Journal of biochemistry最新文献

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Commentary on: Direct binding of calmodulin to the cytosolic C-terminal regions of sweet/umami taste receptors. 甜/鲜味味觉受体细胞质c端区钙调蛋白的直接结合。
IF 1.7 4区 生物学
Journal of biochemistry Pub Date : 2025-08-26 DOI: 10.1093/jb/mvaf050
Takumi Misaka
{"title":"Commentary on: Direct binding of calmodulin to the cytosolic C-terminal regions of sweet/umami taste receptors.","authors":"Takumi Misaka","doi":"10.1093/jb/mvaf050","DOIUrl":"https://doi.org/10.1093/jb/mvaf050","url":null,"abstract":"<p><p>The T1r family of receptors is essential for the detection of sweet and umami tastants, which are categorized as class C G protein-coupled receptors (GPCRs). Although these receptors share structural characteristics with other class C GPCRs, such as metabotropic glutamate receptors, they are uniquely characterized by a significantly shorter C-terminal intracellular domain, consisting of approximately 30-40 amino acid residues. Yoshida et al. recently demonstrated that the C-terminal region of mouse T1rs directly binds to calmodulin (CaM) in a Ca2+-dependent manner. This interaction highlights a previously unrecognized aspect of the intracellular signaling mechanism of T1rs, and indicates that the C-terminal region contributes to taste signal regulation, particularly through Ca2+ dependent feedback mechanisms.</p>","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144955659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Structural analysis of a symbiotic system involving a Nanobdellati archaeon by cryo-electron tomography. 纳米藻古菌共生系统的低温电子断层扫描结构分析。
IF 1.7 4区 生物学
Journal of biochemistry Pub Date : 2025-08-26 DOI: 10.1093/jb/mvaf049
Sakurako Goto-Ito, Shingo Kato, Mari Takahashi, Ayako Sakamoto, Atsushi Yamagata, Yongchan Lee, Haruhiko Ehara, Mayuko Sato, Kiminori Toyooka, Moriya Ohkuma, Takuhiro Ito
{"title":"Structural analysis of a symbiotic system involving a Nanobdellati archaeon by cryo-electron tomography.","authors":"Sakurako Goto-Ito, Shingo Kato, Mari Takahashi, Ayako Sakamoto, Atsushi Yamagata, Yongchan Lee, Haruhiko Ehara, Mayuko Sato, Kiminori Toyooka, Moriya Ohkuma, Takuhiro Ito","doi":"10.1093/jb/mvaf049","DOIUrl":"https://doi.org/10.1093/jb/mvaf049","url":null,"abstract":"<p><p>Nanobdellati (formerly DPANN) archaea are considered as primitive archaeal organisms that often live in symbiosis with archaeal hosts. In this study, we investigated the symbiotic mechanism between a Nanobdellati archaeon, Nanobdella aerobiophila strain MJ1, and its host archaeon Metallosphaera sedula strain MJ1HA, using cryo-electron tomography. In our tomographic observations, we identified a conical attachment organelle at the interface between MJ1 and MJ1HA during symbiosis. This structure consists of a concentric array of short cylindrical shells, consistent with a previous report. Subtomogram averaging, combined with AlphaFold 3 structural predictions, allowed us to identify a potential component of attachment organelles. Additionally, we inferred potential components of the S-layers in MJ1 and MJ1HA based on tomographic data and subtomogram averages. Based on these analyses, we hypothesize that a MJ1 S-layer component may undergo conformational changes to also serve as a component of attachment organelles, warranting further investigation.</p>","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144955592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Neural stem cell-specific deficiency of (pro)renin receptor causes brain malformation and perinatal lethality in mice. 神经干细胞特异性肾素受体(原)缺乏导致小鼠脑畸形和围产期死亡。
IF 1.7 4区 生物学
Journal of biochemistry Pub Date : 2025-08-15 DOI: 10.1093/jb/mvaf047
Misuzu Hashimoto, Misaki Hibi, Koya Matsukubo, Hitoshi Kimura, Kuma Hiraoka, Swapna Paramanya Biswas, Chiharu Suzuki-Nakagawa, Yasuhiko Kizuka, Jun-Dal Kim, Akiyoshi Fukamizu, Atsuhiro Ichihara, Tsutomu Nakagawa
