Biochimica et biophysica acta. Molecular cell research最新文献_第4页

Insights into early cochlear damage induced by potassium channel deficiency 钾通道缺乏致早期耳蜗损伤的研究进展。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2025-08-05 DOI: 10.1016/j.bbamcr.2025.120030

Ezequiel Rías , Camila Carignano , Valeria C. Castagna , Leonardo Dionisio , Jimena A. Ballestero , Giuliana Paolillo , Ingrid Ouwerkerk , María Eugenia Gomez-Casati , Guillermo Spitzmaul

{"title":"Insights into early cochlear damage induced by potassium channel deficiency","authors":"Ezequiel Rías , Camila Carignano , Valeria C. Castagna , Leonardo Dionisio , Jimena A. Ballestero , Giuliana Paolillo , Ingrid Ouwerkerk , María Eugenia Gomez-Casati , Guillermo Spitzmaul","doi":"10.1016/j.bbamcr.2025.120030","DOIUrl":"10.1016/j.bbamcr.2025.120030","url":null,"abstract":"<div><div>Hearing loss (HL) is the most common sensory disorder, caused by genetic mutations and acquired factors like presbycusis and noise exposure. A critical factor in HL development is the dysfunction of potassium (K<sup>+</sup>) channels, essential for sensory cell function in the organ of Corti (OC). Inner and outer hair cells (IHCs and OHCs) convert sound into electrical signals, while supporting cells (SCs) maintain ionic and structural balance. KCNQ4 channels, located in the basal membrane of OHCs, regulate K<sup>+</sup> efflux. Mutations in KCNQ4 are linked to progressive HL (DFNA2), noise-induced hearing loss, and presbycusis, leading to K<sup>+</sup> accumulation, cellular stress, and OHC death. Gene editing or pharmacological activation of KCNQ4 has shown potential in partially preventing HL in mouse models. In this study, we demonstrate KCNQ4 deletion disrupts the localization of key proteins like prestin and BK channels, alters OHC organization, and induces apoptosis in sensory and SC. Spiral ganglion neurons (SGNs) also degenerate over time. Despite these structural changes, noise exposure does not exacerbate OHC damage in our KCNQ4-deficient model. This highlights KCNQ4's role in maintaining ion homeostasis and cochlear function, as its absence triggers widespread dysfunction in the OC. The present study demonstrates that disruptions in a single cell type can have a cascade effect on overall cochlear health. Understanding the molecular and cellular consequences of KCNQ4 mutations is crucial for developing targeted therapies to mitigate progressive HL caused by genetic and environmental factors.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 8","pages":"Article 120030"},"PeriodicalIF":3.7,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144768259","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

MicroRNA-22-3p suppresses hair regrowth in androgenetic alopecia by targeting chloride intracellular channel 4 MicroRNA-22-3p通过靶向氯离子胞内通道4抑制雄激素性脱发的毛发再生

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2025-07-31 DOI: 10.1016/j.bbamcr.2025.120033

Haijing Fu , Chenxi Wu , Tianyi Xu , Wumei Zhao , Leiwei Jiang , Shijun Shan

{"title":"MicroRNA-22-3p suppresses hair regrowth in androgenetic alopecia by targeting chloride intracellular channel 4","authors":"Haijing Fu , Chenxi Wu , Tianyi Xu , Wumei Zhao , Leiwei Jiang , Shijun Shan","doi":"10.1016/j.bbamcr.2025.120033","DOIUrl":"10.1016/j.bbamcr.2025.120033","url":null,"abstract":"<div><div>Androgenetic alopecia (AGA), the most prevalent form of patterned hair loss, manifests through androgen sensitivity, age-dependent progression, and genetic predisposition. Emerging evidence highlights microRNAs as critical post-transcriptional regulators in hair follicle pathophysiology. This study used human hair follicle stem cells (HFSCs), hair follicle samples of AGA patients and AGA mouse model to explore the role of miR-22-3p/CLIC4 signaling in AGA. A significant rise in miR-22-3p expression was observed in balding hair follicles of grade 5 AGA patients. Then we identify chloride intracellular channel 4 (CLIC4) as a novel target of miR-22-3p and CLIC4 is markedly low expressed in balding hair follicle of AGA patients. Functional studies demonstrated that knockdown CLIC4 (shCLIC4) impaired HFSCs proliferative capacity and disrupted sonic hedgehog (SHH) pathway activation, evidenced by decreased Gli1 and Gli2 transcriptional activity. These findings establish the miR-22-3p/CLIC4 axis as a novel regulator of hair follicular miniaturization, proposing CLIC4-mediated SHH modulation as a potential therapeutic target for AGA intervention.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 8","pages":"Article 120033"},"PeriodicalIF":3.7,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144766740","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

