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ISGylation directly modifies hypoxia-inducible factor-2α and enhances its polysome association. isg酰化直接修饰缺氧诱导因子-2α并增强其多体关联。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2022-11-01 DOI: 10.1002/1873-3468.14476
Gaelan Melanson, Antonia C Du Bois, Caroline Webster, James Uniacke
{"title":"ISGylation directly modifies hypoxia-inducible factor-2α and enhances its polysome association.","authors":"Gaelan Melanson,&nbsp;Antonia C Du Bois,&nbsp;Caroline Webster,&nbsp;James Uniacke","doi":"10.1002/1873-3468.14476","DOIUrl":"https://doi.org/10.1002/1873-3468.14476","url":null,"abstract":"<p><p>The hypoxia-inducible factors (HIF)-1α and HIF-2α are central regulators of transcriptional programmes in settings such as development and tumour expansion. HIF-2α moonlights as a cap-dependent translation factor. We provide new insights into how the interferon-stimulated gene 15 (ISG15), a ubiquitin-like modifier, and the HIFs regulate one another in hypoxia and interferon-induced cells. We show that upon ISGylation induction and HIF-α stabilization, both HIFs promote protein ISGylates through transcriptional and/or post-transcriptional pathways. We show the first evidence of HIF-2α modification by ISG15. ISGylation induces system-level alterations to the HIF transcriptional programme and increases the cytoplasmic/nuclear fraction and translation activity of HIF-2α. This work identifies ISG15 as a regulator of hypoxic mRNA translation, which has implications for immune processes and disease progression.</p>","PeriodicalId":50454,"journal":{"name":"FEBS Letters","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10721429","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
The fusion of quantitative molecular proteomics and immune-oncology: a step towards precision medicine in cancer therapeutics. 定量分子蛋白质组学与免疫肿瘤学的融合:癌症治疗迈向精准医学的一步。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2022-11-01 DOI: 10.1002/1873-3468.14480
James Miles, Stephen G Ward, Banafshé Larijani
{"title":"The fusion of quantitative molecular proteomics and immune-oncology: a step towards precision medicine in cancer therapeutics.","authors":"James Miles,&nbsp;Stephen G Ward,&nbsp;Banafshé Larijani","doi":"10.1002/1873-3468.14480","DOIUrl":"https://doi.org/10.1002/1873-3468.14480","url":null,"abstract":"<p><p>Innate and adaptive immune systems are built-in homeostatic functions of many multicellular organisms and protect the host against foreign pathogens and infections. Dysregulation of the molecular mechanisms of the immune system can result in autoimmune diseases. The immune system can also be harnessed and manipulated to provide targeted cancer therapies, some of them relying on the blockade of immune-checkpoint receptors. Two prominent immune checkpoints, PD-1/PD-L1 and CTLA-4/CD80, comprise receptor-ligand pairs that prevent the host immune cells from attacking host tissues. However, cancer cells upregulate the respective PD-L1 and CD80 ligands for PD-1 and CTLA-4 and thereby evade the host-immune response. Therapeutic drugs that block PD-1/PD-L1 and CTLA-4/CD80 interactions re-enable the immune system to attack cancer cells, but their prognostic biomarker remains challenging. In this review, we discuss how the use of quantitative molecular imaging can be exploited to predict the response to anti-PD-1/PD-L1 therapies and to identify cancer patients who would benefit from them.</p>","PeriodicalId":50454,"journal":{"name":"FEBS Letters","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10362339","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: 1
Clinical and mechanistic insights into the roles of DDX41 in haematological malignancies. DDX41在血液系统恶性肿瘤中作用的临床和机制见解。
IF 3 4区 生物学
FEBS Letters Pub Date : 2022-11-01 Epub Date: 2022-09-09 DOI: 10.1002/1873-3468.14487
Joshua T Weinreb, Teresa V Bowman
