Biochimica et biophysica acta. Molecular cell research最新文献

{"title":"Interactions with sulfur acceptors modulate the reactivity of cysteine desulfurases and define their physiological functions","authors":"Jimmy Swindell,&nbsp;Patricia C. Dos Santos","doi":"10.1016/j.bbamcr.2024.119794","DOIUrl":"10.1016/j.bbamcr.2024.119794","url":null,"abstract":"<div><p>Sulfur-containing biomolecules such as [Fe<img>S] clusters, thiamin, biotin, molybdenum cofactor, and sulfur-containing tRNA nucleosides are essential for various biochemical reactions. The amino acid <span>l</span>-cysteine serves as the major sulfur source for the biosynthetic pathways of these sulfur-containing cofactors in prokaryotic and eukaryotic systems. The first reaction in the sulfur mobilization involves a class of pyridoxal-5′-phosphate (PLP) dependent enzymes catalyzing a Cys:sulfur acceptor sulfurtransferase reaction. The first half of the catalytic reaction involves a PLP-dependent C<img>S bond cleavage, resulting in a persulfide enzyme intermediate. The second half of the reaction involves the subsequent transfer of the thiol group to a specific acceptor molecule, which is responsible for the physiological role of the enzyme. Structural and biochemical analysis of these Cys sulfurtransferase enzymes shows that specific protein-protein interactions with sulfur acceptors modulate their catalytic reactivity and restrict their biochemical functions.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1871 7","pages":"Article 119794"},"PeriodicalIF":4.6,"publicationDate":"2024-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141733470","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}

{"title":"Corrigendum to “Mitochondrial DNA has a pro-inflammatory role in AMD” [Biochim. Biophys. Acta 1853 (2015) 2897-2906]","authors":"","doi":"10.1016/j.bbamcr.2024.119790","DOIUrl":"10.1016/j.bbamcr.2024.119790","url":null,"abstract":"","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1871 8","pages":"Article 119790"},"PeriodicalIF":4.6,"publicationDate":"2024-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141465887","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}

{"title":"Proteomic strategies to interrogate the Fe-S proteome","authors":"Daniel W. Bak,&nbsp;Eranthie Weerapana","doi":"10.1016/j.bbamcr.2024.119791","DOIUrl":"10.1016/j.bbamcr.2024.119791","url":null,"abstract":"<div><p>Iron‑sulfur (Fe-S) clusters, inorganic cofactors composed of iron and sulfide, participate in numerous essential redox, non-redox, structural, and regulatory biological processes within the cell. Though structurally and functionally diverse, the list of all proteins in an organism capable of binding one or more Fe-S clusters is referred to as its Fe-S proteome. Importantly, the Fe-S proteome is highly dynamic, with continuous cluster synthesis and delivery by complex Fe-S cluster biogenesis pathways. This cluster delivery is balanced out by processes that can result in loss of Fe-S cluster binding, such as redox state changes, iron availability, and oxygen sensitivity. Despite continued expansion of the Fe-S protein catalogue, it remains a challenge to reliably identify novel Fe-S proteins. As such, high-throughput techniques that can report on native Fe-S cluster binding are required to both identify new Fe-S proteins, as well as characterize the <em>in vivo</em> dynamics of Fe-S cluster binding. Due to the recent rapid growth in mass spectrometry, proteomics, and chemical biology, there has been a host of techniques developed that are applicable to the study of native Fe-S proteins. This review will detail both the current understanding of the Fe-S proteome and Fe-S cluster biology as well as describing state-of-the-art proteomic strategies for the study of Fe-S clusters within the context of a native proteome</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1871 7","pages":"Article 119791"},"PeriodicalIF":4.6,"publicationDate":"2024-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141454986","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}

