EMBO Molecular Medicine最新文献_第10页

A therapeutic regimen using neoantigen-specific TCR-T cells for HLA-A*2402-positive solid tumors. 新抗原特异性TCR-T细胞治疗HLA-A*2402阳性实体瘤的治疗方案

IF 9 1区医学

EMBO Molecular Medicine Pub Date : 2025-02-01 Epub Date: 2025-01-02 DOI: 10.1038/s44321-024-00184-1

Yuncheng Bei, Ying Huang, Nandie Wu, Yishan Li, Ruihan Xu, Baorui Liu, Rutian Li

{"title":"A therapeutic regimen using neoantigen-specific TCR-T cells for HLA-A*2402-positive solid tumors.","authors":"Yuncheng Bei, Ying Huang, Nandie Wu, Yishan Li, Ruihan Xu, Baorui Liu, Rutian Li","doi":"10.1038/s44321-024-00184-1","DOIUrl":"10.1038/s44321-024-00184-1","url":null,"abstract":"The adoptive transfer of TCR-T cells specific to neoantigens preferentially exhibits potent cytotoxicity to tumor cells and has shown promising efficacy in various preclinical human cancers. In this study, we first identified a functional TCR, Tcr-1, which selectively recognized the SYT-SSX fusion neoantigen shared by most synovial sarcomas. Engineered T-cell expressing Tcr-1 (Tcr-T1) demonstrated HLA-A*2402-restricted, antigen-specific anti-tumoral efficacy against synovial sarcoma cells, both in vitro and in vivo. Furthermore, to extend its application, we developed a cooperative therapeutic modality, in which exogenous SYT-SSX fusion neoantigen was loaded into stimuli-responsive nanoparticles (NPs) formed by mPEG-PVGLIG-PCL copolymers (Neo-AgNPs) for tumor targeting delivery. As expected, Neo-AgNPs were proven to have great tumor penetration and local release. In situ, the modification was able to direct engineered Tcr-T1 against other HLA-A*2402-positive malignant cancer cell lines with significant antigen-specific cytotoxicity despite their inherent mutation profiles. With these favorable data, our established cooperative therapeutic modality has great potential for further clinical investigation and provides new insight for future TCR-T cell therapy development.","PeriodicalId":11597,"journal":{"name":"EMBO Molecular Medicine","volume":" ","pages":"365-383"},"PeriodicalIF":9.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11821884/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142920815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Microbial metabolites tune amygdala neuronal hyperexcitability and anxiety-linked behaviors. 微生物代谢物调节杏仁核神经元的过度兴奋性和焦虑相关行为。

IF 9 1区医学

EMBO Molecular Medicine Pub Date : 2025-02-01 Epub Date: 2025-02-05 DOI: 10.1038/s44321-024-00179-y

Weonjin Yu, Yixin Xiao, Anusha Jayaraman, Yi-Chun Yen, Hae Ung Lee, Sven Pettersson, H Shawn Je

{"title":"Microbial metabolites tune amygdala neuronal hyperexcitability and anxiety-linked behaviors.","authors":"Weonjin Yu, Yixin Xiao, Anusha Jayaraman, Yi-Chun Yen, Hae Ung Lee, Sven Pettersson, H Shawn Je","doi":"10.1038/s44321-024-00179-y","DOIUrl":"10.1038/s44321-024-00179-y","url":null,"abstract":"Changes in gut microbiota composition have been linked to anxiety behavior in rodents. However, the underlying neural circuitry linking microbiota and their metabolites to anxiety behavior remains unknown. Using male C57BL/6J germ-free (GF) mice, not exposed to live microbes, increased anxiety-related behavior was observed correlating with a significant increase in the immediate early c-Fos gene in the basolateral amygdala (BLA). This phenomenon coincided with increased intrinsic excitability and spontaneous synaptic activity of BLA pyramidal neurons associated with reduced small conductance calcium-activated potassium (SK) channel currents. Importantly, colonizing GF mice to live microbes or the microbial-derived metabolite indoles reverted SK channel activities in BLA pyramidal neurons and reduced the anxiety behavioral phenotype. These results are consistent with a molecular mechanism by which microbes and or microbial-derived indoles, regulate functional changes in the BLA neurons. Moreover, this microbe metabolite regulation of anxiety links these results to ancient evolutionarily conserved defense mechanisms associated with anxiety-related behaviors in mammals.","PeriodicalId":11597,"journal":{"name":"EMBO Molecular Medicine","volume":" ","pages":"249-264"},"PeriodicalIF":9.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11821874/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143255148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Macrophage-induced enteric neurodegeneration leads to motility impairment during gut inflammation. 巨噬细胞诱导的肠道神经变性导致肠道炎症期间的运动障碍。

