Biochemical Journal最新文献_第7页

Development of circadian rhythms in mammalian systems. 哺乳动物生理节律的发展。

IF 4.4 3区生物学

Biochemical Journal Pub Date : 2024-12-23 DOI: 10.1042/BCJ20210060

Junghyun Lee, Sevde Goker, Sookkyung Lim, Christian I Hong

引用次数: 0

Gα12 and Gα13 proteins are required for transforming growth factor-β-induced myofibroblast differentiation. TGF-β诱导的肌成纤维细胞分化需要Ga12和Ga13蛋白。

IF 4.4 3区生物学

Biochemical Journal Pub Date : 2024-12-18 DOI: 10.1042/BCJ20240317

Eleanor B Reed, Albert Sitikov, Kun Woo D Shin, Robert B Hamanaka, Rengül Cetin-Atalay, Gökhan M Mutlu, Alexander A Mongin, Nickolai O Dulin

{"title":"Gα12 and Gα13 proteins are required for transforming growth factor-β-induced myofibroblast differentiation.","authors":"Eleanor B Reed, Albert Sitikov, Kun Woo D Shin, Robert B Hamanaka, Rengül Cetin-Atalay, Gökhan M Mutlu, Alexander A Mongin, Nickolai O Dulin","doi":"10.1042/BCJ20240317","DOIUrl":"10.1042/BCJ20240317","url":null,"abstract":"Myofibroblast differentiation, characterized by accumulation of cytoskeletal and extracellular matrix proteins by fibroblasts, is a key process in wound healing and pathogenesis of tissue fibrosis. Transforming growth factor-β (TGF-β) is the most powerful known driver of myofibroblast differentiation. TGF-β signals through transmembrane receptor serine/threonine kinases that phosphorylate Smad transcription factors (Smad2/3) leading to activation of transcription of target genes. Heterotrimeric G proteins mediate distinct signaling from seven-transmembrane G protein coupled receptors, which are not known to be linked to Smad activation. We tested whether G protein signaling plays any role in TGF-β-induced myofibroblast differentiation, using primary cultured human lung fibroblasts. Activation of Gαs by cholera toxin blocked TGF-β-induced myofibroblast differentiation without affecting Smad2/3 phosphorylation. Neither inhibition of Gαi by pertussis toxin nor siRNA-mediated combined knockdown of Gαq and Gα11 had a significant effect on TGF-β-induced myofibroblast differentiation. In contrast, combined knockdown of Gα12 and Gα13 significantly inhibited TGF-β-stimulated expression of myofibroblast marker proteins (collagen-1, fibronectin, smooth-muscle α-actin), with siGα12 being significantly more potent than siGα13. Mechanistically, combined knockdown of Gα12 and Gα13 resulted in substantially reduced phosphorylation of Smad2 and Smad3 in response to TGF-β, which was accompanied by a significant decrease in the expression of TGF-β receptors (TGFBR1, TGFBR2) and of Smad3. Thus, our study uncovers a novel role of Gα12/13 proteins in the control of TGF-β signaling and myofibroblast differentiation.","PeriodicalId":8825,"journal":{"name":"Biochemical Journal","volume":" ","pages":"1937-1948"},"PeriodicalIF":4.4,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11668492/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142765758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Opposing regulation of endoplasmic reticulum retention under stress by ERp44 and PDIA6. 应激下ERp44和PDIA6对内质网保留的反向调控。

IF 4.4 3区生物学

Biochemical Journal Pub Date : 2024-12-18 DOI: 10.1042/BCJ20240444

Olaya Yassin, Bellam Praveen, Odai Darawshi, Thomas LaFramboise, Miriam Shmuel, Shakti P Pattanayak, Brian K Law, Maria Hatzoglou, Boaz Tirosh