{"title":"Unraveling radiation-induced skeletal muscle damage: Insights from a 3D human skeletal muscle organoid model","authors":"Yifei Jiang ,&nbsp;Runtao Zhou ,&nbsp;Fawei Liao ,&nbsp;Ganggang Kong ,&nbsp;Jingguang Zeng ,&nbsp;Yixun Wu ,&nbsp;Xubo Li ,&nbsp;Bo Wang ,&nbsp;Fangze Qi ,&nbsp;Shiju Chen ,&nbsp;Qintang Zhu ,&nbsp;Liqiang Gu ,&nbsp;Canbin Zheng","doi":"10.1016/j.bbamcr.2024.119792","DOIUrl":"10.1016/j.bbamcr.2024.119792","url":null,"abstract":"<div><h3>Background</h3><p>Three-dimensional (3D) organoids derived from human pluripotent stem cells (hPSCs) have revolutionized <em>in vitro</em> tissue modeling, offering a unique opportunity to replicate physiological tissue organization and functionality. This study investigates the impact of radiation on skeletal muscle response using an innovative <em>in vitro</em> human 3D skeletal muscle organoids (hSMOs) model derived from hPSCs.</p></div><div><h3>Methods</h3><p>The hSMOs model was established through a differentiation protocol faithfully recapitulating embryonic myogenesis and maturation <em>via</em> paraxial mesodermal differentiation of hPSCs. Key skeletal muscle characteristics were confirmed using immunofluorescent staining and RT-qPCR. Subsequently, the hSMOs were exposed to a clinically relevant dose of 2 Gy of radiation, and their response was analyzed using immunofluorescent staining and RNA-seq.</p></div><div><h3>Results</h3><p>The hSMO model faithfully recapitulated embryonic myogenesis and maturation, maintaining key skeletal muscle characteristics. Following exposure to 2 Gy of radiation, histopathological analysis revealed deficits in hSMOs expansion, differentiation, and repair response across various cell types at early (30 min) and intermediate (18 h) time points post-radiation. Immunofluorescent staining targeting γH2AX and 53BP1 demonstrated elevated levels of foci per cell, particularly in PAX7⁺ cells, during early and intermediate time points, with a distinct kinetic pattern showing a decrease at 72 h. RNA-seq data provided comprehensive insights into the DNA damage response within the hSMOs.</p></div><div><h3>Conclusions</h3><p>Our findings highlight deficits in expansion, differentiation, and repair response in hSMOs following radiation exposure, enhancing our understanding of radiation effects on skeletal muscle and contributing to strategies for mitigating radiation-induced damage in this context.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1871 7","pages":"Article 119792"},"PeriodicalIF":4.6,"publicationDate":"2024-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141465888","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}

{"title":"KLF5 inhibition initiates epithelial-mesenchymal transition in non-transformed human squamous epithelial cells","authors":"Dharmendra Bhargava,&nbsp;David Rusakow,&nbsp;Wilson Zheng,&nbsp;Silina Awad,&nbsp;Jonathan P. Katz","doi":"10.1016/j.bbamcr.2024.119789","DOIUrl":"10.1016/j.bbamcr.2024.119789","url":null,"abstract":"<div><p>The transcriptional regulator <em>Krüppel</em>-like factor 5 (KLF5) is highly expressed in squamous epithelial cells of the esophagus. Increased KLF5 activity induces tumorigenesis and promotes metastasis in several cancers, although this function appears to be context-dependent. Here, we demonstrate that acute KLF5 inhibition, both genetically and with the potent KLF5 inhibitor ML264, causes non-transformed human primary esophageal squamous epithelial cells to enter the epithelial to mesenchymal transition (EMT). Moreover, chronic KLF5 inhibition with ML264 leads to the development of cells with a mesenchymal phenotype characterized by the expression of mesenchymal markers and functionally by reduced cell growth and increased migration and cellular invasion. This EMT resulting from chronic KLF5 inhibition is not driven by β-Catenin or TGF-β signaling. Pharmacologically, ML264 inhibits KLF5 by promoting proteasomal-mediated degradation. Taken together, we demonstrate that reduced KLF5 activity reprograms epithelial cells towards a mesenchymal phenotype and enhances their migratory and invasive potential. These findings have potential implications not only for esophageal cancers but also for normal processes such as esophageal tissue repair following injury.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1871 7","pages":"Article 119789"},"PeriodicalIF":4.6,"publicationDate":"2024-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141442000","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}

