Genes to Cells最新文献_第2页

Identification of the Down Syndrome Critical Region 3 Gene as a Mammalian Cell Size Regulator 唐氏综合征关键区3基因作为哺乳动物细胞大小调节因子的鉴定

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-08-14 DOI: 10.1111/gtc.70142

Kazumi Kimura, Masakazu Souda, Ryotaro Mori, Yoshimi Kato, Hiroki Kurahashi, Masashi Asai, Kazuo Yamamoto

引用次数: 0

Correction to “An Outflow Tract Myocardium-Specific Enhancer at the Sema3c Locus During Heart Development” 更正“心脏发育过程中Sema3c位点流出道心肌特异性增强子”。

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-08-11 DOI: 10.1111/gtc.70144

引用次数: 0

Characterization of Nucleobase Cation Symporter 1 (NCS1) Localized to the Plastids of Nicotiana tabacum 烟草质体核碱基阳离子同调子1 （NCS1）的研究。

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-08-09 DOI: 10.1111/gtc.70143

Nobukazu Shitan, Shota Minami, Taku Tsuyama, Minaho Hayashida, Yasuyuki Yamada, Keita Kato, Yoko Nakahara, Yoshinori Moriyama, Alain Goossens, Kazufumi Yazaki

{"title":"Characterization of Nucleobase Cation Symporter 1 (NCS1) Localized to the Plastids of Nicotiana tabacum","authors":"Nobukazu Shitan, Shota Minami, Taku Tsuyama, Minaho Hayashida, Yasuyuki Yamada, Keita Kato, Yoko Nakahara, Yoshinori Moriyama, Alain Goossens, Kazufumi Yazaki","doi":"10.1111/gtc.70143","DOIUrl":"10.1111/gtc.70143","url":null,"abstract":"<div>\u0000 \u0000 Jasmonate-mediated defense responses redirect plant resources from growth to defense, imposing significant demands on the nitrogen economy to produce nitrogenous compounds, such as alkaloids. However, the mechanisms by which plants maintain essential central metabolic processes, such as nucleotide synthesis, under nitrogen resource competition remain unclear. Therefore, in this study, we characterized the nucleobase cation symporter NtNCS1 in Nicotiana tabacum. Notably, NtNCS1 mRNA exhibited opposing organ-specific regulation by jasmonic acid, with induction in roots (the site of nicotine synthesis) but repression in leaves. NtNCS1 was localized to the plastid envelope in metabolically active cells, including mesophyll, phloem-associated, and, notably, guard cells. This dual regulation suggests that NtNCS1 plays a key role in reallocating nitrogen resources. In roots, its expression possibly contributes to maintaining the essential nucleotide pools for basal metabolism when nitrogen is diverted to alkaloid production. Conversely, its repression in leaves possibly conserves nitrogen by downregulating growth, thereby reallocating resources to defense. Overall, this study highlights the potential roles of NCS1 transporters in safeguarding central metabolism and mediating the plant growth–defense trade-off.\u0000 </div>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 5","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148703231","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

EXPRESSION OF CONCERN: Ser46 Phosphorylation of p53 Is Not Always Sufficient to Induce Apoptosis: Multiple Mechanisms of Regulation of p53-Dependent Apoptosis 关注表达：p53的Ser46磷酸化并不总是足以诱导细胞凋亡：p53依赖性细胞凋亡的多种调节机制。

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-08-05 DOI: 10.1111/gtc.70141

{"title":"EXPRESSION OF CONCERN: Ser46 Phosphorylation of p53 Is Not Always Sufficient to Induce Apoptosis: Multiple Mechanisms of Regulation of p53-Dependent Apoptosis","authors":"","doi":"10.1111/gtc.70141","DOIUrl":"10.1111/gtc.70141","url":null,"abstract":"EXPRESSION OF CONCERN: A. Kurihara, H. Nagoshi, M. Yabuki, R. Okuyama, M. Obinata and S. Ikawa, “ Ser46 Phosphorylation of p53 Is Not Always Sufficient to Induce Apoptosis: Multiple Mechanisms of Regulation of p53-Dependent Apoptosis,” Genes to Cells 12, no. 7 (2007): 853–861, https://doi.org/10.1111/j.1365-2443.2007.01097.x.This Expression of Concern is for the above article, published online on 20 June 2007 in Wiley Online Library (https://onlinelibrary.wiley.com), and has been issued by agreement between the journal Editor-in-Chief, Tadashi Uemura; The Molecular Biology Society of Japan; and John Wiley & Sons Australia, Ltd. The Expression of Concern has been agreed following concerns raised by a third party. An investigation identified apparent duplication between bands in the p53 ser20 panel of the IP anti-p53 experiment and bands in the p53 panel of the lysate experiment shown in Figure 2A. The authors were contacted to provide original data and an explanation but did not respond. As the conclusions are not believed to be affected, the journal has issued this Expression of Concern to inform and alert readers about these concerns.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 5","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13443350/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148681941","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