{"title":"Opposing regulation of endoplasmic reticulum retention under stress by ERp44 and PDIA6.","authors":"Olaya Yassin, Bellam Praveen, Odai Darawshi, Thomas LaFramboise, Miriam Shmuel, Shakti P Pattanayak, Brian K Law, Maria Hatzoglou, Boaz Tirosh","doi":"10.1042/BCJ20240444","DOIUrl":"10.1042/BCJ20240444","url":null,"abstract":"Conditions of endoplasmic reticulum (ER) stress reduce protein synthesis by provoking translation regulation, governed by the eIF2α kinase PERK. When PERK is inhibited during ER stress, retention of a selective subset of glycoproteins occurs, a phenomenon we termed selective ER retention (sERr). sERr clients are enriched with tyrosine kinase receptors (RTKs), which form large molecular weight disulfide bonded complexes in the ER. The protein disulfide isomerase ERp44 promotes sERr and increases the size of sERr complexes. Here we show that sERr is reversible upon washout. Pulse chase analyses show that upon recovery, only a small fraction of the sERr complexes disintegrates and contributes to the matured proteins, while most are newly synthesized. Sequential inductions of sERr and washouts demonstrate an accelerated recovery that is dependent on the unfolded protein response transducer IRE1. Since IRE1 regulates the expression level PDIA6, we analyzed its contribution to sERr. We found that PDIA6 and ERp44 constitutively interact by disulfides and have opposite effects on resumed recovery of trafficking following removal of sERr conditions. Deletion of ERp44 accelerates, while deletion of PDIA6 slows down recovery with a minimal effect on total protein synthesis. ERp44 is a primary interactor with sERr clients. When missing, PDIA6 partitions more into sERr complexes. Deletion of the tumor suppressor PTEN, which induces RTK signaling, promoted sERr formation kinetics, and accelerated the recovery, suggesting feedback between RTKs signaling and sERr. This study suggests that sERr, should develop physiologically or pathologically, is counteracted by adaptation responses that involve IRE1 and PDIA6.","PeriodicalId":8825,"journal":{"name":"Biochemical Journal","volume":" ","pages":"1921-1935"},"PeriodicalIF":4.4,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142765778","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}

引用次数: 0

On the function of TRAP substrate-binding proteins: the isethionate-specific binding protein IseP. 关于 TRAP 底物结合蛋白的功能：异蛋氨酸特异性结合蛋白 IseP。

IF 4.4 3区生物学

Biochemical Journal Pub Date : 2024-12-18 DOI: 10.1042/BCJ20240540

Michael C Newton-Vesty, Michael J Currie, James S Davies, Santosh Panjikar, Ashish Sethi, Andrew E Whitten, Zachary D Tillett, David M Wood, Joshua D Wright, Michael J Love, Timothy M Allison, Sam A Jamieson, Peter D Mace, Rachel A North, Renwick C J Dobson

{"title":"On the function of TRAP substrate-binding proteins: the isethionate-specific binding protein IseP.","authors":"Michael C Newton-Vesty, Michael J Currie, James S Davies, Santosh Panjikar, Ashish Sethi, Andrew E Whitten, Zachary D Tillett, David M Wood, Joshua D Wright, Michael J Love, Timothy M Allison, Sam A Jamieson, Peter D Mace, Rachel A North, Renwick C J Dobson","doi":"10.1042/BCJ20240540","DOIUrl":"10.1042/BCJ20240540","url":null,"abstract":"Bacteria evolve mechanisms to compete for limited resources and survive in new niches. Here we study the mechanism of isethionate import from the sulfate-reducing bacterium Oleidesulfovibrio alaskensis. The catabolism of isethionate by Desulfovibrio species has been implicated in human disease, due to hydrogen sulfide production, and has potential for industrial applications. O. alaskensis employs a tripartite ATP-independent periplasmic (TRAP) transporter (OaIsePQM) to import isethionate, which relies on the substrate-binding protein (OaIseP) to scavenge isethionate and deliver it to the membrane transporter component (OaIseQM) for import into the cell. We determined the binding affinity of isethionate to OaIseP by isothermal titration calorimetry, KD = 0.95 µM (68% CI = 0.6-1.4 µM), which is weaker compared with other TRAP substrate-binding proteins. The X-ray crystal structures of OaIseP in the ligand-free and isethionate-bound forms were obtained and showed that in the presence of isethionate, OaIseP adopts a closed conformation whereby two domains of the protein fold over the substrate. We serendipitously discovered two crystal forms with sulfonate-containing buffers (HEPES and MES) bound in the isethionate-binding site. However, these do not evoke domain closure, presumably because of the larger ligand size. Together, our data elucidate the molecular details of how a TRAP substrate-binding protein binds a sulfonate-containing substrate, rather than a typical carboxylate-containing substrate. These results may inform future antibiotic development to target TRAP transporters and provide insights into protein engineering of TRAP transporter substrate-binding proteins.","PeriodicalId":8825,"journal":{"name":"Biochemical Journal","volume":" ","pages":"1901-1920"},"PeriodicalIF":4.4,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11668362/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142667211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Ubiquitin E3 ligases in the plant Arg/N-degron pathway. 植物Arg/N-degron通路中的泛素E3连接酶。