{"title":"Clinical and mechanistic insights into the roles of DDX41 in haematological malignancies.","authors":"Joshua T Weinreb, Teresa V Bowman","doi":"10.1002/1873-3468.14487","DOIUrl":"10.1002/1873-3468.14487","url":null,"abstract":"<p><p>DEAD-box Helicase 41 (DDX41) is a member of the DExD/H-box helicase family that has a variety of cellular functions. Of note, germline and somatic mutations in the DDX41 gene are prevalently found in myeloid malignancies. Here, we present a comprehensive and analytic review covering relevant clinical, translational and basic science findings on DDX41. We first describe the initial characterisation of DDX41 mutations in patients affected by myelodysplastic syndromes, their associated clinical characteristics, and current treatment modalities. We then cover the known cellular functions of DDX41, spanning from its discovery in Drosophila as a neuroregulator through its more recently described roles in inflammatory signalling, R-loop metabolism and snoRNA processing. We end with a summary of the identified basic functions of DDX41 that when perturbed may contribute to the underlying pathology of haematologic neoplasms.</p>","PeriodicalId":50454,"journal":{"name":"FEBS Letters","volume":null,"pages":null},"PeriodicalIF":3.0,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9669125/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10739576","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
Discoidin domain receptor 1 regulates ErbB2/ErbB3 signaling in mammary epithelial cells. 盘状蛋白结构域受体1调控乳腺上皮细胞ErbB2/ErbB3信号通路。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2022-11-01 DOI: 10.1002/1873-3468.14522
Andrés Martin Toscani, Pablo Aguilera, Federico Coluccio Leskow
{"title":"Discoidin domain receptor 1 regulates ErbB2/ErbB3 signaling in mammary epithelial cells.","authors":"Andrés Martin Toscani,&nbsp;Pablo Aguilera,&nbsp;Federico Coluccio Leskow","doi":"10.1002/1873-3468.14522","DOIUrl":"https://doi.org/10.1002/1873-3468.14522","url":null,"abstract":"<p><p>The ErbB2 receptor tyrosine kinase plays a key role in mammary gland development. It forms large clusters which serve as signaling platforms for integration of extracellular information. The discoidin domain receptor (DDR) family are collagen receptor tyrosine kinases which, together with ErbB2, are involved in many physiological and pathological processes. Here, we investigated the interaction of ErbB2 and DDR1 receptors in breast cancer cells. In contrast to beta1-integrin, DDR1 colocalizes with ErbB2 in membrane clusters regardless of their expression levels. We demonstrated that this spatial coexistence is a consequence of the physical interaction between these receptors. In addition, these receptors are coexpressed in the normal mammary gland but not in breast tumor samples. Together, these results present DDR1 as a novel modulator of the ErbB2/ErbB3 signaling pathway.</p>","PeriodicalId":50454,"journal":{"name":"FEBS Letters","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10376801","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: 2
Activity of the nonreceptor tyrosine kinase Ack1 is regulated by tyrosine phosphorylation of its Mig6 homology region. 非受体酪氨酸激酶Ack1的活性受其Mig6同源区酪氨酸磷酸化的调节。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2022-11-01 DOI: 10.1002/1873-3468.14505
Yağmur Kan, W Todd Miller
{"title":"Activity of the nonreceptor tyrosine kinase Ack1 is regulated by tyrosine phosphorylation of its Mig6 homology region.","authors":"Yağmur Kan,&nbsp;W Todd Miller","doi":"10.1002/1873-3468.14505","DOIUrl":"https://doi.org/10.1002/1873-3468.14505","url":null,"abstract":"<p><p>Ack1 is a proto-oncogenic tyrosine kinase with homology to the tumour suppressor Mig6, an inhibitor of the epidermal growth factor receptor (EGFR). The residues critical for binding of Mig6 to EGFR are conserved within the Mig6 homology region (MHR) of Ack1. We tested whether intramolecular interactions between the Ack1 MHR and kinase domain (KD) are regulated by phosphorylation. We identified two Src phosphorylation sites within the MHR (Y859, Y860). Addition of Src-phosphorylated MHR to the Ack1 KD enhanced enzymatic activity. Co-expression of Src in cells led to increased Ack1 activity; mutation of Y859/Y860 blocked this increase. Collectively, the data suggest that phosphorylation of the Ack1 MHR regulates its kinase activity. Phosphorylation of Y859/Y860 occurs in cancers of the brain, breast, colon, and prostate, where genomic amplification or somatic mutations of Ack1 play a role in disease progression. Our findings suggest that MHR phosphorylation could contribute to Ack1 dysregulation in tumours.</p>","PeriodicalId":50454,"journal":{"name":"FEBS Letters","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9879303/pdf/nihms-1864192.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10620160","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: 2