SYT13: An underestimated synaptotagmin SYT13：一种被低估的突触联合蛋白

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2025-07-30 DOI: 10.1016/j.bbamcr.2025.120031

Johannes Lehmann , Alberto Catanese

引用次数: 0

HMGB1 activates caspase-1 and induces hepatic stellate cell activation via GABPA-ASC HMGB1激活caspase-1，通过GABPA-ASC诱导肝星状细胞活化

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2025-07-30 DOI: 10.1016/j.bbamcr.2025.120032

Mengjia Jing , Yixing Luo , Lumiao Zhang , Yu Fu , Wei Yan

{"title":"HMGB1 activates caspase-1 and induces hepatic stellate cell activation via GABPA-ASC","authors":"Mengjia Jing , Yixing Luo , Lumiao Zhang , Yu Fu , Wei Yan","doi":"10.1016/j.bbamcr.2025.120032","DOIUrl":"10.1016/j.bbamcr.2025.120032","url":null,"abstract":"<div><div>In the intricate process leading to liver fibrosis, which frequently correlates with inflammation, the activation of hepatic stellate cells (HSCs) is critical. High mobility group box 1(HMGB1), as endogenous danger signal in the extracellular environment, governs the activation of caspase-1 and hepatic stellate cell. Constructing a liver fibrosis model via intraperitoneal thioacetamide (TAA) administration unveiled excessive HMGB1 expression and serum release during the TAA-induced fibrosis progression. Intraperitoneal injection of ethyl pyruvate (EP, which inhibits the release of HMGB1) or AAV-shHMGB1 can significantly reverse the progression of liver fibrosis induced by TAA. Recombinant HMGB1 (rHMGB1) and <em>Z</em>-YVAD-FMK (Caspase-1 inhibitor) were used to treat HSCs. It was found that HMGB1 could activate caspase-1, while Z-YVAD-FMK could prevent HMGB1-induced activation of HSCs. Through immunofluorescence, immunoblotting, lentiviral transfection, luciferase reporter assay and chromatin immunoprecipitation assay, it was found that HMGB1 activated caspase-1 through GABPA-regulated ASC transcription, which not only participates in the activation of caspase-1, but also promotes the process of liver fibrosis. Taken together, HMGB1 significantly drives HSC activation. It boosts ASC transcriptional activity via GABPA leading to caspase-1 activation and fostering liver fibrosis development.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 8","pages":"Article 120032"},"PeriodicalIF":3.7,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144757271","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

Corrigendum to “USP47 enhances NRP1-mediated angiogenesis to promote gastric cancer progression” [Volume 1872, Issue 7, October 2025, 120004] “USP47增强nrp1介导的血管生成以促进胃癌进展”的勘误表[1872卷，第7期，2025年10月，120004]。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2025-07-23 DOI: 10.1016/j.bbamcr.2025.120025

Wei Chen , Huizhi Wang , Haitao Sun , Junbo Zuo , Pengcheng Jiang , Wen Feng , Zhenhua Huang

引用次数: 0

XCL1: a multifunctional chemokine with metamorphic properties and therapeutic potential after injury to the nervous system – review XCL1：一种具有神经系统损伤后变质特性和治疗潜力的多功能趋化因子。

