Genes to Cells最新文献_第10页

Isoliquiritigenin inhibits NLRP3 inflammasome activation with CAPS mutations by suppressing caspase-1 activation and mutated NLRP3 aggregation 异桔梗甙元通过抑制 Caspase-1 的激活和突变 NLRP3 的聚集，抑制了 CAPS 突变的 NLRP3 炎性体的激活。

IF 2.1 4区生物学

Genes to Cells Pub Date : 2024-02-17 DOI: 10.1111/gtc.13108

Fumitake Usui-Kawanishi, Koudai Kani, Tadayoshi Karasawa, Hiroe Honda, Nobuyuki Takayama, Masafumi Takahashi, Kiyoshi Takatsu, Yoshinori Nagai

{"title":"Isoliquiritigenin inhibits NLRP3 inflammasome activation with CAPS mutations by suppressing caspase-1 activation and mutated NLRP3 aggregation","authors":"Fumitake Usui-Kawanishi, Koudai Kani, Tadayoshi Karasawa, Hiroe Honda, Nobuyuki Takayama, Masafumi Takahashi, Kiyoshi Takatsu, Yoshinori Nagai","doi":"10.1111/gtc.13108","DOIUrl":"10.1111/gtc.13108","url":null,"abstract":"The nucleotide-binding oligomerization domain leucine-rich repeat and pyrin domain containing 3 (NLRP3) inflammasome contributes to the development of inflammatory diseases. Cryopyrin-associated periodic syndrome (CAPS) is an autoinflammatory disease caused by NLRP3 gene mutations that results in excessive IL-1β production. We previously identified isoliquiritigenin (ILG), a component of Glycyrrhiza uralensis extracts, as a potent inhibitor of the NLRP3 inflammasome. Here, we aimed to investigate whether ILG inhibits the activation of NLRP3 inflammasome caused by NLRP3 gene mutations. We demonstrated that ILG significantly inhibited NLRP3 inflammasome-mediated lactate dehydrogenase (LDH) release and IL-1β production in two CAPS model THP-1 cell lines, NLRP3-D303N and NLRP3-L353P, in a dose-dependent manner. Interestingly, the NLRP3 inhibitor MCC950 inhibited LDH release and IL-1β production in NLRP3-D303N cells, but not in NLRP3-L353P cells. Western blotting and caspase-1 activity assays showed that ILG, as well as caspase inhibitors, including Z-VAD and YVAD, suppressed caspase-1 activation. Notably, ILG prevented cryo-sensitive foci formation of NLRP3 without affecting the levels of intracellular Ca2+. We concluded that ILG effectively prevents the constitutive activation of the inflammasome associated with NLRP3 gene mutations by inhibiting the aggregation of cryo-sensitive mutated NLRP3.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"29 5","pages":"423-431"},"PeriodicalIF":2.1,"publicationDate":"2024-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139746516","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

Analysis of the responsiveness to antiandrogens in multiple breast cancer cell lines 分析多种乳腺癌细胞系对抗雄激素的反应性。

IF 2.1 4区生物学

Genes to Cells Pub Date : 2024-02-17 DOI: 10.1111/gtc.13105

Yuka Kuroiwa, Kagenori Ito, Jun Nakayama, Kentaro Semba, Yusuke Yamamoto

{"title":"Analysis of the responsiveness to antiandrogens in multiple breast cancer cell lines","authors":"Yuka Kuroiwa, Kagenori Ito, Jun Nakayama, Kentaro Semba, Yusuke Yamamoto","doi":"10.1111/gtc.13105","DOIUrl":"10.1111/gtc.13105","url":null,"abstract":"Antiandrogens were originally developed as therapeutic agents for prostate cancer but are also expected to be effective for breast cancer. However, the role of androgen signaling in breast cancer has long been controversial due to the limited number of experimental models. Our study aimed to comprehensively investigate the efficacy of antiandrogens on breast cancer. In the present study, a total of 18 breast cancer cell lines were treated with the agonist or antagonists of the androgen receptor (AR). Among the 18 cell lines tested, only T-47D cells proliferated in an androgen-dependent manner, while the other cell lines were almost irresponsive to AR stimulation. On the other hand, treatment with AR antagonists at relatively high doses suppressed the proliferation of not only T-47D cells but also some other cell lines including AR-low/negative cells. In addition, expression of the full-length AR and constitutively active AR splice variants, AR-V7 and ARV567es, was not correlated with sensitivity to AR antagonists. These data suggest that the antiproliferative effect of AR antagonists is AR-independent in some cases. Consistently, proliferation of AR-knockout BT-549 cells was inhibited by AR antagonists. Identification of biomarkers would be necessary to determine which breast cancer patients will benefit from these drugs.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"29 4","pages":"301-315"},"PeriodicalIF":2.1,"publicationDate":"2024-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139746514","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

