IUBMB Life最新文献_第4页

Genomic features of lichen-associated black fungi 与地衣相关的黑色真菌的基因组特征。

IF 3.7 3区生物学

IUBMB Life Pub Date : 2024-12-22 DOI: 10.1002/iub.2934

Victoria Keller, Anjuli Calchera, Jürgen Otte, Imke Schmitt

{"title":"Genomic features of lichen-associated black fungi","authors":"Victoria Keller, Anjuli Calchera, Jürgen Otte, Imke Schmitt","doi":"10.1002/iub.2934","DOIUrl":"10.1002/iub.2934","url":null,"abstract":"Lichens are mutualistic associations consisting of a primary fungal host, and one to few primary phototrophic symbiont(s), usually a green alga and/or a cyanobacterium. They form complex thallus structures, which provide unique and stable habitats for many other microorganisms. Frequently isolated from lichens are the so-called black fungi, or black yeasts, which are mainly characterized by melanized cell walls and extremophilic lifestyles. It is presently unclear in which ways these fungi interact with other members of the lichen symbiosis. Genomic resources of lichen-associated black fungi are needed to better understand the physiological potential of these fungi and shed light on the complexity of the lichen consortium. Here, we present high-quality genomes of 14 black fungal lineages, isolated from lichens of the rock-dwelling genus Umbilicaria. Nine of the lineages belong to the Eurotiomycetes (Chaetothyriales), four to the Dothideomycetes, and one to the Arthoniomycetes, representing the first genome of a black fungus in this class. The PacBio-based assemblies are highly contiguous (5–42 contigs per genome, mean coverage of 79–502, N50 of 1.0–7.3 mega-base-pair (Mb), Benchmarking Universal Single-Copy Orthologs (BUSCO) completeness generally ≥95.4%). Most contigs are flanked by a telomere sequence, suggesting we achieved near chromosome-level assemblies. Genome sizes range between 26 and 44 Mb. Transcriptome-based annotations yielded ~11,000–18,000 genes per genome. We analyzed genome content with respect to repetitive elements, biosynthetic genes, and effector genes. Each genome contained a polyketide synthase gene related to the dihydroxynaphthalene-melanin pathway. This research provides insights into genome content and metabolic potential of these relatively unknown, but frequently encountered lichen associates.","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11664114/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142877237","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

Human disease-causing missense genetic variants are enriched in the evolutionarily ancient domains of the cytosolic aminoacyl-tRNA synthetase proteins 人类致病的错义遗传变异富集于进化上古老的胞质氨基酰基- trna合成酶蛋白结构域。

IF 3.7 3区生物学

IUBMB Life Pub Date : 2024-12-22 DOI: 10.1002/iub.2932

Alexandra K. Turvey, André R. O. Cavalcanti

{"title":"Human disease-causing missense genetic variants are enriched in the evolutionarily ancient domains of the cytosolic aminoacyl-tRNA synthetase proteins","authors":"Alexandra K. Turvey, André R. O. Cavalcanti","doi":"10.1002/iub.2932","DOIUrl":"10.1002/iub.2932","url":null,"abstract":"All life depends on accurate and efficient protein synthesis. The aminoacyl-tRNA synthetases (aaRSs) are a family of proteins that play an essential role in protein translation, as they catalyze the esterification reaction that charges a transfer RNA (tRNA) with its cognate amino acid. However, new domains added to the aaRSs over the course of evolution in eukaryotes confer novel functions unrelated to protein translation. To date, damaging variants that affect aaRS-encoding genes have been linked to over 50 human diseases. In this study, we leverage the evolutionary history of the aaRS proteins to better understand the distribution of disease-causing missense variants in human cytosolic aaRSs. We hypothesized that disease-causing missense variants in human aaRSs were more likely to be located in the ancient domains of the aaRS, essential for the aminoacylation reaction, rather than in the evolutionarily more recent domains found in eukaryotes. We determined the locations of the modern and ancient domains in each aaRS protein found in humans. We then statistically assessed the positional conservation across each domain and examined the distribution of pathogenic and benign/unknown missense human genetic variants across these domains. We establish that pathogenic missense variants in the human aaRS proteins are enriched in the evolutionarily ancient domains while benign/unknown missense variants are enriched in the modern domains. In addition to defining the evolutionary history of human aaRS proteins through domain identification, we anticipate that this work will improve the ability to diagnose patients affected by damaging genetic variants in the aaRS protein family.","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11664165/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142877239","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