IF 4.4 3区生物学

Biochemical Journal Pub Date : 2024-12-18 DOI: 10.1042/BCJ20240132

Keely E A Oldham, Peter D Mabbitt

{"title":"Ubiquitin E3 ligases in the plant Arg/N-degron pathway.","authors":"Keely E A Oldham, Peter D Mabbitt","doi":"10.1042/BCJ20240132","DOIUrl":"10.1042/BCJ20240132","url":null,"abstract":"Regulation of protein longevity via the ubiquitin (Ub) - proteasome pathway is fundamental to eukaryotic biology. Ubiquitin E3 ligases (E3s) interact with substrate proteins and provide specificity to the pathway. A small subset of E3s bind to specific exposed N-termini (N-degrons) and promote the ubiquitination of the bound protein. Collectively these E3s, and other N-degron binding proteins, are known as N-recognins. There is considerable functional divergence between fungi, animal, and plant N-recognins. In plants, at least three proteins (PRT1, PRT6, and BIG) participate in the Arg/N-degron pathway. PRT1 has demonstrated E3 ligase activity, whereas PRT6 and BIG are candidate E3s. The Arg/N-degron pathway plays a central role in plant development, germination, and submersion tolerance. The pathway has been manipulated both to improve crop performance and for conditional protein degradation. A more detailed structural and biochemical understanding of the Arg/N-recognins and their substrates is required to fully realise the biotechnological potential of the pathway. This perspective focuses on the structural and molecular details of substrate recognition and ubiquitination in the plant Arg/N-degron pathway. While PRT1 appears to be plant specific, the PRT6 and BIG proteins are similar to UBR1 and UBR4, respectively. Analysis of the cryo-EM structures of Saccharomyces UBR1 suggests that the mode of ubiquitin conjugating enzyme (E2) and substrate recruitment is conserved in PRT6, but regulation of the two N-recognins may be significantly different. The structurally characterised domains from human UBR4 are also likely to be conserved in BIG, however, there are sizeable gaps in our understanding of both proteins.","PeriodicalId":8825,"journal":{"name":"Biochemical Journal","volume":"481 24","pages":"1949-1965"},"PeriodicalIF":4.4,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11668491/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

USP10 deubiquitinates and stabilizes CD44 leading to enhanced breast cancer cell proliferation, stemness and metastasis. USP10 可使 CD44 去泛素化和稳定化，从而增强乳腺癌细胞的增殖、干性和转移。

IF 4.4 3区生物学

Biochemical Journal Pub Date : 2024-12-18 DOI: 10.1042/BCJ20240611

Arppita Sethi, Shivkant Mishra, Vishal Upadhyay, Parul Dubey, Shumaila Siddiqui, Anil Kumar Singh, Sangita Chowdhury, Swati Srivastava, Pragya Srivastava, Prasannajit Sahoo, Madan L B Bhatt, Anand Mishra, Arun Kumar Trivedi