Cathepsin L prevents the accumulation of alpha-synuclein fibrils in the cell Cathepsin L 可防止 alpha-synuclein 纤维在细胞内积聚。

IF 2.1 4区生物学

Genes to Cells Pub Date : 2024-02-17 DOI: 10.1111/gtc.13099

Ayumi Matsuki, Yoshihisa Watanabe, Sho Hashimoto, Atsushi Hoshino, Satoaki Matoba

引用次数: 0

Roles of linker region flanked by transmembrane and peptidoglycan binding region of PomB in energy conversion of the Vibrio flagellar motor PomB 跨膜和肽聚糖结合区两侧的连接区在弧菌鞭毛运动的能量转换中的作用。

IF 2.1 4区生物学

Genes to Cells Pub Date : 2024-02-14 DOI: 10.1111/gtc.13102

Yusuke Miyamura, Tatsuro Nishikino, Hiroaki Koiwa, Michio Homma, Seiji Kojima

{"title":"Roles of linker region flanked by transmembrane and peptidoglycan binding region of PomB in energy conversion of the Vibrio flagellar motor","authors":"Yusuke Miyamura, Tatsuro Nishikino, Hiroaki Koiwa, Michio Homma, Seiji Kojima","doi":"10.1111/gtc.13102","DOIUrl":"10.1111/gtc.13102","url":null,"abstract":"The flagellar components of Vibrio spp., PomA and PomB, form a complex that transduces sodium ion and contributes to rotate flagella. The transmembrane protein PomB is attached to the basal body T-ring by its periplasmic region and has a plug segment following the transmembrane helix to prevent ion flux. Previously we showed that PomB deleted from E41 to R120 (Δ41–120) was functionally comparable to the full-length PomB. In this study, three deletions after the plug region, PomB (Δ61–120), PomB (Δ61–140), and PomB (Δ71–150), were generated. PomB (Δ61–120) conferred motility, whereas the other two mutants showed almost no motility in soft agar plate; however, we observed some swimming cells with speed comparable for the wild-type cells. When the two PomB mutants were introduced into a wild-type strain, the swimming ability was not affected by the mutant PomBs. Then, we purified the mutant PomAB complexes to confirm the stator formation. When plug mutations were introduced into the PomB mutants, the reduced motility by the deletion was rescued, suggesting that the stator was activated. Our results indicate that the deletions prevent the stator activation and the linker and plug regions, from E41 to S150, are not essential for the motor function of PomB but are important for its regulation.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"29 4","pages":"282-289"},"PeriodicalIF":2.1,"publicationDate":"2024-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139729429","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

CdsA, a CDP-diacylglycerol synthase involved in phospholipid and glycolipid MPIase biosynthesis, possesses multiple initiation codons CdsA 是一种参与磷脂和糖脂 MPI 酶生物合成的 CDP-二酰甘油合成酶，具有多个起始密码子。

IF 2.1 4区生物学

Genes to Cells Pub Date : 2024-02-13 DOI: 10.1111/gtc.13104

Runa Hikage, Yusei Sekiya, Katsuhiro Sawasato, Ken-ichi Nishiyama

{"title":"CdsA, a CDP-diacylglycerol synthase involved in phospholipid and glycolipid MPIase biosynthesis, possesses multiple initiation codons","authors":"Runa Hikage, Yusei Sekiya, Katsuhiro Sawasato, Ken-ichi Nishiyama","doi":"10.1111/gtc.13104","DOIUrl":"10.1111/gtc.13104","url":null,"abstract":"CdsA is a CDP-diacylglycerol synthase essential for phospholipid and glycolipid MPIase biosynthesis, and therefore for growth. The initiation codon of CdsA has been assigned as “TTG,” while methionine at the 37th codon was reported to be an initiation codon in the original report. Since a vector containing the open reading frame starting with “TTG” under a controllable promoter complemented the cdsA knockout, “TTG” could function as an initiation codon. However, no evidence supporting that this “TTG” is the sole initiation codon has been reported. We determined the initiation codon by examining the ability of mutants around the N-terminal region to complement cdsA mutants. Even if the “TTG” was substituted with a stop codon, the clear complementation was observed. Moreover, the clones with multiple mutations of stop codons complemented the cdsA mutant up to the 37th codon, indicating that cdsA possesses multiple codons that can function as initiation codons. We constructed an experimental system in which the chromosomal expression of cdsA can be analyzed. By means of this system, we found that the cdsA mutant with substitution of “TTG” with a stop codon is fully functional. Thus, we concluded that CdsA contains multiple initiation codons.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"29 4","pages":"347-355"},"PeriodicalIF":2.1,"publicationDate":"2024-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.13104","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139729427","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