Treatment With Ruxolitinib and TAK-779 Enhances GII.17 Human Norovirus Replication and Enables Serial Passaging in Human Intestinal Enteroids Ruxolitinib和TAK-779治疗增强GII.17人诺如病毒复制并使其在人肠道中连续传代

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-08-01 DOI: 10.1111/gtc.70139

Eri Hiraishi, Tsuyoshi Hayashi, Yoshiki Fujii, Hirokazu Kimura, Kosuke Murakami

{"title":"Treatment With Ruxolitinib and TAK-779 Enhances GII.17 Human Norovirus Replication and Enables Serial Passaging in Human Intestinal Enteroids","authors":"Eri Hiraishi, Tsuyoshi Hayashi, Yoshiki Fujii, Hirokazu Kimura, Kosuke Murakami","doi":"10.1111/gtc.70139","DOIUrl":"https://doi.org/10.1111/gtc.70139","url":null,"abstract":"Human norovirus (HuNoV) is a major cause of acute viral gastroenteritis. Although it can be replicated in vitro using human intestinal enteroids (HIEs), generating high-titer viral laboratory stocks remains challenging due to low infection and passage efficiencies. Interferon response and chemokine signaling may be key host pathways that restrict efficient HuNoV replication. Here, we evaluated the effect of their inhibitors, ruxolitinib—a Janus kinase (JAK) 1/JAK2 inhibitor—and TAK-779—a C-X-C motif chemokine receptor 3 (CXCR3)/C-C motif chemokine receptor (CCR) 5/CCR2 antagonist—on HuNoV replication in wild-type jejunal HIEs. TAK-779 increased GII.17 HuNoV replication by 2.3- and 6.0-fold at 48 and 96 h postinfection (hpi), respectively, compared with the DMSO-treated control. In contrast, ruxolitinib alone did not affect viral replication. Notably, simultaneous treatment with these compounds further enhanced GII.17 replication by 6.0- and 10.7-fold at 48 and 96 hpi, respectively, which enabled serial passaging. These findings imply that the simultaneous suppression of these pathways potentially benefits GII.17 HuNoV replication.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 5","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.70139","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148647643","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

Combined Inhibition of Wee1 and Checkpoint Kinases Synergistically Provokes S-Phase Progression and Mitotic Entry, and Promotes Cell Death Under Heat Stress 联合抑制Wee1和检查点激酶协同刺激s期进展和有丝分裂进入，并促进热应激下的细胞死亡。

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-07-29 DOI: 10.1111/gtc.70140

Tamaki Muratani, Honoka Takeya, Riko Ishibashi, Takuto Kurakawa, Shin-ichi Ikushiro, Yoshinori Nagai, Yoshiaki Tabuchi, Takashi Kondo, Yukihiro Furusawa