Integrated multi-omics and machine learning reveal a gefitinib resistance signature for prognosis and treatment response in lung adenocarcinoma 综合多组学和机器学习揭示了肺腺癌预后和治疗反应的吉非替尼耐药特征。

IF 3.7 3区生物学

IUBMB Life Pub Date : 2024-11-29 DOI: 10.1002/iub.2930

Dong Zhou, Zhi Zheng, Yanqi Li, Jiao Zhang, Xiao Lu, Hong Zheng, Jigang Dai

{"title":"Integrated multi-omics and machine learning reveal a gefitinib resistance signature for prognosis and treatment response in lung adenocarcinoma","authors":"Dong Zhou, Zhi Zheng, Yanqi Li, Jiao Zhang, Xiao Lu, Hong Zheng, Jigang Dai","doi":"10.1002/iub.2930","DOIUrl":"10.1002/iub.2930","url":null,"abstract":"Gefitinib resistance (GR) presents a significant challenge in treating lung adenocarcinoma (LUAD), highlighting the need for alternative therapies. This study explores the genetic basis of GR to improve prediction, prevention, and treatment strategies. We utilized public databases to obtain GR gene sets, single-cell data, and transcriptome data, applying univariate and multivariate regression analyses alongside machine learning to identify key genes and develop a predictive signature. The signature's performance was evaluated using survival analysis and time-dependent ROC curves on internal and external datasets. Enrichment and tumor immune microenvironment analyses were conducted to understand the mechanistic roles of the signature genes in GR. Our analysis identified a robust 22-gene signature with strong predictive performance across validation datasets. This signature was significantly associated with chromosomal processes, DNA replication, immune cell infiltration, and various immune scores based on enrichment and tumor microenvironment analyses. Importantly, the signature also showed potential in predicting the efficacy of immunotherapy in LUAD patients. Moreover, we identified alternative agents to gefitinib that could offer improved therapeutic outcomes for high-risk and low-risk patient groups, thereby guiding treatment strategies for gefitinib-resistant patients. In conclusion, the 22-gene signature not only predicts prognosis and immunotherapy efficacy in gefitinib-resistant LUAD patients but also provides novel insights into non-immunotherapy treatment options.","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755016","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

Role of the initiation factor 3 in the fidelity of initiator tRNA selection on ribosome 启动因子 3 在核糖体上选择启动子 tRNA 的保真度中的作用。

IF 3.7 3区生物学

IUBMB Life Pub Date : 2024-11-23 DOI: 10.1002/iub.2927

Jitendra Singh, Umesh Varshney

引用次数: 0

YTHDF3 rs7464 A > G polymorphism increases Chinese neuroblastoma risk: A multiple-center case–control study YTHDF3 rs7464 A > G 多态性增加中国人患神经母细胞瘤的风险：一项多中心病例对照研究。

IF 3.7 3区生物学

IUBMB Life Pub Date : 2024-11-22 DOI: 10.1002/iub.2923

Huiran Lin, Yongping Chen, Liping Chen, Wenli Zhang, Jinhong Zhu, Xinxin Zhang, Zhonghua Yang, Jiao Zhang, Jiwen Cheng, Li Li, Haixia Zhou, Suhong Li, Zhenjian Zhuo, Jing He