IF 9 1区医学

EMBO Molecular Medicine Pub Date : 2025-02-01 Epub Date: 2025-01-06 DOI: 10.1038/s44321-024-00189-w

Mona Breßer, Kevin D Siemens, Linda Schneider, Jonah E Lunnebach, Patrick Leven, Tim R Glowka, Kristin Oberländer, Elena De Domenico, Joachim L Schultze, Joachim Schmidt, Jörg C Kalff, Anja Schneider, Sven Wehner, Reiner Schneider

{"title":"Macrophage-induced enteric neurodegeneration leads to motility impairment during gut inflammation.","authors":"Mona Breßer, Kevin D Siemens, Linda Schneider, Jonah E Lunnebach, Patrick Leven, Tim R Glowka, Kristin Oberländer, Elena De Domenico, Joachim L Schultze, Joachim Schmidt, Jörg C Kalff, Anja Schneider, Sven Wehner, Reiner Schneider","doi":"10.1038/s44321-024-00189-w","DOIUrl":"10.1038/s44321-024-00189-w","url":null,"abstract":"Current studies pictured the enteric nervous system and macrophages as modulators of neuroimmune processes in the inflamed gut. Expanding this view, we investigated the impact of enteric neuron-macrophage interactions on postoperative trauma and subsequent motility disturbances, i.e., postoperative ileus. In the early postsurgical phase, we detected strong neuronal activation, followed by transcriptional and translational signatures indicating neuronal death and synaptic damage. Simultaneously, our study revealed neurodegenerative profiles in macrophage-specific transcriptomes after postoperative trauma. Validating the role of resident and monocyte-derived macrophages, we depleted macrophages by CSF-1R-antibodies and used CCR2-/- mice, known for reduced monocyte infiltration, in POI studies. Only CSF-1R-antibody-treated animals showed decreased neuronal death and lessened synaptic decay, emphasizing the significance of resident macrophages. In human gut samples taken early and late during abdominal surgery, we substantiated the mouse model data and found reactive and apoptotic neurons and dysregulation in synaptic genes, indicating a species' overarching mechanism. Our study demonstrates that surgical trauma activates enteric neurons and induces neurodegeneration, mediated by resident macrophages, introducing neuroprotection as an option for faster recovery after surgery.","PeriodicalId":11597,"journal":{"name":"EMBO Molecular Medicine","volume":"17 2","pages":"301-335"},"PeriodicalIF":9.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11822118/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143406508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Gut microbiota interact with breast cancer therapeutics to modulate efficacy. 肠道微生物群与乳腺癌治疗药物相互作用以调节疗效。

IF 11.1 1区医学

EMBO Molecular Medicine Pub Date : 2025-01-16 DOI: 10.1038/s44321-024-00185-0

Alana A Arnone,Katherine Ansley,Arielle L Heeke,Marissa Howard-McNatt,Katherine L Cook

引用次数: 0

A novel anti-epileptogenesis strategy of temporal lobe epilepsy based on nitric oxide donor. 一种新的基于一氧化氮供体的颞叶癫痫抗癫痫策略。

IF 9 1区医学

EMBO Molecular Medicine Pub Date : 2025-01-01 Epub Date: 2024-12-09 DOI: 10.1038/s44321-024-00168-1

Xian-Hui Zhu, Ya-Ping Zhou, Qiao Zhang, Ming-Yi Zhu, Xiao-Wei Song, Jun Li, Jiang Chen, Yun Shi, Kang-Jian Sun, Yong-Jie Zhang, Jing Zhang, Tian Xia, Bao-Sheng Huang, Fan Meng, Qi-Gang Zhou