IF 4.6 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2025-07-21 DOI: 10.1016/j.bbamcr.2025.120028

Agata Ciechanowska, Joanna Mika

{"title":"XCL1: a multifunctional chemokine with metamorphic properties and therapeutic potential after injury to the nervous system – review","authors":"Agata Ciechanowska, Joanna Mika","doi":"10.1016/j.bbamcr.2025.120028","DOIUrl":"10.1016/j.bbamcr.2025.120028","url":null,"abstract":"<div><div>XC Motif Chemokine Ligand 1 (XCL1, known as lymphotactin), acting via XCR1, is a member of the chemokine family which includes molecules with chemotactic functions. However, subsequent years of research on this chemokine, while simultaneously exploring and understanding the complexity of the processes taking place in living organisms, have revealed a plethora of interesting information about its properties. This review aims to combine the current knowledge on the properties of XCL1 under pathological conditions, particularly in neuropathy. We wanted to draw attention to the unusual properties of XCL1 that have not yet been considered, such as its metamorphic properties and its mutual connections with glycosaminoglycans and integrin subunit alpha 9 (ITGA9). Furthermore, given the well-documented roles of XCL1 in the coordination of homeostatic and immune responses, we anticipate that a comprehensive understanding of the molecular interactions regulating XCL1 binding and activation of its receptors may facilitate the development of novel drugs targeting XCR1 or ITGA9 in various diseases. This point of view may be of great importance in the future for the modulation of systems related to this chemokine for therapeutic applications. This review aims to outline new areas of interest, to break out of following old patterns and dead ends and to sketch further research paths.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 7","pages":"Article 120028"},"PeriodicalIF":4.6,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144697507","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

Histone deacetylase 11 regulates stress granule formation to promote endothelial-to-mesenchymal transition in atherosclerosis 组蛋白去乙酰化酶11调节应激颗粒形成，促进动脉粥样硬化中内皮向间质转化。

IF 4.6 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2025-07-19 DOI: 10.1016/j.bbamcr.2025.120026

Lingxuan Ren , Yizhen Liu , Danli Chen , Xiaoyu Rong , Jiazheng Wen , Zihan Zheng , Lifang Chen , Jianyu He , Weirong Wang , Rong Lin

{"title":"Histone deacetylase 11 regulates stress granule formation to promote endothelial-to-mesenchymal transition in atherosclerosis","authors":"Lingxuan Ren , Yizhen Liu , Danli Chen , Xiaoyu Rong , Jiazheng Wen , Zihan Zheng , Lifang Chen , Jianyu He , Weirong Wang , Rong Lin","doi":"10.1016/j.bbamcr.2025.120026","DOIUrl":"10.1016/j.bbamcr.2025.120026","url":null,"abstract":"<div><div>Histone deacetylase 11 (HDAC11) is the only member of the class IV HDAC family and is involved in cardiovascular diseases (CVDs). Stress granule (SG) is non-membranous cytoplasmic foci induced by various stress conditions, and also has emerged as a key player for CVDs. However, the regulatory role of HDAC11 in SG formation and underlying mechanism during atherosclerosis remain elusive. Therefore, we aimed to investigate the effect of HDAC11 on SG in ApoE<sup>−/−</sup> mice fed with a HFD and HUVECs induced by H<sub>2</sub>O<sub>2</sub>. Firstly, we found that the expression levels of SG core proteins G3BP1/2 and HDAC11 were increased in the aorta of ApoE<sup>−/−</sup> mice fed with a HFD for 12w via analyses of Western blotting, Real-time PCR and immunofluorescence staining. In addition, endothelial-to-mesenchymal transition (EndMT) was occurred in the aorta of ApoE<sup>−/−</sup> mice. Then, in vitro experiments demonstrated that treatment of HUVECs with H<sub>2</sub>O<sub>2</sub> resulted in SG formation, HDAC11 upregulation, and EndMT occurrence. Furthermore, knockdown of HDAC11 by siRNA significantly attenuated SG formation and EndMT activation in HUVECs induced by H<sub>2</sub>O<sub>2</sub>. Silencing of HDAC11 suppressed H<sub>2</sub>O<sub>2</sub>-induced EndMT activation in HUVECs, which may be attributed to increased acetylation of G3BP1/2 and the consequent impairment of SG formation. Further studies found that suppression of SG formation not only facilitated the expression of endothelial markers, but also decreased the levels of mesenchymal cell markers. Taken together, these findings identified that HDAC11 may regulate SG formation to promote EndMT in atherosclerosis, targeting SG could represent a novel therapeutic strategy for addressing the underlying mechanisms of atherosclerosis.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 7","pages":"Article 120026"},"PeriodicalIF":4.6,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144681929","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