{"title":"YTHDF3 rs7464 A > G polymorphism increases Chinese neuroblastoma risk: A multiple-center case–control study","authors":"Huiran Lin, Yongping Chen, Liping Chen, Wenli Zhang, Jinhong Zhu, Xinxin Zhang, Zhonghua Yang, Jiao Zhang, Jiwen Cheng, Li Li, Haixia Zhou, Suhong Li, Zhenjian Zhuo, Jing He","doi":"10.1002/iub.2923","DOIUrl":"10.1002/iub.2923","url":null,"abstract":"Neuroblastoma (NB), a rare childhood cancer originating in nerve tissue. YTHDF3, a member of the YTH domain protein family, is involved in RNA m6A modification and cancer progression. Polymorphisms in YTHDF3 may influence its expression and biological function. Herein, this study estimated the association between YTHDF3 polymorphisms (rs2241753, rs2241754, and rs7464) and NB susceptibility in a multicenter study comprising 898 cases and 1734 controls. We genotyped YTHDF3 candidate polymorphisms by the TaqMan assay. Logistic regression analysis was applied to indicate the possible relationships between these polymorphisms and NB susceptibility, using odds ratios (ORs) and 95% confidence intervals (CIs). Logistic regression analysis revealed that the rs2241753 GA versus GG decreased NB risk (Adjusted OR = 0.84, 95% CI = 0.71–0.997, p = .047), while the rs7464 GG versus AA enhanced NB risk (Adjusted OR = 1.62, 95% CI = 1.20–2.18, p = .002). Additionally, rs7464 GG versus AA/AG showed a higher risk (Adjusted OR = 1.66, 95% CI = 1.24–2.22, p = .0006). Combination analysis showed that having 1–3 risk genotypes versus 0 was associated with increased NB risk (Adjusted OR = 1.28, 95%CI = 1.09–1.51, p = .003). The significance of rs7464 and the risk genotypes combination persisted across multiple subgroups, whereas rs2241754 was significant only in mediastinal NB. False-positive report probability (FPRP) confirmed the reliability of results. Notably, the interaction between rs7464 and rs2241754 may increase NB risk dramatically. Our study demonstrated that YTHDF3 rs7464 A > G significantly affected NB susceptibility, warranting validation in larger sample sizes.","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142687044","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

KRT80 in hepatocellular carcinoma plays oncogenic role via epithelial–mesenchymal transition and PI3K/AKT pathway 肝细胞癌中的 KRT80 通过上皮-间质转化和 PI3K/AKT 通路发挥致癌作用。

IF 3.7 3区生物学

IUBMB Life Pub Date : 2024-11-21 DOI: 10.1002/iub.2925

Ruheng Hua, Xiyue Yan, Jun He, Nuwa Wu, Wangjianfei Yu, Pengfei Yu, Lei Qin

引用次数: 0

Depletion of macrophages and osteoclast precursors mitigates iron overload-mediated bone loss 消耗巨噬细胞和破骨细胞前体可减轻铁超载介导的骨质流失。

IF 3.7 3区生物学

IUBMB Life Pub Date : 2024-11-18 DOI: 10.1002/iub.2928

Vanessa Passin, Maria G. Ledesma-Colunga, Sandro Altamura, Martina U. Muckenthaler, Ulrike Baschant, Lorenz C. Hofbauer, Martina Rauner

{"title":"Depletion of macrophages and osteoclast precursors mitigates iron overload-mediated bone loss","authors":"Vanessa Passin, Maria G. Ledesma-Colunga, Sandro Altamura, Martina U. Muckenthaler, Ulrike Baschant, Lorenz C. Hofbauer, Martina Rauner","doi":"10.1002/iub.2928","DOIUrl":"10.1002/iub.2928","url":null,"abstract":"Iron is an essential element for physiological cellular processes, but is toxic in excess. Iron overload diseases are commonly associated with low bone mass. Increased bone resorption by osteoclasts as well as decreased bone formation by osteoblasts have been implicated in bone loss under iron overload conditions. However, the exact contribution of individual cell types has not yet been formally tested. In this study, we aimed to investigate the role of osteoclast precursors in iron overload-induced bone loss. To that end, we used clodronate liposomes to deplete phagocytic cells (including macrophages and osteoclast precursors) in male C57BL/6J mice that were exposed to ferric derisomaltose. Bone microarchitecture and bone turnover were assessed after 4 weeks. The application of clodronate resulted in the efficient depletion of circulating myeloid-lineage cells by about 70%. Depletion of osteoclast precursors mitigated iron overload-induced trabecular bone loss at the lumbar vertebrae and distal femur. While clodronate treatment led to a profound inhibition of bone turnover in control mice, it significantly reduced osteoclast numbers in iron-treated mice without further impacting the bone formation rate or serum PINP levels. Our observations suggest that even though bone formation is markedly suppressed by iron overload, osteoclasts also play a key role in iron overload-induced bone loss and highlight them as potential therapeutic targets.","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iub.2928","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142648266","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