{"title":"A novel anti-epileptogenesis strategy of temporal lobe epilepsy based on nitric oxide donor.","authors":"Xian-Hui Zhu, Ya-Ping Zhou, Qiao Zhang, Ming-Yi Zhu, Xiao-Wei Song, Jun Li, Jiang Chen, Yun Shi, Kang-Jian Sun, Yong-Jie Zhang, Jing Zhang, Tian Xia, Bao-Sheng Huang, Fan Meng, Qi-Gang Zhou","doi":"10.1038/s44321-024-00168-1","DOIUrl":"10.1038/s44321-024-00168-1","url":null,"abstract":"The molecular mechanism underlying the role of hippocampal hilar interneuron degeneration in temporal lobe epilepsy (TLE) remains unclear. Especially, very few studies have focused on the role of neuronal nitric oxide synthase (nNOS, encoded by Nos1) containing hilar interneurons in TLE. In the present study, Nos1 conditional knockout mice were constructed, and we found that selective deletion of Nos1 in hilar interneurons rather than dentate granular cells (DGCs) triggered epileptogenesis. The level of nNOS was downregulated in patients and mice with TLE. Nos1 deletion led to excessive epilepsy-like excitatory input circuit formation and hyperexcitation of DGCs. Replenishment of hilar nNOS protein blocked epileptogenic development and memory impairment in pilocarpine-induced TLE mice. Moreover, chronic treatment with DETA/NONOate, a slowly released exogenous nitric oxide (NO) donor, prevented aberrant neural circuits of DGCs and the consequent epileptogenesis without acute antiseizure effects. Therefore, we concluded that NO donor therapy may be a novel anti-epileptogenesis strategy, different from existing antiseizure medications (ASMs), for curing TLE.","PeriodicalId":11597,"journal":{"name":"EMBO Molecular Medicine","volume":" ","pages":"85-111"},"PeriodicalIF":9.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11730642/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

BMP-9 mediates fibroproliferation in fibrodysplasia ossificans progressiva through TGF-β signaling. BMP-9通过TGF-β信号介导进行性骨化纤维发育不良的纤维增殖。

IF 9 1区医学

EMBO Molecular Medicine Pub Date : 2025-01-01 Epub Date: 2024-12-03 DOI: 10.1038/s44321-024-00174-3

Chengzhu Zhao, Yoshiko Inada, Souta Motoike, Daisuke Kamiya, Kyosuke Hino, Makoto Ikeya

{"title":"BMP-9 mediates fibroproliferation in fibrodysplasia ossificans progressiva through TGF-β signaling.","authors":"Chengzhu Zhao, Yoshiko Inada, Souta Motoike, Daisuke Kamiya, Kyosuke Hino, Makoto Ikeya","doi":"10.1038/s44321-024-00174-3","DOIUrl":"10.1038/s44321-024-00174-3","url":null,"abstract":"Fibrodysplasia ossificans progressiva (FOP) is a rare genetic disorder presenting with progressive heterotopic ossification (HO) in soft tissues. Early-stage FOP is characterized by recurrent episodes of painful tissue swelling (flare-ups), with numerous proliferation-activated mesenchymal stromal cells (MSCs) subsequently causing HO. However, the mechanisms underlying flare-up progression remain unclear. In this study, we evaluated the proliferation of MSCs obtained from FOP patient-derived induced pluripotent stem cells (FOP-iPSCs) to elucidate the mechanisms underlying flare-ups and found that bone morphogenetic protein (BMP)-9 mediated enhanced proliferation by abnormal activation of transforming growth factor (TGF)-β signaling pathway in MSCs from FOP-iPSCs. In FOP model mice, elevated BMP-9 levels correlated with elevated phosphorylation of SMAD2/3 and increased cellular proliferation in the affected tissues, while systemic BMP-9 neutralization and knockout mitigated flare-ups and HO. Thus, BMP-9 aberrantly transduces TGF-β signaling and induces fibroproliferation, initiating flare-ups. This study provides novel insights into the development of future FOP therapies.","PeriodicalId":11597,"journal":{"name":"EMBO Molecular Medicine","volume":" ","pages":"112-128"},"PeriodicalIF":9.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11729865/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142767249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bi-allelic variants in WDR47 cause a complex neurodevelopmental syndrome. WDR47的双等位基因变异导致复杂的神经发育综合征。

IF 9 1区医学

EMBO Molecular Medicine Pub Date : 2025-01-01 Epub Date: 2024-11-28 DOI: 10.1038/s44321-024-00178-z