Publishing in the Open Access and Open Science era 开放获取和开放科学时代的出版。

IF 2.1 4区生物学

Genes to Cells Pub Date : 2024-02-13 DOI: 10.1111/gtc.13100

Masanori Arita, Bernd Pulverer, Tadashi Uemura, Chisako Sakuma, Shigeo Hayashi

{"title":"Publishing in the Open Access and Open Science era","authors":"Masanori Arita, Bernd Pulverer, Tadashi Uemura, Chisako Sakuma, Shigeo Hayashi","doi":"10.1111/gtc.13100","DOIUrl":"10.1111/gtc.13100","url":null,"abstract":"Our research activities would be better served if they were communicated in a manner that is openly accessible to the public and all researchers. The research we share is often limited to representative data included in research papers—science would be much more efficient if all reproducible research data were shared alongside detailed methods and protocols, in the paradigm called Open Science. On the other hand, one primary function of research journals is to select manuscripts of good quality, verify the authenticity of the data and its impact, and deliver to the appropriate audience for critical evaluation and verification. In the current paradigm, where publication in a subset of journals is intimately linked to research evaluation, a hypercompetitive “market” has emerged where authors compete to access a limited number of top-tier journals, leading to high rejection rates. Competition among publishers and scientific journals for market dominance resulted in an increase in both the number of journals and the cost of publishing and accessing scientific papers. Here we summarize the current problems and potential solutions from the development of AI technology discussed in the seminar at the 46th Annual Meeting of the Molecular Biology Society of Japan.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"29 4","pages":"275-281"},"PeriodicalIF":2.1,"publicationDate":"2024-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.13100","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139729428","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

C9orf10/Ossa regulates the bone metastasis of established lung adenocarcinoma cell subline H322L-BO4 in a mouse model 在小鼠模型中，C9orf10/Ossa调节已建立的肺腺癌细胞亚系H322L-BO4的骨转移。

IF 2.1 4区生物学

Genes to Cells Pub Date : 2024-02-10 DOI: 10.1111/gtc.13103

Takamasa Uekita, Reiko Yagi, Tohru Ichimura, Ryuichi Sakai

{"title":"C9orf10/Ossa regulates the bone metastasis of established lung adenocarcinoma cell subline H322L-BO4 in a mouse model","authors":"Takamasa Uekita, Reiko Yagi, Tohru Ichimura, Ryuichi Sakai","doi":"10.1111/gtc.13103","DOIUrl":"10.1111/gtc.13103","url":null,"abstract":"Lung cancer frequently metastasizes to the bones. An in vivo model is urgently required to identify potential therapeutic targets for the prevention and treatment of lung cancer with bone metastasis. We established a lung adenocarcinoma cell subline (H322L-BO4) that specifically showed metastasis to the leg bones and adrenal glands. This was achieved by repeated isolation of metastatic cells from the leg bones of mice. The cells were intracardially injected into nude mice. Survival was prolonged for mice that received H322L-BO4 cells versus original cells (H322L). H322L-BO4 cells did not exhibit obvious changes in general in vitro properties associated with the metastatic potential (e.g., cell growth, migration, and invasion) compared with H322L cells. However, the phosphorylation of chromosome 9 open reading frame 10/oxidative stress-associated Src activator (C9orf10/Ossa) was increased in H322L-BO4 cells. This result confirmed the increased anchorage independence through C9orf10/Ossa-mediated activation of Src family tyrosine kinase. Reduction of C9orf10/Ossa by shRNA reduced cells' metastasis to the leg bone and prolonged survival in mice. These findings indicate that H322L-BO4 cells can be used to evaluate the effect of candidate therapeutic targets against bone metastatic lung cancer cells. Moreover, C9orf10/Ossa may be a useful target for treatment of lung cancer with bone metastasis.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"29 4","pages":"290-300"},"PeriodicalIF":2.1,"publicationDate":"2024-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.13103","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139711824","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

Microtubule-affinity regulating kinase family members distinctively affect tau phosphorylation and promote its toxicity in a Drosophila model 在果蝇模型中，微管亲和性调节激酶家族成员会明显影响 tau 的磷酸化并促进其毒性。