{"title":"Fe-S cluster biosynthesis and maturation: Mass spectrometry-based methods advancing the field","authors":"Shelby D. Oney-Hawthorne,&nbsp;David P. Barondeau","doi":"10.1016/j.bbamcr.2024.119784","DOIUrl":"10.1016/j.bbamcr.2024.119784","url":null,"abstract":"<div><p>Iron‑sulfur (Fe<img>S) clusters are inorganic protein cofactors that perform essential functions in many physiological processes. Spectroscopic techniques have historically been used to elucidate details of Fe<img>S cluster type, their assembly and transfer, and changes in redox and ligand binding properties. Structural probes of protein topology, complex formation, and conformational dynamics are also necessary to fully understand these Fe<img>S protein systems. Recent developments in mass spectrometry (MS) instrumentation and methods provide new tools to investigate Fe<img>S cluster and structural properties. With the unique advantage of sampling all species in a mixture, MS-based methods can be utilized as a powerful complementary approach to probe native dynamic heterogeneity, interrogate protein folding and unfolding equilibria, and provide extensive insight into protein binding partners within an entire proteome. Here, we highlight key advances in Fe<img>S protein studies made possible by MS methodology and contribute an outlook for its role in the field.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1871 7","pages":"Article 119784"},"PeriodicalIF":4.6,"publicationDate":"2024-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141440158","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}

{"title":"Structural aspects of iron‑sulfur protein biogenesis: An NMR view","authors":"Leonardo Querci ,&nbsp;Mario Piccioli ,&nbsp;Simone Ciofi-Baffoni ,&nbsp;Lucia Banci","doi":"10.1016/j.bbamcr.2024.119786","DOIUrl":"10.1016/j.bbamcr.2024.119786","url":null,"abstract":"<div><p>Over the last decade, structural aspects involving iron‑sulfur (Fe/S) protein biogenesis have played an increasingly important role in understanding the high mechanistic complexity of mitochondrial and cytosolic machineries maturing Fe/S proteins. In this respect, solution NMR has had a significant impact because of its ability to monitor transient protein-protein interactions, which are abundant in the networks of pathways leading to Fe/S cluster biosynthesis and transfer, as well as thanks to the developments of paramagnetic NMR in both terms of new methodologies and accurate data interpretation. Here, we review the use of solution NMR in characterizing the structural aspects of human Fe/S proteins and their interactions in the framework of Fe/S protein biogenesis. We will first present a summary of the recent advances that have been achieved by paramagnetic NMR and then we will focus our attention on the role of solution NMR in the field of human Fe/S protein biogenesis.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1871 7","pages":"Article 119786"},"PeriodicalIF":4.6,"publicationDate":"2024-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141431262","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}

{"title":"Vimentin, inversely correlating with infiltration of CD8 + T lymphocytes, promotes nuclear translocation of PD-L1 in esophageal squamous cell carcinoma","authors":"Yan Liang ,&nbsp;Shuo He ,&nbsp;Qing Liu ,&nbsp;Tao Liu ,&nbsp;Yiyi Tan ,&nbsp;Tianyuan Peng ,&nbsp;Conggai Huang ,&nbsp;Xiaomei Lu ,&nbsp;Shutao Zheng","doi":"10.1016/j.bbamcr.2024.119781","DOIUrl":"10.1016/j.bbamcr.2024.119781","url":null,"abstract":"<div><p>Vimentin has been considered a canonical marker of epithelial-mesenchymal transition (EMT) and is associated with tumor escape characterized by aberrant PD-L1 expression. However, whether there is a relationship between vimentin and PD-L1 in esophageal squamous cell carcinoma (ESCC) remains poorly understood. The immunological involvement of vimentin in ESCC was first analyzed by multiplex immunofluorescence staining in ESCC tissue microarray followed by a xenografted mouse model. <em>In vivo</em>, C57BL/6 mice were subcutaneously transplanted with AKR cells after stable silencing of vimentin. <em>In vivo</em> results showed that in addition to PD-L1 and PD-L2 expression, vimentin expression was inversely correlated with CD8+ T-cell infiltration. Mechanistically, vimentin can directly interact with PD-L1 and promote nuclear translocation of PD-L1 in AKR cells. In addition, SEMA6C, STC-2 and TRAILR2 were identified as cytokines modulated by vimentin. Blockade of STC-2 and TRAILR2 in co-culture with their own primary antibodies was shown to recruit more CD8+ T cells than controls. Together, these data strongly suggest targeting Vimenin to overcome the immune cycle in ESCC.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1871 7","pages":"Article 119781"},"PeriodicalIF":4.6,"publicationDate":"2024-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141431263","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}