Efil Bayam, Peggy Tilly, Stephan C Collins, José Rivera Alvarez, Meghna Kannan, Lucile Tonneau, Elena Brivio, Bruno Rinaldi, Romain Lecat, Noémie Schwaller, Ludovica Cotellessa, Sateesh Maddirevula, Fabiola Monteiro, Carlos M Guardia, João Paulo Kitajima, Fernando Kok, Mitsuhiro Kato, Ahlam A A Hamed, Mustafa A Salih, Saeed Al Tala, Mais O Hashem, Hiroko Tada, Hirotomo Saitsu, Mariano Stabile, Paolo Giacobini, Sylvie Friant, Zafer Yüksel, Mitsuko Nakashima, Fowzan S Alkuraya, Binnaz Yalcin, Juliette D Godin

{"title":"Bi-allelic variants in WDR47 cause a complex neurodevelopmental syndrome.","authors":"Efil Bayam, Peggy Tilly, Stephan C Collins, José Rivera Alvarez, Meghna Kannan, Lucile Tonneau, Elena Brivio, Bruno Rinaldi, Romain Lecat, Noémie Schwaller, Ludovica Cotellessa, Sateesh Maddirevula, Fabiola Monteiro, Carlos M Guardia, João Paulo Kitajima, Fernando Kok, Mitsuhiro Kato, Ahlam A A Hamed, Mustafa A Salih, Saeed Al Tala, Mais O Hashem, Hiroko Tada, Hirotomo Saitsu, Mariano Stabile, Paolo Giacobini, Sylvie Friant, Zafer Yüksel, Mitsuko Nakashima, Fowzan S Alkuraya, Binnaz Yalcin, Juliette D Godin","doi":"10.1038/s44321-024-00178-z","DOIUrl":"10.1038/s44321-024-00178-z","url":null,"abstract":"Brain development requires the coordinated growth of structures and cues that are essential for forming neural circuits and cognitive functions. The corpus callosum, the largest interhemispheric connection, is formed by the axons of callosal projection neurons through a series of tightly regulated cellular events, including neuronal specification, migration, axon extension and branching. Defects in any of those steps can lead to a range of disorders known as syndromic corpus callosum dysgenesis (CCD). We report five unrelated families carrying bi-allelic variants in WDR47 presenting with CCD together with other neuroanatomical phenotypes such as microcephaly and enlarged ventricles. Using in vitro and in vivo mouse models and complementation assays, we show that WDR47 is required for survival of callosal neurons by contributing to the maintenance of mitochondrial and microtubule homeostasis. We further propose that severity of the CCD phenotype is determined by the degree of the loss of function caused by the human variants. Taken together, we identify WDR47 as a causative gene of a new neurodevelopmental syndrome characterized by corpus callosum abnormalities and other neuroanatomical malformations.","PeriodicalId":11597,"journal":{"name":"EMBO Molecular Medicine","volume":" ","pages":"129-168"},"PeriodicalIF":9.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11730659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142749651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Melanin-like nanoparticles slow cyst growth in ADPKD by dual inhibition of oxidative stress and CREB. 类黑色素纳米粒子通过氧化应激和 CREB 的双重抑制作用减缓 ADPKD 囊肿的生长。

IF 9 1区医学

EMBO Molecular Medicine Pub Date : 2025-01-01 Epub Date: 2024-11-20 DOI: 10.1038/s44321-024-00167-2

Yongzhan Sun, Quan Zou, Huizheng Yu, Xiaoping Yi, Xudan Dou, Yu Yang, Zhiheng Liu, Hong Yang, Junya Jia, Yupeng Chen, Shao-Kai Sun, Lirong Zhang