{"title":"Neural stem cell-specific deficiency of (pro)renin receptor causes brain malformation and perinatal lethality in mice.","authors":"Misuzu Hashimoto, Misaki Hibi, Koya Matsukubo, Hitoshi Kimura, Kuma Hiraoka, Swapna Paramanya Biswas, Chiharu Suzuki-Nakagawa, Yasuhiko Kizuka, Jun-Dal Kim, Akiyoshi Fukamizu, Atsuhiro Ichihara, Tsutomu Nakagawa","doi":"10.1093/jb/mvaf047","DOIUrl":"https://doi.org/10.1093/jb/mvaf047","url":null,"abstract":"<p><p>(Pro)renin receptor [(P)RR], encoded by Atp6ap2, is a transmembrane protein found in many organs. It functions in lysosomes as part of the vacuolar-ATPase complex, facilitating autophagy and degradation. Mutations in ATP6AP2 are linked to neurological conditions, including X-linked parkinsonism with spasticity. However, our understanding of the role of (P)RR in whole brain development remains incomplete. Here, we generated mice with neural stem cell (NSC)-specific (P)RR deficiency (CKO). CKO mice exhibited significant brain atrophy during mid-gestation, leading to perinatal lethality. Fetal CKO brains showed lateral ventricular enlargement with malformation of neocortex and ganglionic eminence (GE) from mid-gestation. CKO brains showed massive apoptosis in multiple regions along with microglial activation at E15. On the contrary, CKO NSCs showed normal self-renewal ability, suggesting that (P)RR is critical for survival of differentiated cells. In line with this, the mechanistic study using RNA-seq of primary NSCs revealed downregulation of genes related to neurodevelopment and myelination. We also found p62 and LC3-II protein accumulation, hallmarks of deregulated autophagic pathways, in CKO fetal brains and NSCs. These findings demonstrate that (P)RR is crucial for guiding NSC differentiation and ensuring the coordinated construction of brain architecture during development.</p>","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144855330","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Comprehensive characterization of the interaction between prototypical drug-site markers and multiple sites on human serum albumin by microbore frontal gel chromatography. 用微孔正面凝胶色谱法综合表征典型药物位点标记物与人血清白蛋白多个位点之间的相互作用。
IF 1.7 4区 生物学
Journal of biochemistry Pub Date : 2025-08-14 DOI: 10.1093/jb/mvaf045
Marie Yamauchi, Hiromasa Tojo, Takemitsu Arakaki, Tetsuo Ishida
{"title":"Comprehensive characterization of the interaction between prototypical drug-site markers and multiple sites on human serum albumin by microbore frontal gel chromatography.","authors":"Marie Yamauchi, Hiromasa Tojo, Takemitsu Arakaki, Tetsuo Ishida","doi":"10.1093/jb/mvaf045","DOIUrl":"https://doi.org/10.1093/jb/mvaf045","url":null,"abstract":"<p><p>Human serum albumin (HSA) has three major binding sites for drugs, site I, site II, and FA1 site. Dansyl amino acids (Dans-AAs) have long been used as convenient markers to judge whether a low molecular weight molecule of interest (ligand) binds to sites I or II. However, crystal structures of HSA-Dans-AA complexes have revealed that Dans-AAs with strict site specificity are also bound to non-marker sites. To characterize the multiple binding of Dans-AAs in detail, the average number of the bound ligands per HSA molecule were obtained in a free ligand concentration of 1-400 μM for dansylate (DA) and seventeen Dans-AAs using microbore frontal gel filtration chromatography. Analysis of the binding curves indicated that there are three specific binding sites for Dans-AAs. Four Dans-AAs with hydrophobic sidechain bind to all the sites with identical affinity, whereas DA and four Dans-AAs bind equally to two of them. Nine Dans-AAs bind to one of the three sites with the maximum occupancy ranging from 72% to 94%. The UV-vis absorption spectrum of HSA-ligand complex was obtained for DA and ten Dans-AAs, revealing that the dansyl moiety is in hydrophobic environment and conformational changes in the binding site residues are induced.</p>","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144846636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Substrate Structure Determines p97- and RAD23A/B-Mediated Proteasomal Degradation in Human Cells. 底物结构决定p97-和RAD23A/ b介导的人细胞蛋白酶体降解。