KGF secreted from HSCs activates PAK4/BMI1, promotes HCC stemness through PI3K/AKT pathway 造血干细胞分泌的KGF可激活PAK4/BMI1，并通过PI3K/AKT途径促进HCC干细胞的形成。

IF 3.7 3区生物学

IUBMB Life Pub Date : 2024-11-15 DOI: 10.1002/iub.2929

Qinghua Li, Qiuyang Chen, Wenchao Wang, Rongrong Xie, Zhen Li, Dawei Chen

{"title":"KGF secreted from HSCs activates PAK4/BMI1, promotes HCC stemness through PI3K/AKT pathway","authors":"Qinghua Li, Qiuyang Chen, Wenchao Wang, Rongrong Xie, Zhen Li, Dawei Chen","doi":"10.1002/iub.2929","DOIUrl":"10.1002/iub.2929","url":null,"abstract":"In our present study, we investigated the interaction between HSCs and HCC, also explored the molecular mechanism. Clinical samples were collected from HCC and adjacent tissue with different degree of liver fibrosis. HCC cells were co-cultured with LX-2 cell by Transwell system or cultured with conditioned medium (CM), which was collected from LX-2. The tumor spheroid growth and colony formation analyses were performed to evaluate the cell stemness. Flow cytometry analysis was conducted on cell apoptosis after 5-Fu treatment. Co-immunoprecipitation assay confirmed the interaction between BMI1 and PAK4. Our results showed that BMI1 was highly expressed in HCC and was correlated with HCC liver fibrosis. Both co-cultured with LX-2 and cultured with CM promoted HCC stemness, also increased KGF level and BMI1 expression. KGF treatment had a similar effect with co-culture with LX-2 on HCC. BMI1 overexpression promoted HCC stemness and activated PI3K/AKT pathway, which was reversed by PI3K inhibition. PAK4 was activated by KGF, then phosphorylated S315 site and promoted protein stability of BMI1, therefore enhanced HCC stemness. BMI1 also had a promote effect on liver fibrosis. In summary, we found that KGF secreted by HSCs activated PAK4, which phosphorylated S315 and promoted protein stability of BMI1, and further promoted liver fibrosis and HCC stemness through the PI3K/AKT signaling pathway. Our present study deeply studied the interaction and mechanism between HSCs and HCC, which might provide a new insight for HCC therapy.","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142620671","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

RETRACTION: Nutritional Flavonoids Modulate Estrogen Receptor α Signaling 回归：营养类黄酮调节雌激素受体 α 信号传导

IF 3.7 3区生物学

IUBMB Life Pub Date : 2024-11-07 DOI: 10.1002/iub.2926

{"title":"RETRACTION: Nutritional Flavonoids Modulate Estrogen Receptor α Signaling","authors":"","doi":"10.1002/iub.2926","DOIUrl":"10.1002/iub.2926","url":null,"abstract":"\u0000 F. Virgili, F. Acconcia, R. Ambra, A. Rinna, P. Totta, and M. Marino, “ Nutritional Flavonoids Modulate Estrogen Receptor α Signaling,” IUBMB Life 56, no. 3 (2004): 145–151, https://doi.org/10.1080/15216540410001685083.The above article, published online on 3 January 2008 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Efstathios S. Gonos; the International Union of Biochemistry and Molecular Biology; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Specifically, duplication of several Western Blot bands has been detected within Figure 2a. The relative raw data could no longer be accessed due to the considerable time elapsed since the article's publication. The corresponding author, Maria Marino, maintains that the concerns do not impact the overall results and conclusions of the study, and disagrees with the decision of retraction. However, the article is retracted as the editors have lost trust in the integrity of the data presented and consider the conclusions invalid.","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iub.2926","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142604560","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

Aminoacyl-tRNA synthetase defects in neurological diseases 神经系统疾病中的氨基酰-tRNA 合成酶缺陷。

IF 3.7 3区生物学

IUBMB Life Pub Date : 2024-11-02 DOI: 10.1002/iub.2924

Hong Zhang, Jiqiang Ling

引用次数: 0