{"title":"Melanin-like nanoparticles slow cyst growth in ADPKD by dual inhibition of oxidative stress and CREB.","authors":"Yongzhan Sun, Quan Zou, Huizheng Yu, Xiaoping Yi, Xudan Dou, Yu Yang, Zhiheng Liu, Hong Yang, Junya Jia, Yupeng Chen, Shao-Kai Sun, Lirong Zhang","doi":"10.1038/s44321-024-00167-2","DOIUrl":"10.1038/s44321-024-00167-2","url":null,"abstract":"Melanin-like nanoparticles (MNPs) have recently emerged as valuable agents in antioxidant therapy due to their excellent biocompatibility and potent capacity to scavenge various reactive oxygen species (ROS). However, previous studies have mainly focused on acute ROS-related diseases, leaving a knowledge gap regarding their potential in chronic conditions. Furthermore, apart from their well-established antioxidant effects, it remains unclear whether MNPs target other intracellular molecular pathways. In this study, we synthesized ultra-small polyethylene glycol-incorporated Mn2+-chelated MNP (MMPP). We found that MMPP traversed the glomerular filtration barrier and specifically accumulated in renal tubules. Autosomal dominant polycystic kidney disease (ADPKD) is a chronic genetic disorder closely associated with increased oxidative stress and featured by the progressive enlargement of cysts originating from various segments of the renal tubules. Treatment with MMPP markedly attenuated oxidative stress levels, inhibited cyst growth, thereby improving renal function. Interestingly, we found that MMPP effectively inhibits a cyst-promoting gene program downstream of the cAMP-CREB pathway, a crucial signaling pathway implicated in ADPKD progression. Mechanistically, we observed that MMPP directly binds to the bZIP DNA-binding domain of CREB, leading to competitive inhibition of CREB's DNA binding ability and subsequent reduction in CREB target gene expression. In summary, our findings identify an intracellular target of MMPP and demonstrate its potential for treating ADPKD by simultaneously targeting oxidative stress and CREB transcriptional activity.","PeriodicalId":11597,"journal":{"name":"EMBO Molecular Medicine","volume":" ","pages":"169-192"},"PeriodicalIF":9.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11730739/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Beneficial microbiome and diet interplay in early-onset colorectal cancer. 有益微生物群与饮食在早期结直肠癌中的相互作用

IF 9 1区医学

EMBO Molecular Medicine Pub Date : 2025-01-01 Epub Date: 2024-12-09 DOI: 10.1038/s44321-024-00177-0

Zhengyuan Zhou, Linda Kleis, Ana Depetris-Chauvin, Stefanie Jaskulski, Victoria Damerell, Karin B Michels, Biljana Gigic, Ute Nöthlings, Gianni Panagiotou

{"title":"Beneficial microbiome and diet interplay in early-onset colorectal cancer.","authors":"Zhengyuan Zhou, Linda Kleis, Ana Depetris-Chauvin, Stefanie Jaskulski, Victoria Damerell, Karin B Michels, Biljana Gigic, Ute Nöthlings, Gianni Panagiotou","doi":"10.1038/s44321-024-00177-0","DOIUrl":"10.1038/s44321-024-00177-0","url":null,"abstract":"Colorectal cancer (CRC) is the third most commonly diagnosed cancer and the second leading cause of cancer-related deaths worldwide. Although the risk of developing CRC increases with age, approximately 10% of newly diagnosed cases occur in individuals under the age of 50. Significant changes in dietary habits in young adults since industrialization create a favorable microenvironment for colorectal carcinogenesis. We aim here to shed light on the complex interplay between diet and gut microbiome in the pathogenesis and prevention of early-onset CRC (EO-CRC). We provide an overview of dietary risk factors associated with EO-CRC and contrast them with the general trends for CRC. We delve into gut bacteria, fungi, and phages with potential benefits against CRC and discuss the underlying molecular mechanisms. Furthermore, based on recent findings from human studies, we offer insights into how dietary modifications could potentially enhance gut microbiome composition to mitigate CRC risk. All together, we outline the current research landscape in this area and propose directions for future investigations that could pave the way for novel preventive and therapeutic strategies.","PeriodicalId":11597,"journal":{"name":"EMBO Molecular Medicine","volume":" ","pages":"9-30"},"PeriodicalIF":9.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11730345/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

PDE12 mediated pruning of the poly-A tail of mitochondrial DNA-encoded tRNAs is essential for survival. PDE12 介导的线粒体 DNA 编码的 tRNA 的 poly-A 尾部修剪对生存至关重要。

IF 9 1区医学

EMBO Molecular Medicine Pub Date : 2025-01-01 Epub Date: 2024-11-20 DOI: 10.1038/s44321-024-00171-6

Chenxiao Yu, Marco Tigano, Erin L Seifert

引用次数: 0