{"title":"Combined Inhibition of Wee1 and Checkpoint Kinases Synergistically Provokes S-Phase Progression and Mitotic Entry, and Promotes Cell Death Under Heat Stress","authors":"Tamaki Muratani, Honoka Takeya, Riko Ishibashi, Takuto Kurakawa, Shin-ichi Ikushiro, Yoshinori Nagai, Yoshiaki Tabuchi, Takashi Kondo, Yukihiro Furusawa","doi":"10.1111/gtc.70140","DOIUrl":"10.1111/gtc.70140","url":null,"abstract":"<div>\u0000 \u0000 Hyperthermia, induced by heat stress (HS), inhibits cancer cell proliferation and induces cell death. We have previously demonstrated that the inhibition of checkpoint kinase 1/2 (Chk1/2) abrogated G2/M arrest and promoted cell death under HS conditions. Here, we investigated whether Wee1 inhibition promoted mitotic entry and cell death in cells exposed to HS in combination with a Chk1/2 inhibitor. MK-1775, a selective Wee1 inhibitor, promoted HS-induced loss of cell viability and increased the SubG1 population in HeLa S3 cells, accompanied by enhanced recovery of EdU incorporation and reduced G2-phase accumulation following HS. Either MK-1775 or AZD-7762, a Chk1/2 inhibitor, alone counteracted HS-induced suppression of EdU incorporation and G2 arrest, whereas their combination further promoted EdU incorporation, mitotic entry, and loss of cell viability under HS. These findings suggest that Wee1 and Chk1/2 cooperatively regulate both S-phase progression and mitotic entry under HS, thereby contributing to cell survival. Moreover, the combination of MK-1775 and AZD-7762 abrogated G2 arrest and enhanced HS-induced cell death in MG-63 and HSC-3 cells. These findings indicate that simultaneous inhibition of Wee1 and Chk1/2 could be a promising strategy for augmenting the therapeutic efficacy of hyperthermia.\u0000 </div>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 5","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148612306","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

RNA-Seq Profiling Reveals Transcriptional Changes in Phosphorylation-Site Mutants of Brg1 RNA-Seq分析揭示Brg1磷酸化位点突变体的转录变化

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-07-17 DOI: 10.1111/gtc.70137

Ayuko Kimura, Jun Nakabayashi, Osamu Ohara, Yayoi Kimura

{"title":"RNA-Seq Profiling Reveals Transcriptional Changes in Phosphorylation-Site Mutants of Brg1","authors":"Ayuko Kimura, Jun Nakabayashi, Osamu Ohara, Yayoi Kimura","doi":"10.1111/gtc.70137","DOIUrl":"https://doi.org/10.1111/gtc.70137","url":null,"abstract":"<div>\u0000 \u0000 Brg1 is a core ATPase subunit of the SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin-remodeling complex that regulates DNA accessibility for RNA polymerase II (Pol II), transcription factors, and DNA repair enzymes. Phosphoproteomic profiling of highly malignant ovarian clear cell carcinoma (OCCC) cell lines revealed reduced levels of several SWI/SNF components and decreased Brg1 phosphorylation within its histone-binding region. Prior work showed that phosphorylation-mimic and phosphorylation-deficient mutants alter chromatin-silencing factors, producing chromatin condensation and decondensation, respectively. Here, we performed RNA-seq in Brg1-deficient JHOC-5 cells and in isogenic cells expressing Brg1-WT, phosphorylation-mimic brg1-S1452D, or phosphorylation-deficient brg1-S1452A. PCA and hierarchical clustering separated brg1-S1452A from the other lines, indicating a strong transcriptional impact of Ser1452 dephosphorylation. JHOC-5 and brg1-S1452A shared altered expression of Pol II–promoter-regulated genes. Apoptosis genes (BCL2, FGFR2, ZC3H12A, and NFKBIA) showed reciprocal expression between brg1-S1452D and brg1-S1452A, consistent with increased and decreased apoptosis, respectively. Genes linked to cell adhesion/migration and neuronal development also differed, accompanied by reduced cell circularity in brg1-S1452A. Overall, Brg1 phosphorylation at Ser1452 shapes SWI/SNF-mediated chromatin remodeling to regulate transcriptional programs controlling apoptosis and cell morphology.\u0000 </div>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 4","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148467176","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

Cancer-Associated STAT3 Mutations Maintain ES Cell Self-Renewal Through Phosphorylation-Independent Mechanisms 癌症相关的STAT3突变通过磷酸化独立机制维持ES细胞的自我更新。

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-07-14 DOI: 10.1111/gtc.70136

Tadayuki Akagi, Shota Nakamura, Tomoya Tamaru, Atsushi Ueda, Takashi Yokota

引用次数: 0

A Combination of Variants in SEPTIN9 and MSX1 Genes Leads to the Formation of Orofacial Clefts SEPTIN9和MSX1基因的变异组合导致口面裂的形成。

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-07-10 DOI: 10.1111/gtc.70138