IF 1.7 4区 生物学
Journal of biochemistry Pub Date : 2025-08-11 DOI: 10.1093/jb/mvaf046
Yi Ding, Takuya Tomita, Hikaru Tsuchiya, Yasushi Saeki
{"title":"Substrate Structure Determines p97- and RAD23A/B-Mediated Proteasomal Degradation in Human Cells.","authors":"Yi Ding, Takuya Tomita, Hikaru Tsuchiya, Yasushi Saeki","doi":"10.1093/jb/mvaf046","DOIUrl":"https://doi.org/10.1093/jb/mvaf046","url":null,"abstract":"<p><p>Proteasomal degradation of ubiquitinated proteins involves various accessory factors, including p97 and shuttle factors, but their requirements and relationship with substrate structural properties are not fully understood, especially in human cells. Here, we demonstrate that substrate structure dictates the dependency on p97 and RAD23A/B for proteasomal degradation in human cells, using two ubiquitin-fusion model substrates, Ub-GFP (well-folded) and Ub-GFP-tail (with an unstructured tail). Both substrates exhibited similar ubiquitin chain composition, primarily mediated by the UBR4-KCMF1 E3 ligase. Interactome analyses revealed that Ub-GFP preferentially interacts with p97 and RAD23B, while Ub-GFP-tail binds more strongly with the proteasome. The degradation of Ub-GFP depends on p97 and RAD23A/B, whereas that of Ub-GFP-tail bypasses these accessory factors. RAD23A/B knockdown resulted in a reduction in the apparent lengths of ubiquitin chains on both substrates, yet only affected Ub-GFP degradation, suggesting that even a lower level of ubiquitination is sufficient to support proteasomal degradation of substrates with an unstructured tail. Overall, our findings highlight substrate structure as a key determinant of accessory factor requirement, offering valuable insights for the development of targeted protein degradation.</p>","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144835209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Innate immune responses to lysosomal nucleic acid stress. 先天免疫对溶酶体核酸应激的反应。
IF 1.7 4区 生物学
Journal of biochemistry Pub Date : 2025-07-31 DOI: 10.1093/jb/mvaf011
Kensuke Miyake, Takuma Shibata, Ryota Sato, Ryutaro Fukui
{"title":"Innate immune responses to lysosomal nucleic acid stress.","authors":"Kensuke Miyake, Takuma Shibata, Ryota Sato, Ryutaro Fukui","doi":"10.1093/jb/mvaf011","DOIUrl":"10.1093/jb/mvaf011","url":null,"abstract":"<p><p>Nucleic acids (NAs) are recognized by endosomal Toll-like receptors (TLRs) and cytoplasmic sensors in innate immune cells. NAs accumulate within lysosomes due to either excessive NA influx or defective lysosomal degradation. The resultant storage of NAs and/or NA metabolites in the lysosome, referred to here as lysosomal NA stress, elicits a spectrum of responses, ranging from inflammation to tissue repair, through NA sensor activation. Although these responses contribute to host defence against infection, they may also drive diseases. For instance, loss of function of the lysosomal nucleoside transporter SLC29A3 drives lysosomal nucleoside stress, which activates TLR8 in macrophages to cause histiocytic diseases collectively called SLC29A3 disorders. Similarly, DNase II deficiency promotes lysosomal DNA stress, leading to activation of cytoplasmic double-stranded DNA sensors, such as cGAS-STING and AIM2, and thereby autoinflammatory and autoimmune diseases. Thus, lysosomal NA stress is viewed as a pivotal environmental signal that initiates innate immune responses.</p>","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":"89-96"},"PeriodicalIF":1.7,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12319223/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143556969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Histone H2B isoform H2bc27 is expressed in the developing brain of mouse embryos. 组蛋白H2B异构体H2bc27在小鼠胚胎发育中的大脑中表达。