The thylakoidal Tat receptor complex appears as a homo-trimeric TatC core with three associated TatB subunits 类囊体Tat受体复合物表现为具有三个相关TatB亚基的同源三聚体TatC核心。

IF 4.6 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2025-07-18 DOI: 10.1016/j.bbamcr.2025.120024

Matthias Reimers , Mario Jakob , Ralf Bernd Klösgen

{"title":"The thylakoidal Tat receptor complex appears as a homo-trimeric TatC core with three associated TatB subunits","authors":"Matthias Reimers , Mario Jakob , Ralf Bernd Klösgen","doi":"10.1016/j.bbamcr.2025.120024","DOIUrl":"10.1016/j.bbamcr.2025.120024","url":null,"abstract":"<div><div>The Twin-arginine translocation (Tat) machinery, which is found in most cellular membranes containing a respiratory or photosynthetic electron transport chain, is characterized by its unique ability to catalyze membrane transport of folded proteins without impairing the membrane potential. In plant thylakoids, Tat machinery consists of three subunits, TatA, TatB, and TatC, with the latter two, TatB and TatC, forming membrane-integral multimeric TatBC receptor complexes. Here we have analyzed the stability and the subunit composition of these complexes after solubilization of thylakoids with the mild detergent digitonin as well as after additional affinity-purification. Employing different detergent combinations and/or heat treatment (40 °C) followed by BN-PAGE and Western analysis we could identify four distinct Tat complexes with apparent molecular masses ranging from approximately 230 kDa to 620 kDa. Treatment of the largest Tat complex with either heat or detergents like DDM or Triton X-114 led to its stepwise breakdown into the three smaller complexes resulting from the successive release of TatB subunits from a relatively stable TatC core complex. From these data we postulate that the fully assembled, physiologically active TatBC receptor complex consists of a stable, trimeric TatC core to which three TatB subunits are bound independently from each other.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 7","pages":"Article 120024"},"PeriodicalIF":4.6,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144673877","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

M6A-mediated uc003pes.1 stability regulates proliferation and migration of human coronary artery smooth muscle cells via scaffolding STAT1 and USP10 M6A-mediated uc003pes。1稳定性通过支架STAT1和USP10调控人冠状动脉平滑肌细胞的增殖和迁移。

IF 4.6 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2025-07-15 DOI: 10.1016/j.bbamcr.2025.120023

Rongli Jiang , Qiaowei Jia , Chengcheng Li , Shu He , Hanxiao Zhou , Mengmeng Ren , Lanyu Liang , Enzhi Jia