Ubiquitin receptors play redundant roles in the proteasomal degradation of the p53 repressor MDM2. 泛素受体在p53抑制因子MDM2的蛋白酶体降解中发挥冗余作用。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2022-11-01 DOI: 10.1002/1873-3468.14436
Alison Sparks, Christopher J Kelly, Mark K Saville
{"title":"Ubiquitin receptors play redundant roles in the proteasomal degradation of the p53 repressor MDM2.","authors":"Alison Sparks,&nbsp;Christopher J Kelly,&nbsp;Mark K Saville","doi":"10.1002/1873-3468.14436","DOIUrl":"https://doi.org/10.1002/1873-3468.14436","url":null,"abstract":"<p><p>Much remains to be determined about the participation of ubiquitin receptors in proteasomal degradation and their potential as therapeutic targets. Suppression of the ubiquitin receptor S5A/PSMD4/hRpn10 alone stabilises p53/TP53 but not the key p53 repressor MDM2. Here, we observed S5A and the ubiquitin receptors ADRM1/PSMD16/hRpn13 and RAD23A and B functionally overlap in MDM2 degradation. We provide further evidence that degradation of only a subset of ubiquitinated proteins is sensitive to S5A knockdown because ubiquitin receptor redundancy is commonplace. p53 can be upregulated by S5A modulation while degradation of substrates with redundant receptors is maintained. Our observations and analysis of Cancer Dependency Map (DepMap) screens show S5A depletion/loss substantially reduces cancer cell line viability. This and selective S5A dependency of proteasomal substrates make S5A a target of interest for cancer therapy.</p>","PeriodicalId":50454,"journal":{"name":"FEBS Letters","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9796813/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10485920","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
Integrin β1 transduces the signal for LY6D-induced macropinocytosis and mediates senescence-inducing stress-evoked vacuole formation via FAK. 整合素β1通过FAK传导ly6d诱导的巨噬细胞增多症信号并介导诱导衰老的应激诱导液泡形成。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2022-11-01 DOI: 10.1002/1873-3468.14477
Keitaro Nakagawa, Taiki Nagano, Ryoko Katasho, Tetsushi Iwasaki, Shinji Kamada
{"title":"Integrin β1 transduces the signal for LY6D-induced macropinocytosis and mediates senescence-inducing stress-evoked vacuole formation via FAK.","authors":"Keitaro Nakagawa,&nbsp;Taiki Nagano,&nbsp;Ryoko Katasho,&nbsp;Tetsushi Iwasaki,&nbsp;Shinji Kamada","doi":"10.1002/1873-3468.14477","DOIUrl":"https://doi.org/10.1002/1873-3468.14477","url":null,"abstract":"<p><p>Cellular senescence is a highly stable cell-cycle arrest induced by DNA damage and various cellular stresses. Recently, we have revealed that lymphocyte antigen 6 complex, locus D (LY6D) is responsible for senescence-inducing stress-evoked vacuole formation through induction of Src family kinase (SFK)-mediated macropinocytosis. However, the signaling molecule(s) transducing the macropinocytosis signal from extracellular LY6D to the cytoplasmic SFK are unknown. In this study, we identified integrin β1, a transmembrane signaling protein, as an interactor of LY6D by proteomic analysis and co-immunoprecipitation assays. Inhibition of integrin β1 impaired LY6D-induced macropinocytosis, and integrin β1 activated SFK through focal adhesion kinase to mediate macropinocytosis. These results indicate that integrin β1 is a crucial mediator of the LY6D-induced vacuole formation in senescent cells.</p>","PeriodicalId":50454,"journal":{"name":"FEBS Letters","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10370164","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: 1
Small RNA sequencing in hypoxic naked mole-rat hearts suggests microRNA regulation of RNA- and translation-related processes. 低氧裸鼹鼠心脏的小RNA测序表明，microRNA调控RNA和翻译相关过程。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2022-11-01 DOI: 10.1002/1873-3468.14499
W Aline Ingelson-Filpula, Hang Cheng, Liam Eaton, Matthew E Pamenter, Kenneth B Storey