IF 1.7 4区 生物学
Journal of biochemistry Pub Date : 2025-07-31 DOI: 10.1093/jb/mvaf026
Saki Egashira, Kazumitsu Maehara, Kaori Tanaka, Mako Nakamura, Tatsuya Takemoto, Yasuyuki Ohkawa, Akihito Harada
{"title":"Histone H2B isoform H2bc27 is expressed in the developing brain of mouse embryos.","authors":"Saki Egashira, Kazumitsu Maehara, Kaori Tanaka, Mako Nakamura, Tatsuya Takemoto, Yasuyuki Ohkawa, Akihito Harada","doi":"10.1093/jb/mvaf026","DOIUrl":"10.1093/jb/mvaf026","url":null,"abstract":"<p><p>Histones bind directly to DNA and play a role in regulating gene expression in part by influencing chromatin structure. The DNA sequences of these histone genes are quite similar, which has hindered individual analyses. The exact function of the 13 different isoforms of histone H2B remains unclear. In this study, we performed a comprehensive gene expression analysis of the H2B isoforms, focusing on tissue specificity. Our results revealed that the H2bc27 gene exhibited brain-specific expression in mice at E14.5. We generated mice lacking the H2bc27 gene using the CRISPR/Cas9 system. While the phenotype of H2bc27 knockout mouse brains was not different from that of wild-type mouse brains, transcriptome analysis indicated that H2bc27 is associated with regulating the expression of several functional genes involved in mouse brain development. The methods used in this study may serve to facilitate comprehensive H2B isoform analysis.</p>","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":"109-119"},"PeriodicalIF":1.7,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144078321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Autophagy promotes the acquisition of genotoxic resistance in cancer cells in a paracrine manner via upregulation of PLK1-RAD9A axis. 自噬通过上调PLK1-RAD9A轴,以旁分泌方式促进癌细胞获得基因毒性抗性。
IF 1.7 4区 生物学
Journal of biochemistry Pub Date : 2025-07-31 DOI: 10.1093/jb/mvaf027
Masae Ikura, Takuma Shiraki, Tsuyoshi Ikura, Kanji Furuya
{"title":"Autophagy promotes the acquisition of genotoxic resistance in cancer cells in a paracrine manner via upregulation of PLK1-RAD9A axis.","authors":"Masae Ikura, Takuma Shiraki, Tsuyoshi Ikura, Kanji Furuya","doi":"10.1093/jb/mvaf027","DOIUrl":"10.1093/jb/mvaf027","url":null,"abstract":"<p><p>Autophagy suppresses tumourigenesis in normal cells, but in established tumours, it can promote tumour progression, particularly by enhancing resistance to stress. However, the mechanism underlying this tumour-promoting function remains unclear. To investigate this, we adopted an interdisciplinary approach combining database analysis with experimental validation. Specifically, by classifying the autophagy-related genes using AutoML analysis on their expression patterns in the COSMIC database, we identified an autophagy subnetwork that correlated with the PLK1-RAD9A axis, a pathway we had previously linked to genotoxic resistance. Cell-based experiments confirmed that autophagy enhanced polo-like-kinase1 (PLK1) expression at both the transcriptional and translational levels, facilitating genotoxic resistance. Notably, in stressed S-phase cells, we found that PLK1 expression levels varied among individual cells, yet overall cell population acquired genotoxin resistance. The genotoxin resistance in the cell population with heterogeneous PLK1 expression was driven by autophagy by facilitating the secretion of currently unidentified factors, likely by switching function of RAD9A from DNA checkpoint to substance secretion. Together our data demonstrate that intra-tumour heterogeneity contributes to the malignant features of tumours through an autophagy-PLK-RAD9A axis that promotes intercellular communication via secretion.</p>","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":"97-107"},"PeriodicalIF":1.7,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144180505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Acquisition mechanism of heme oxygenase-1 induction by heat shock in human monocytic cell line THP-1 after differentiation to macrophage-like cells. 热休克诱导单核细胞THP-1向巨噬细胞样细胞分化后血红素氧合酶-1的获取机制
