Liu , Changyou Gao","doi":"10.1016/j.bbrc.2025.152253","DOIUrl":"10.1016/j.bbrc.2025.152253","url":null,"abstract":"<div><div>Hyperbranched polylysine (HBPL) has shown broad-spectrum antibacterial activity and cell adhesion promoting effect, which are inherited mainly from its ε- and α-structures, respectively. Although the effectiveness of HBPL in wound anti-infection, tissue regeneration and surface modification has been thoroughly demonstrated, its systematic biosafety evaluation and influence on bacterial cohorts in the gut remain unknown. In this study, the biosafety of HBPL was systematically analyzed <em>via</em> endotoxin detection, cytotoxicity test, and acute systemic toxicity test (oral and intravenous injection). On the basis of its excellent biocompatibility (i.e. endotoxin-free, low cytotoxicity, LD50 (oral) ≥ 5000 mg/kg and intravenous injection safety), HBPL was added to high-fat feed for mice. Serum biochemical and hepatic histopathological results revealed that feeding HBPL can significantly reduce lipid accumulation and thus improve mouse liver functions. Additionally, HBPL assists in optimizing gut microbiota <em>via</em> increasing the abundance of beneficial probiotics, including <em>Akkermansia</em>, <em>Butyricicoccus</em> and <em>Romboutsia</em>. These findings suggest that an appropriate dose of HBPL can significantly ameliorate NAFLD through simultaneous lipase inhibition and gut microbiota modulation, providing new insights into the potential application of HBPL in NAFLD treatment.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"777 ","pages":"Article 152253"},"PeriodicalIF":2.5,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144490187","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":"RFFL inhibition increases cell surface CFTR and reduces IL-8 production in airway epithelial cells upon COPD-associated environmental pathogen exposure","authors":"Daichi Hinata, Shiori Beppu, Yuka Kamada, Tsukasa Okiyoneda","doi":"10.1016/j.bbrc.2025.152251","DOIUrl":"10.1016/j.bbrc.2025.152251","url":null,"abstract":"<div><div>Chronic exposure to environmental pathogens and pollutants can impair CFTR chloride channel function, contributing to chronic obstructive pulmonary disease (COPD). Our previous study demonstrated that pyocyanin (PYO), a COPD-associated pathogen factor, significantly reduces the functional expression of R75Q- or M470V-CFTR, two CFTR polymorphisms found in COPD patients, leading to increased IL-8 production in airway epithelial cells (AEC). In this study, we report that inhibition of RFFL, a ubiquitin ligase that targets CFTR mutants for removal from the plasma membrane (PM), mitigates excessive IL-8 production in AECs expressing R75Q- or M470V-CFTR, even in the presence of PYO. RFFL knockdown (KD) enhanced the functional PM expression of R75Q- or M470V-CFTR under PYO exposure, although it did not prevent PYO-induced CFTR downregulation. Our results indicate that RFFL likely regulates constitutive IL-8 production independently of CFTR, while also modulating pathogen-induced IL-8 expression through a CFTR-dependent mechanism. This highlights the potential of RFFL inhibitors to enhance CFTR function and reduce IL-8 secretion, even amid chronic exposure to environmental pathogens and pollutants, underscoring RFFL inhibition as a promising therapeutic approach for COPD management.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"777 ","pages":"Article 152251"},"PeriodicalIF":2.5,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144490190","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}
Cong Yan , Yongqing Ye , Nan Liu , Dongdong Zhang , Wenzhong Du , Ying Li , GuoFu Li , Chen Li , Jingwei Li , Shengji Ma , Zifeng Dai , ZiYu Xiong , Yuwen Wang , Chunyang Men , Rui Bi , Qianpeng Duan , Weishi Xu , Husilengtu , Yuan Cao , Jiapei Du , Changbin Shi
{"title":"Metformin limits cerebral cavernous malformation development by targeting KLF4-mediated mitochondrial damage","authors":"Cong Yan , Yongqing Ye , Nan Liu , Dongdong Zhang , Wenzhong Du , Ying Li , GuoFu Li , Chen Li , Jingwei Li , Shengji Ma , Zifeng Dai , ZiYu Xiong , Yuwen Wang , Chunyang Men , Rui Bi , Qianpeng Duan , Weishi Xu , Husilengtu , Yuan Cao , Jiapei Du , Changbin Shi","doi":"10.1016/j.bbrc.2025.152241","DOIUrl":"10.1016/j.bbrc.2025.152241","url":null,"abstract":"<div><div>Cerebral cavernous malformations (CCM) present prevalent vascular diseases of the central nervous system, which can result in hemorrhage and seizures. Metformin, a first-line antidiabetic with established safety profiles, demonstrates pleiotropic effects, including the inhibition of cellular proliferation, inflammation, and angiogenesis, all of which are implicated in the pathogenesis of CCM. However, the therapeutic benefits of metformin in the realm of CCM remain unclear. This study aims to investigate the effect of metformin on the growth of CCM lesions in <em>Slco1c1</em> CreERT2; <em>Pdcd10</em> <sup>fl/fl</sup> (<em>Pdcd10</em><sup>BECKO</sup>) mice. Super-resolution confocal microscopy and transmission electron microscopy (TEM) were employed to evaluate mitochondrial structure. The results showed that metformin administration significantly attenuated CCM lesion burden, reduced iron deposition, and decreased collagen accumulation in <em>Pdcd10</em><sup>BECKO</sup> mice. Metformin also normalized the defects from PDCD10 deficiency, including disruption of tight junctions and excessive proliferation of endothelial cells. Moreover, metformin significantly improved mitochondrial structural anomalies and dysfunction associated with PDCD10 deficiency, characterized by the presence of mitochondrial puncta and the loss of cristae, followed by impaired mitochondrial membrane potential and increased mitoROS in endothelial cells with the mutation. Metformin provided these beneficial effects by downregulating KLF4. In conclusion, these findings indicate that metformin suppresses the development of CCM in <em>Pdcd10</em><sup>BECKO</sup> mice by targeting KLF4-mediated mitochondrial damage, thereby providing promising prospects as a novel therapeutic approach for CCM.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"777 ","pages":"Article 152241"},"PeriodicalIF":2.5,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144471722","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}