{"title":"Eml1 promotes axonal growth by enhancing αTAT1-mediated microtubule acetylation","authors":"Yufang Zhang ,&nbsp;Tuchen Guan ,&nbsp;Zhen Li ,&nbsp;Beibei Guo ,&nbsp;Xiaoqian Luo ,&nbsp;Longyu Guo ,&nbsp;Mingxuan Li ,&nbsp;Man Xu ,&nbsp;Mei Liu ,&nbsp;Yan Liu","doi":"10.1016/j.bbamcr.2024.119770","DOIUrl":"10.1016/j.bbamcr.2024.119770","url":null,"abstract":"<div><p>Microtubule stabilization is critical for axonal growth and regeneration, and many microtubule-associated proteins are involved in this process. In this study, we found that the knockdown of echinoderm microtubule-associated protein-like 1 (EML1) hindered axonal growth in cultured cortical and dorsal root ganglion neurons. We further revealed that EML1 facilitated the acetylation of microtubules and that the impairment of axonal growth due to EML1 inhibition could be restored by treatment with deacetylase inhibitors, suggesting that EML1 affected tubulin acetylation. Moreover, we verified an interaction between EML1 and the alpha-tubulin acetyltransferase 1, which is responsible for the acetylation of alpha-tubulin. We thus proposed that EML1 might regulate microtubule acetylation and stabilization via alpha-tubulin acetyltransferase 1 and then promote axon growth. Finally, we verified that the knockdown of EML1 in vivo also inhibited sciatic nerve regeneration. Our findings revealed a novel effect of EML1 on microtubule acetylation during axonal regeneration.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1871 7","pages":"Article 119770"},"PeriodicalIF":5.1,"publicationDate":"2024-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141426223","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}

{"title":"Promoter hypermethylation-induced downregulation of ITGA7 promotes colorectal cancer proliferation and migration by activating the PI3K/AKT/NF-κB pathway","authors":"Jianjun Wang ,&nbsp;Yu Wang ,&nbsp;Jijun Zhu ,&nbsp;Lili Wang ,&nbsp;Yanlin Huang ,&nbsp;Huiru Zhang ,&nbsp;Xiaoyan Wang ,&nbsp;Xiaomin Li","doi":"10.1016/j.bbamcr.2024.119785","DOIUrl":"10.1016/j.bbamcr.2024.119785","url":null,"abstract":"<div><p>We previously reported that integrin alpha 7 (ITGA7) was downregulated in colorectal cancer (CRC) tissues and CRC cell lines and that the lower expression of ITGA7 in CRC tissues was correlated with distant metastasis, suggesting that ITGA7 may function as a suppressor in CRC. The present research was conducted to further investigate the role and mechanisms of ITGA7 in CRC progression. First, bisulfite modification and genomic sequencing (BSP) results showed that the methylation rate of ITGA7 promoter was higher in 10 CRC tissues than in the matched normal tissues. Additionally, 5-Aza-CdR treatment increased ITGA7 expression in CRC cells. Gain-of-function assays revealed the inhibitory role of ITGA7 in CRC cell proliferation and migration. Mechanistically, RNA sequencing, RT-qPCR, and cytoplasm and nuclear separation and rescue assays indicated that knockdown of ITGA7 activated the transcription of MMP9, SETD7, and ADAM15 by enhancing the nuclear translocation of NF-κB. Moreover, CoIP and Western blot suggested a mechanistic model in which ITGA7 binds to CKAP4 to block the interaction of CKAP4 and PI3K p85α and thereby suppress the PI3K/AKT/NF-κB pathway. Accordingly, the current study suggests that ITGA7 functions as a suppressor in CRC progression and that its expression is controlled by promoter methylation.</p></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1871 7","pages":"Article 119785"},"PeriodicalIF":5.1,"publicationDate":"2024-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141410999","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}