IF 2.1 4区生物学

Genes to Cells Pub Date : 2024-02-08 DOI: 10.1111/gtc.13101

Grigorii Sultanakhmetov, Iori Kato, Akiko Asada, Taro Saito, Kanae Ando

{"title":"Microtubule-affinity regulating kinase family members distinctively affect tau phosphorylation and promote its toxicity in a Drosophila model","authors":"Grigorii Sultanakhmetov, Iori Kato, Akiko Asada, Taro Saito, Kanae Ando","doi":"10.1111/gtc.13101","DOIUrl":"10.1111/gtc.13101","url":null,"abstract":"Accumulation of abnormally phosphorylated tau and its aggregation constitute a significant hallmark of Alzheimer's disease (AD). Tau phosphorylation at Ser262 and Ser356 in the KXGS motifs of microtubule-binding repeats plays a critical role in its physiological function and AD disease progression. Major tau kinases to phosphorylate tau at Ser262 and Ser356 belong to the Microtubule Affinity Regulating Kinase family (MARK1-4), which are considered one of the major contributors to tau abnormalities in AD. However, whether and how each member affects tau toxicity in vivo is unclear. We used transgenic Drosophila as a model to compare the effect on tau-induced neurodegeneration among MARKs in vivo. MARK4 specifically promotes tau accumulation and Ser396 phosphorylation, which yields more tau toxicity than was caused by other MARKs. Interestingly, MARK1, 2, and 4 increased tau phosphorylation at Ser262 and Ser356, but only MARK4 caused tau accumulation, indicating that these sites alone did not cause pathological tau accumulation. Our results revealed MARKs are different in their effect on tau toxicity, and also in tau phosphorylation at pathological sites other than Ser262 and Ser356. Understanding the implementation of each MARK into neurodegenerative disease helps to develop more target and safety therapies to overcome AD and related tauopathies.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"29 4","pages":"337-346"},"PeriodicalIF":2.1,"publicationDate":"2024-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.13101","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139702295","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

The anti-inflammatory effect of metformin: The molecular targets 二甲双胍的抗炎作用：分子靶点。

IF 2.1 4区生物学

Genes to Cells Pub Date : 2024-02-04 DOI: 10.1111/gtc.13098

Natsumi Sakata

引用次数: 0

Transcriptional features of low-grade neuroepithelial tumors with the BRAF V600E mutation associated with epileptogenicity 与致痫性相关的 BRAF V600E 突变低级别神经上皮肿瘤的转录特征。

IF 2.1 4区生物学

Genes to Cells Pub Date : 2024-01-25 DOI: 10.1111/gtc.13096

Keiya Iijima, Kanako Komatsu, Satoshi Miyashita, Kyoka Suyama, Kumiko Murayama, Koichi Hashizume, Nao K. Tabe, Hajime Miyata, Masaki Iwasaki, Shinichiro Taya, Mikio Hoshino

{"title":"Transcriptional features of low-grade neuroepithelial tumors with the BRAF V600E mutation associated with epileptogenicity","authors":"Keiya Iijima, Kanako Komatsu, Satoshi Miyashita, Kyoka Suyama, Kumiko Murayama, Koichi Hashizume, Nao K. Tabe, Hajime Miyata, Masaki Iwasaki, Shinichiro Taya, Mikio Hoshino","doi":"10.1111/gtc.13096","DOIUrl":"10.1111/gtc.13096","url":null,"abstract":"Low-grade neuroepithelial tumors are major causes of drug-resistant focal epilepsy. Clinically, these tumors are defined as low-grade epilepsy-associated neuroepithelial tumors (LEATs). The BRAF V600E mutation is frequently observed in LEAT and linked to poor seizure outcomes. However, its molecular role in epileptogenicity remains elusive. To understand the molecular mechanism underlying the epileptogenicity in LEAT with the BRAF V600E genetic mutation (BRAF V600E-LEAT), we conducted RNA sequencing (RNA-seq) analysis using surgical specimens of BRAF V600E-LEAT obtained and stored at a single institute. We obtained 21 BRAF V600E-LEAT specimens and 4 control specimens, including 24 from Japanese patients and 1 from a patient of Central Asian origin, along with comprehensive clinical data. We submitted the transcriptome dataset of 21 BRAF V600E-LEAT plus 4 controls, as well as detailed clinical information, to a public database. Preliminary bioinformatics analysis using this dataset identified 2134 differentially expressed genes between BRAF V600E-LEAT and control. Additionally, gene set enrichment analysis provided novel insights into the association between estrogen response-related pathways and the epileptogenicity of BRAF V600E-LEAT patients. Our datasets and findings will contribute toward the understanding of the pathology of epilepsy caused by LEAT and the identification of new therapeutic targets.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"29 3","pages":"192-206"},"PeriodicalIF":2.1,"publicationDate":"2024-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139545773","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