{"title":"USP10 deubiquitinates and stabilizes CD44 leading to enhanced breast cancer cell proliferation, stemness and metastasis.","authors":"Arppita Sethi, Shivkant Mishra, Vishal Upadhyay, Parul Dubey, Shumaila Siddiqui, Anil Kumar Singh, Sangita Chowdhury, Swati Srivastava, Pragya Srivastava, Prasannajit Sahoo, Madan L B Bhatt, Anand Mishra, Arun Kumar Trivedi","doi":"10.1042/BCJ20240611","DOIUrl":"10.1042/BCJ20240611","url":null,"abstract":"Despite extensive research, strategies to effectively combat breast cancer stemness and achieve a definitive cure remains elusive. CD44, a well-defined cancer stem cell (CSC) marker is reported to promote breast cancer tumorigenesis, metastasis, and chemoresistance. However, mechanisms leading to its enhanced expression and function is poorly understood. Here, we demonstrate that USP10 positively regulates CD44 protein levels and its downstream actions. While USP10 depletion prominently down-regulates CD44 protein levels and functions, its overexpression significantly enhances CD44 protein levels, leading to enhanced cluster tumor cell formation, stemness, and metastasis in breast cancer cells both in vitro and ex vivo in primary human breast tumor cells. USP10 interacts with CD44 and stabilizes it through deubiquitination both in breast cancer cell lines and human breast cancer-derived primary tumor cells. Stabilized CD44 shows enhanced interaction with cytoskeleton proteins Ezrin/Radixin/Moesin and potently activates PDGFRβ/STAT3 signaling which are involved in promoting CSC traits. Using USP10 stably expressing 4T1 cells, we further demonstrate that the USP10-CD44 axis potently promotes tumorigenicity in vivo in mice, while simultaneous depletion of CD44 in these cells renders them ineffective. In line with these findings, we further showed that inhibition of USP10 either through RNAi or the pharmacological inhibitor Spautin-1 significantly mitigated CD44 levels and its downstream function ex vivo in primary breast tumor cells. Finally, we demonstrated that primary breast tumor cells are more susceptible to chemotherapy when co-treated with USP10 inhibitor indicating that the USP10-CD44 axis could be an attractive therapeutic target in combination with chemotherapy in CD44 expressing breast cancers.","PeriodicalId":8825,"journal":{"name":"Biochemical Journal","volume":" ","pages":"1877-1900"},"PeriodicalIF":4.4,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142674935","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}

引用次数: 0

Biochemical basis and therapeutic potential of mitochondrial uncoupling in cardiometabolic syndrome. 线粒体解偶联在心脏代谢综合征中的生化基础和治疗潜力。

IF 4.4 3区生物学

Biochemical Journal Pub Date : 2024-12-04 DOI: 10.1042/BCJ20240005

Bernardo Gindri Dos Santos, Niki F Brisnovali, Leigh Goedeke

{"title":"Biochemical basis and therapeutic potential of mitochondrial uncoupling in cardiometabolic syndrome.","authors":"Bernardo Gindri Dos Santos, Niki F Brisnovali, Leigh Goedeke","doi":"10.1042/BCJ20240005","DOIUrl":"10.1042/BCJ20240005","url":null,"abstract":"Mild uncoupling of oxidative phosphorylation is an intrinsic property of all mitochondria, allowing for adjustments in cellular energy metabolism to maintain metabolic homeostasis. Small molecule uncouplers have been extensively studied for their potential to increase metabolic rate, and recent research has focused on developing safe and effective mitochondrial uncoupling agents for the treatment of obesity and cardiometabolic syndrome (CMS). Here, we provide a brief overview of CMS and cover the recent mechanisms by which chemical uncouplers regulate CMS-associated risk-factors and comorbidities, including dyslipidemia, insulin resistance, steatotic liver disease, type 2 diabetes, and atherosclerosis. Additionally, we review the current landscape of uncoupling agents, focusing on repurposed FDA-approved drugs and compounds in advanced preclinical or early-stage clinical development. Lastly, we discuss recent molecular insights by which chemical uncouplers enhance cellular energy expenditure, highlighting their potential as a new addition to the current CMS drug landscape, and outline several limitations that need to be addressed before these agents can successfully be introduced into clinical practice.","PeriodicalId":8825,"journal":{"name":"Biochemical Journal","volume":"481 23","pages":"1831-1854"},"PeriodicalIF":4.4,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142765735","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}

引用次数: 0

Macromolecular crowding and bicarbonate enhance the hydrogen peroxide-induced inactivation of glyceraldehyde-3-phosphate dehydrogenase. 大分子拥挤和碳酸氢盐会增强过氧化氢诱导的甘油醛-3-磷酸脱氢酶失活。