Udval Uuganbayar, Zarko Manojlovic, Nao Ito, Reiko Yamaguchi, Hiromasa Ninomiya, Issei S. Shimada, Chisato Yamada, Devin Feigelson, Gretchen Schulz, Allyn Auslander, Sylvia Rakotoarison, William Magee III, Yutaka Hashimoto, Yoichi Kato

{"title":"A Combination of Variants in SEPTIN9 and MSX1 Genes Leads to the Formation of Orofacial Clefts","authors":"Udval Uuganbayar, Zarko Manojlovic, Nao Ito, Reiko Yamaguchi, Hiromasa Ninomiya, Issei S. Shimada, Chisato Yamada, Devin Feigelson, Gretchen Schulz, Allyn Auslander, Sylvia Rakotoarison, William Magee III, Yutaka Hashimoto, Yoichi Kato","doi":"10.1111/gtc.70138","DOIUrl":"10.1111/gtc.70138","url":null,"abstract":"Nonsyndromic cleft lip with or without palate (nCL/P) is a common congenital anomaly with a complex genetic basis. Previous whole-exome sequencing of Malagasy case-parent trios identified variants in several craniofacial development genes, including SEPTIN9, SKI, WNT5B, GPC4, and MSX1, enriched on East Asian ancestry segments. To assess functional contributions, we used Xenopus laevis embryos to evaluate the effects of individual and combined perturbations of candidate genes. Neither single-gene depletion nor ectopic expression of candidate genes induced orofacial clefts, although some craniofacial malformations were observed. In contrast, double knockdown of SEPTIN9 and MSX1 reproducibly produced orofacial clefts. These defects were rescued by co-injection of wild type human SEPTIN9 and MSX1 mRNAs, but not by variant alleles such as SEPTIN9 p.Glu370Lys and MSX1 p.Glu84Val. Our findings reveal a functional interaction between SEPTIN9 and MSX1 in craniofacial morphogenesis and provide experimental evidence for digenic inheritance in nCL/P. This work underscores the importance of ancestry-enriched variant combinations in the etiology of complex congenital anomalies.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 4","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.70138","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148428552","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 Nuclear Export Signal of IκBα Drives RelB Oscillations in the Noncanonical NF-κB Pathway i -κB α核输出信号在非典型NF-κB通路中驱动RelB振荡。

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-07-02 DOI: 10.1111/gtc.70135

Takao Seki, Shelly Davis, Shigeki Miyamoto, Taishin Akiyama, Hiroyasu Nakano, Jun-ichiro Inoue, Katsuhide Okunishi

{"title":"The Nuclear Export Signal of IκBα Drives RelB Oscillations in the Noncanonical NF-κB Pathway","authors":"Takao Seki, Shelly Davis, Shigeki Miyamoto, Taishin Akiyama, Hiroyasu Nakano, Jun-ichiro Inoue, Katsuhide Okunishi","doi":"10.1111/gtc.70135","DOIUrl":"10.1111/gtc.70135","url":null,"abstract":"The noncanonical NF-κB pathway regulates immune development and inflammation through RelB nuclear translocation, yet the dynamics of this process at the single-cell level remain poorly understood. Using live-cell imaging of RelB-Venus knock-in mouse embryonic fibroblasts, we show that LTβR or TWEAK stimulation induces four distinct RelB nuclear translocation patterns: oscillating, prolonged activation, transient activation, and non-responding. Approximately 40% of cells exhibited oscillatory behavior with a predominant period of 1.5–2.0 h, similar to RelA oscillations in the canonical pathway. Mechanistically, RelB oscillations required CRM1-mediated nuclear export, ongoing protein synthesis, NIK-dependent noncanonical signaling, and the IκBα nuclear export signal. Knockdown or knockout of Nfkb2 (encoding p100) induced spontaneous RelB oscillations without stimulation, identifying p100 as a threshold regulator that controls oscillation probability through cytoplasmic sequestration of RelB. Co-immunoprecipitation analysis revealed dynamic RelB-IκBα complex formation in both cytoplasmic and nuclear fractions following LTβR stimulation. Furthermore, disruption of RelB oscillations in NfkbiaNES/NES cells was associated with impaired induction of NF-κB target genes. These findings provide the first experimental characterization of RelB oscillatory dynamics and reveal both conserved and pathway-specific mechanisms governing noncanonical NF-κB signaling.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 4","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.70135","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148371773","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