{"title":"M6A-mediated uc003pes.1 stability regulates proliferation and migration of human coronary artery smooth muscle cells via scaffolding STAT1 and USP10","authors":"Rongli Jiang , Qiaowei Jia , Chengcheng Li , Shu He , Hanxiao Zhou , Mengmeng Ren , Lanyu Liang , Enzhi Jia","doi":"10.1016/j.bbamcr.2025.120023","DOIUrl":"10.1016/j.bbamcr.2025.120023","url":null,"abstract":"<div><h3>Background</h3><div>The <em>uc003pes.1</em> has been identified as a potential diagnostic biomarker for coronary artery disease (CAD) and is associated with the risk of CAD. However, the precise function and intricate mechanism of <em>uc003pes.1</em> in CAD remain elusive.</div></div><div><h3>Methods</h3><div>To elucidate the underlying mechanism we employed various techniques including RNA pull-down assays coupled with mass spectrometry analysis, RIP, RNA MeRIP, as well as luciferase reporter gene analysis.</div></div><div><h3>Results</h3><div>Overexpression of uc003pes.1 suppressed the proliferation and migration of HCASMCs. The upregulation of uc003pes.1 can be attributed to m6A modification mediated by the methylase RBM15. In terms of downstream mechanisms, uc003pes.1 acts as a molecular scaffold facilitating the interaction between STAT1 and the USP10, thereby impeding ubiquitination degradation of STAT1 and promoting phosphorylation levels at Tyr701 and Ser727, ultimately influencing HCASMCs' proliferation and migration.</div></div><div><h3>Conclusion</h3><div>Our study has discovered, for the first time, that uc003pes.1, regulated by m6A modification, functions as a molecular scaffold for STAT1 and USP10. This interaction plays a crucial role in regulating the proliferation and migration of HCASMCs, thereby offering novel insights into the diagnosis and treatment of CAD.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 7","pages":"Article 120023"},"PeriodicalIF":4.6,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144648360","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

GRK5 regulates mitotic progression and promotes resistance against anti-mitotic agents in a CDK1 and AKT1 dependent manner GRK5以CDK1和AKT1依赖的方式调节有丝分裂进程并促进对抗有丝分裂药物的抗性。

IF 4.6 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2025-07-13 DOI: 10.1016/j.bbamcr.2025.120020

Nusrat Nabi , Syed Qaaifah Gillani , Marjan Fatima , Misbah Un Nisa , Zarka Sarwar , Sameer Ahmed Bhat , Irfana Reshi , Shareen Bashir , Fazl Q Parray , Shaida Andrabi

{"title":"GRK5 regulates mitotic progression and promotes resistance against anti-mitotic agents in a CDK1 and AKT1 dependent manner","authors":"Nusrat Nabi , Syed Qaaifah Gillani , Marjan Fatima , Misbah Un Nisa , Zarka Sarwar , Sameer Ahmed Bhat , Irfana Reshi , Shareen Bashir , Fazl Q Parray , Shaida Andrabi","doi":"10.1016/j.bbamcr.2025.120020","DOIUrl":"10.1016/j.bbamcr.2025.120020","url":null,"abstract":"<div><div>G protein receptor kinase 5 (GRK5) is a serine/threonine protein kinase that belongs to the family of G protein receptor kinases (GRKs), which are important regulators of G protein-coupled receptor (GPCR) functions. GRK5 regulates signaling by binding to various receptors on the plasma membrane or by regulating transcription within the nucleus. It also has been found to critically regulate several physiological processes including vascular remodelling, invasion, metastasis and migration of the cells. Although its role in cancer progression and metastasis is known, its role in cell division, and particularly in mitosis has not been investigated much. Here, we report that GRK5 is an important mitotic protein and is regulated by well-known cellular proteins that have a critical role in cell cycle regulation, especially mitosis. In particular, we show that GRK5 is regulated by two key players of mitosis, AKT1 and CDK1, which regulate GRK5 by interacting with it. We also provide evidence that GRK5 protein levels fluctuate throughout the cell cycle and reach their maximum during mitosis. Further, we report that overexpression of GRK5 promotes resistance against cell death that is induced by polyomavirus small T (PolST) antigen and different chemotherapeutic drugs including paclitaxel. Additionally, we found that GRK5 levels are upregulated in colorectal cancers supporting a potential role in tumor progression. Our findings thus add GRK5 to the growing list of mitotic kinases, which play a role in the regulation of cell cycle and promotion of drug resistance in cancer.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 7","pages":"Article 120020"},"PeriodicalIF":4.6,"publicationDate":"2025-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641644","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