IF 4.4 3区生物学

Biochemical Journal Pub Date : 2024-12-04 DOI: 10.1042/BCJ20240597

Rebecca H J Bloemen, Rafael Radi, Michael J Davies, Eduardo Fuentes-Lemus

{"title":"Macromolecular crowding and bicarbonate enhance the hydrogen peroxide-induced inactivation of glyceraldehyde-3-phosphate dehydrogenase.","authors":"Rebecca H J Bloemen, Rafael Radi, Michael J Davies, Eduardo Fuentes-Lemus","doi":"10.1042/BCJ20240597","DOIUrl":"10.1042/BCJ20240597","url":null,"abstract":"The active site Cys residue in glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is sensitive to oxidation by hydrogen peroxide (H2O2), with this resulting in enzyme inactivation. This re-routes the carbon flux from glycolysis to the pentose phosphate pathway favoring the formation of NADPH and synthetic intermediates required for antioxidant defense and repair systems. Consequently, GAPDH inactivation serves as a redox switch for metabolic adaptation under conditions of oxidative stress. However, there is a major knowledge gap as to how GAPDH is efficiently oxidized and inactivated, when the increase in intracellular H2O2 is modest, and there is a high concentration of alternative (non-signaling) thiols and efficient peroxide removing systems. We have therefore explored whether GAPDH inactivation is enhanced by two factors of in vivo relevance: macromolecular crowding, an inherent property of biological environments, and the presence of bicarbonate, an abundant biological buffer. Bicarbonate is already known to modulate H2O2 metabolism via formation of peroxymonocarbonate. GAPDH activity was assessed in experiments with low doses of H2O2 under both dilute and crowded conditions (induced by inert high molecular mass polymers and small molecules), in both the absence and presence of 25 mM sodium bicarbonate. H2O2-induced inactivation of GAPDH was observed to be significantly enhanced under macromolecular crowding conditions, with bicarbonate having an additional effect. These data strongly suggest that these two factors are of major importance in redox switch mechanisms involving GAPDH (and possibly other thiol-dependent systems) within the cellular environment.","PeriodicalId":8825,"journal":{"name":"Biochemical Journal","volume":" ","pages":"1855-1866"},"PeriodicalIF":4.4,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11668361/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142646879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Editorial Note: Camelid single-domain antibodies raised by DNA immunization are potent inhibitors of EGFR signaling. 编辑注：DNA免疫引起的骆驼单域抗体是EGFR信号传导的有效抑制剂。

IF 4.4 3区生物学

Biochemical Journal Pub Date : 2024-12-04 DOI: 10.1042/BCJ20180795_EDN

引用次数: 0

Investigating the differential structural organization and gene expression regulatory networks of lamin A Ig fold domain mutants of muscular dystrophy. 研究肌肉萎缩症的层粘连A Ig折叠结构域突变体的不同结构组织和基因表达调控网络。

IF 4.4 3区生物学

Biochemical Journal Pub Date : 2024-12-04 DOI: 10.1042/BCJ20240474

Subarna Dutta, Vikas Kumar, Arnab Barua, Madavan Vasudevan

{"title":"Investigating the differential structural organization and gene expression regulatory networks of lamin A Ig fold domain mutants of muscular dystrophy.","authors":"Subarna Dutta, Vikas Kumar, Arnab Barua, Madavan Vasudevan","doi":"10.1042/BCJ20240474","DOIUrl":"10.1042/BCJ20240474","url":null,"abstract":"Lamins form a proteinaceous meshwork as a major structural component of the nucleus. Lamins, along with their interactors, act as determinants for chromatin organization throughout the nucleus. The major dominant missense mutations responsible for autosomal dominant forms of muscular dystrophies reside in the Ig fold domain of lamin A. However, how lamin A contributes to the distribution of heterochromatin and balances euchromatin, and how it relocates epigenetic marks to shape chromatin states, remains poorly defined, making it difficult to draw conclusions about the prognosis of lamin A-mediated muscular dystrophies. In the first part of this report, we identified the in vitro organization of full-length lamin A proteins due to two well-documented Ig LMNA mutations, R453W and W514R. We further demonstrated that both lamin A/C mutant cells predominantly expressed nucleoplasmic aggregates. Labeling specific markers of epigenetics allowed correlation of lamin A mutations with epigenetic mechanisms. In addition to manipulating epigenetic mechanisms, our proteomic studies traced diverse expressions of transcription regulators, RNA synthesis and processing proteins, protein translation components, and posttranslational modifications. These data suggest severe perturbations in targeting other proteins to the nucleus.","PeriodicalId":8825,"journal":{"name":"Biochemical Journal","volume":" ","pages":"1803-1827"},"PeriodicalIF":4.4,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142602290","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}

引用次数: 0