Jeong-Hwa Baek , Min Ji Bae , Hye Min Kim , Eun Kyoung Shin , Yong Uk Kye , HyoJin Kim , Yeong-Rok Kang , Wol Soon Jo , Joong Sun Kim , Min Kook Kang , Chang Geun Lee
{"title":"Differential toxicity of radiation with different dose-rates between testis and bone marrow cells via the differential regulation of ROS, Ca2+, and mitochondria membrane potential","authors":"Jeong-Hwa Baek , Min Ji Bae , Hye Min Kim , Eun Kyoung Shin , Yong Uk Kye , HyoJin Kim , Yeong-Rok Kang , Wol Soon Jo , Joong Sun Kim , Min Kook Kang , Chang Geun Lee","doi":"10.1016/j.bbrc.2025.152248","DOIUrl":"10.1016/j.bbrc.2025.152248","url":null,"abstract":"<div><div>It is believed that there may be a proportional relationship between the dose-rate and adverse effects of radiation for a given dose. However, we have previously shown that low dose-rate (LDR) radiation induces greater toxicity in the testes than that induced by high-dose rate (HDR) radiation, in contrast to results for the thymic lymphoma induction rate. Since cell/organ toxicity and cancer induction rates may not be directly comparable, we compared toxicities following LDR and HDR radiation between testis/spermatogenesis and bone marrow/hematopoiesis, similar organs/cells in terms of continuously producing progenitor cells. The two organs showed opposite patterns of toxicity due to LDR and HDR radiation, supporting the differential dose-rate effect between the two organs. Furthermore, reactive oxygen species (ROS), Ca<sup>2+</sup> and mitochondria membrane potential (MMP) were specifically regulated between the two organs by LDR and HDR. These results suggest that LDR radiation may enhance toxicity specifically in the testes but not in the bone marrow via the specific regulation of ROS, Ca<sup>2+</sup>, and MMP in single testis/spermatogonia. This report provides the evidence that radiation at different dose rates induces differential toxicity depending on the organ, accompanied by the differential regulation of key cellular parameters, such as ROS, Ca<sup>2+</sup> and MMP.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"777 ","pages":"Article 152248"},"PeriodicalIF":2.5,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144480307","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":"Biochemical characteristics of spacer amino acid determine phase-separating behavior and induction of nucleolar stress by arginine-rich dipeptide repeat proteins","authors":"Tamami Miyagi , Mikiro Nawa , Shinya Kusakari , Rio Yamazaki , Hiroshi Uji-i , Yuhei Hayamizu , Hiroaki Suzuki , Kohsuke Kanekura","doi":"10.1016/j.bbrc.2025.152252","DOIUrl":"10.1016/j.bbrc.2025.152252","url":null,"abstract":"<div><div>Arginine-rich dipeptide repeat proteins (R-DPRs), produced from hexanucleotide repeat expansions via repeat-associated non-AUG translation, are linked to neurodegenerative disorders. While novel, potentially pathogenic R-DPRs have been identified, their intracellular signaling mechanisms remain unclear. To explore their biological roles, we examined R-DPR liquid–liquid phase separation behavior <em>in vitro</em> and their impact on nucleolar function. We found that the spacer hydrophobicity is a key determinant of R-DPR phase separation. Specifically, R-DPRs with hydrophobic spacers formed aggregates with RNA and recombinant nucleophosmin <em>in vitro,</em> inducing nucleolar stress and impairing ribosomal RNA synthesis in cells. These findings provide insights into the mechanisms by which R-DPRs exert nucleolar stress, advancing our understanding of their pathological roles.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"777 ","pages":"Article 152252"},"PeriodicalIF":2.5,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144480265","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":"Structure of quercetin 3,4′-dimethyl ether in complex with tubulin provides a rationale for drug design","authors":"Yang Su , Wei Yan , Jianhong Yang , Falong Yang","doi":"10.1016/j.bbrc.2025.152245","DOIUrl":"10.1016/j.bbrc.2025.152245","url":null,"abstract":"<div><div>Microtubules, composed of αβ-tubulin heterodimers, serve as key targets for anticancer therapeutics due to their critical role in cell division. Numerous compounds have been discovered to interact with tubulin and disrupt microtubule dynamics, particularly those targeting the colchicine-binding domain. Certain flavones, for instance, have demonstrated the ability to bind to this site and suppress microtubule polymerization. Despite their potential, progress in developing flavone-based drugs has been limited by insufficient structural data on tubulin-ligand complexes. Here, we present the high-resolution (1.92 Å) crystal structure of tubulin in complex with a flavone derivative, quercetin 3,4′-dimethyl ether (QU34), elucidating the specific molecular interactions at atomic detail. By analyzing this structure alongside other colchicine-site inhibitors, we clarify prior structure-activity relationship (SAR) findings and offer a framework for designing optimized flavone analogs targeting this site.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"777 ","pages":"Article 152245"},"PeriodicalIF":2.5,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144480305","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}