{"title":"Small RNA sequencing in hypoxic naked mole-rat hearts suggests microRNA regulation of RNA- and translation-related processes.","authors":"W Aline Ingelson-Filpula,&nbsp;Hang Cheng,&nbsp;Liam Eaton,&nbsp;Matthew E Pamenter,&nbsp;Kenneth B Storey","doi":"10.1002/1873-3468.14499","DOIUrl":"https://doi.org/10.1002/1873-3468.14499","url":null,"abstract":"<p><p>The naked mole-rat (Heterocephalus glaber) regularly endures intermittent periods of hypoxia in its burrows, surviving in part due to metabolic rate depression (MRD)-a strategy of conserving cellular resources by downregulating nonessential gene expression and reorganizing cellular processes. miRNA are short, noncoding RNAs already implicated for their roles in numerous models of extreme environmental stress; given their rapid, reversible nature, they are ideal for implementing MRD. We performed small RNA sequencing on cardiac tissue from normoxic versus 24 h hypoxic naked mole-rats, and used bioinformatics to predict 18 miRNAs which may be differentially regulated during hypoxia. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway mapping further suggest these miRNAs play roles in largely translation-related functions, including RNA processing and catabolism.</p>","PeriodicalId":50454,"journal":{"name":"FEBS Letters","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10376784","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: 2
The mitochondrial enzyme FAHD1 regulates complex II activity in breast cancer cells and is indispensable for basal BT-20 cells in vitro. 线粒体酶FAHD1调节乳腺癌细胞中复合物II的活性，是体外基础BT-20细胞不可缺少的。
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2022-11-01 DOI: 10.1002/1873-3468.14462
Max Holzknecht, Lena Guerrero-Navarro, Michele Petit, Eva Albertini, Elisabeth Damisch, Anna Simonini, Fernando Schmitt, Walther Parson, Heidelinde Fiegl, Alexander Weiss, Pidder Jansen-Duerr
{"title":"The mitochondrial enzyme FAHD1 regulates complex II activity in breast cancer cells and is indispensable for basal BT-20 cells in vitro.","authors":"Max Holzknecht,&nbsp;Lena Guerrero-Navarro,&nbsp;Michele Petit,&nbsp;Eva Albertini,&nbsp;Elisabeth Damisch,&nbsp;Anna Simonini,&nbsp;Fernando Schmitt,&nbsp;Walther Parson,&nbsp;Heidelinde Fiegl,&nbsp;Alexander Weiss,&nbsp;Pidder Jansen-Duerr","doi":"10.1002/1873-3468.14462","DOIUrl":"https://doi.org/10.1002/1873-3468.14462","url":null,"abstract":"<p><p>The mitochondrial enzyme fumarylacetoacetate hydrolase domain-containing protein 1 (FAHD1) was identified to be upregulated in breast cancer tissues. Here, we show that FAHD1 is indispensable for the survival of BT-20 cells, representing the basal breast cancer cell type. A lentiviral knock-down of FAHD1 in the breast cancer cell lines MCF-7 and BT-20 results in lower succinate dehydrogenase (complex II) activity. In luminal MCF-7 cells, this leads to reduced proliferation when cultured in medium containing only glutamine as the carbon source. Of note, both cell lines show attenuated protein levels of the enzyme glutaminase (GLS) which activates programmed cell death in BT-20. These findings demonstrate that FAHD1 is crucial for the functionality of complex II in breast cancer cells and acts on glutaminolysis in the mitochondria.</p>","PeriodicalId":50454,"journal":{"name":"FEBS Letters","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7613834/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10739557","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: 1
Retraction Statement: The circadian rhythm regulator RpaA modulates photosynthetic electron transport and alters the preferable temperature range for growth in a cyanobacterium 撤回声明：昼夜节律调节因子RpaA调节光合电子传输，并改变蓝藻生长的最佳温度范围
IF 3.5 4区 生物学
FEBS Letters Pub Date : 2022-06-09 DOI: 10.1002/1873-3468.14363
{"title":"Retraction Statement: The circadian rhythm regulator RpaA modulates photosynthetic electron transport and alters the preferable temperature range for growth in a cyanobacterium","authors":"","doi":"10.1002/1873-3468.14363","DOIUrl":"https://doi.org/10.1002/1873-3468.14363","url":null,"abstract":"The above article, published online on 17 March 2021 in Wiley Online Library (https://febs.onlinelibrary.wiley. com/doi/10.1002/1873-3468.14075), has been retracted by agreement between the authors, the journal Editor in Chief, Michael Brunner, and John Wiley and Sons Ltd. The retraction has been agreed because, following publication, the authors realized that the clone used as WT strain (PCC7942) and reference in their study had acquired a spontaneous mutation that affected its temperature sensitivity, which impacted the conclusions about the role of RpaA. Therefore, the interpretation of the results was considered incorrect.","PeriodicalId":50454,"journal":{"name":"FEBS Letters","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2022-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42126236","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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