IF 1.7 4区 生物学
Journal of biochemistry Pub Date : 2025-07-31 DOI: 10.1093/jb/mvaf029
Daisuke Tsuji, Nodoka Ishida, Takafumi Miyamoto, Sachiye Inouye, Reiko Akagi
{"title":"Acquisition mechanism of heme oxygenase-1 induction by heat shock in human monocytic cell line THP-1 after differentiation to macrophage-like cells.","authors":"Daisuke Tsuji, Nodoka Ishida, Takafumi Miyamoto, Sachiye Inouye, Reiko Akagi","doi":"10.1093/jb/mvaf029","DOIUrl":"10.1093/jb/mvaf029","url":null,"abstract":"<p><p>Heme oxygenase-1 (HO-1) is unique to be directly regulated by diverse stress-responsible transcription factors; however, the cross-talk between oxidative stress and heat shock stress has not been completely elucidated. It is widely accepted that HO activity is not induced by heat shock in cultured cells derived from humans and mice but from rats. Previously, we reported that the discrepancies in heat shock-induced HO-1 expression in different animal species were caused by the access of heat shock factor 1 (HSF1) to heat shock element (HSE) in the different regions of the HO-1 gene. Recently, we found that the human monocyte-derived cell line THP-1, which has been extensively used to study monocyte/macrophage functions, represents the heat shock induction of HO-1 after differentiation to macrophage-like cells, although not responsible before differentiation. In this study, we demonstrated that heat shock loading to macrophage-like cells derived from THP-1 specifically activated HSF1 to bind to HSE in the promotor region in the HO-1 gene, resulting in the induction of HO-1. Our finding is significant in understanding the regulation system by macrophages for inflammation caused by oxidative insults and associated with hyperthermia in vivo.</p>","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":"135-143"},"PeriodicalIF":1.7,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144187100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Mitochondrial DNA: leakage, recognition and associated human diseases. 线粒体DNA:泄漏、识别和相关的人类疾病。
IF 1.7 4区 生物学
Journal of biochemistry Pub Date : 2025-07-31 DOI: 10.1093/jb/mvaf037
Hyota Takamatsu
{"title":"Mitochondrial DNA: leakage, recognition and associated human diseases.","authors":"Hyota Takamatsu","doi":"10.1093/jb/mvaf037","DOIUrl":"10.1093/jb/mvaf037","url":null,"abstract":"<p><p>Mitochondria are intracellular organelles originating from intracellular symbiotic bacteria that play essential roles in life activities such as energy production, metabolism, Ca2+ storage, signal transduction and cell death. Mitochondria also function as hubs for host defence against harmful stimuli such as infection and inflammation control. However, when cells are exposed to stress, mitochondrial homeostasis is disrupted, and mitochondrial DNA (mtDNA) can leak into the cytoplasm or extracellular space. Leaked mtDNA activates innate immune sensors, causing severe inflammation and contributing to the pathogenesis of human diseases. In this review, we summarize the mechanisms by which mtDNA leaks from the mitochondria and subsequently induces inflammation. We also review the relationship between mtDNA leakage and human diseases.</p>","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":"79-87"},"PeriodicalIF":1.7,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144512024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
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