Genes to Cells最新文献_第7页

Changes in brain proteasome dynamics associated with aging 与衰老相关的大脑蛋白酶体动力学变化

IF 2.1 4区生物学

Genes to Cells Pub Date : 2024-03-25 DOI: 10.1111/gtc.13113

Nodoka Nago, Shigeo Murata, Keiji Tanaka, Nobuyuki Tanahashi

{"title":"Changes in brain proteasome dynamics associated with aging","authors":"Nodoka Nago, Shigeo Murata, Keiji Tanaka, Nobuyuki Tanahashi","doi":"10.1111/gtc.13113","DOIUrl":"10.1111/gtc.13113","url":null,"abstract":"In the nervous system, proteasomes are important for proteolysis and cellular homeostasis of neurons and glial cells and for brain health. Proteasome function declines with age in many tissues, including the nervous system, and this decline affects many of the nervous system processes important to brain health and may be related to age-related cognitive decline. Therefore, we analyzed the factors that contribute to this decline in function using the brain of mice from different months of life. Peptidase activity of proteasomes in crude extracts decreased with aging, while ubiquitinated proteins increased with aging. Additionally, there was a tendency for the number of subunits that form proteasomes to decrease slightly with age. On the other hand, ump1, which is required for proteasome formation, accumulated with age. Therefore, analysis of proteasome dynamics in each month revealed that proteasome formation decreased with aging. This study suggests that with aging, not only 20S proteasome function but also 26 proteasome function decreases, the decline in proteasome function is due to the lack of proteasome formation, the PA28-20S-PA700 complex, which is involved in immunity, increases in the brain, and one factor in this lack of proteasome formation is that the proteins called UMP1.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140287363","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

Long-term sorbitol consumption affects the hippocampus and alters cognitive function in aged mice 长期食用山梨醇会影响老年小鼠的海马并改变其认知功能。

IF 2.1 4区生物学

Genes to Cells Pub Date : 2024-03-11 DOI: 10.1111/gtc.13112

Haruna Yokoi, Jingshu Wang, Yoriko Ikuyo, Mitsuyoshi Yamada, Yosuke Shikama, Masae Furukawa, Kenji Matsushita

引用次数: 0

Staphylococcal superantigen-like protein 3 triggers murine mast cell adhesion by binding to CD43 and augments mast cell activation 葡萄球菌超抗原样蛋白 3 通过与 CD43 结合引发小鼠肥大细胞粘附并增强肥大细胞活化。

IF 2.1 4区生物学

Genes to Cells Pub Date : 2024-03-07 DOI: 10.1111/gtc.13111

Sae Kawano, Chisaki Noda, Saotomo Itoh, Ayaka Urabe, Chifumi Fujii, Isamu Ogawa, Ryo Suzuki, Shigeaki Hida

{"title":"Staphylococcal superantigen-like protein 3 triggers murine mast cell adhesion by binding to CD43 and augments mast cell activation","authors":"Sae Kawano, Chisaki Noda, Saotomo Itoh, Ayaka Urabe, Chifumi Fujii, Isamu Ogawa, Ryo Suzuki, Shigeaki Hida","doi":"10.1111/gtc.13111","DOIUrl":"10.1111/gtc.13111","url":null,"abstract":"Staphylococcus aureus is a noteworthy pathogen in allergic diseases, as four staphylococcal exotoxins activate mast cells, a significant contributor to inflammation, in an IgE-independent manner. Although the adhesion of mast cells is an essential process for their immune responses, only a small number of exotoxins have been reported to affect the process. Here, we demonstrated that staphylococcal superantigen-like (SSL) 3, previously identified as a toll-like receptor 2 agonist, induced the adhesion of murine bone marrow-derived mast cells to culture substratum. SSL3-induced adhesion was mediated by fibronectin in an Arg-Gly-Asp (RGD) sequence-dependent manner, suggesting the integrins were involved in the process. Additionally, SSL3 was found to bind to an anti-adhesive surface protein CD43. SSL3 induced the adhesion of HEK293 cells expressing exogenous CD43, suggesting that CD43 is the target molecule for adhesion induced by SSL3. Evaluation of SSL3-derived mutants showed that the C-terminal region (253–326), specifically T285 and H307, are necessary to induce adhesion. SSL3 augmented the IL-13 production of mast cells in response to immunocomplex and SSL12. These findings reveal a novel function of SSL3, triggering cell adhesion and enhancing mast cell activation. This study would clarify the correlation between S. aureus and allergic diseases such as atopic dermatitis.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140059127","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

Left–right Myosin-Is, Myosin1C, and Myosin1D exhibit distinct single molecule behaviors on the plasma membrane of Drosophila macrophages 左-右肌球蛋白-Is、肌球蛋白1C和肌球蛋白1D在果蝇巨噬细胞质膜上表现出不同的单分子行为。

IF 2.1 4区生物学

Genes to Cells Pub Date : 2024-03-07 DOI: 10.1111/gtc.13110

Sosuke Utsunomiya, Kazutoshi Takebayashi, Asuka Yamaguchi, Takeshi Sasamura, Mikiko Inaki, Masahiro Ueda, Kenji Matsuno

{"title":"Left–right Myosin-Is, Myosin1C, and Myosin1D exhibit distinct single molecule behaviors on the plasma membrane of Drosophila macrophages","authors":"Sosuke Utsunomiya, Kazutoshi Takebayashi, Asuka Yamaguchi, Takeshi Sasamura, Mikiko Inaki, Masahiro Ueda, Kenji Matsuno","doi":"10.1111/gtc.13110","DOIUrl":"10.1111/gtc.13110","url":null,"abstract":"Left–right (LR) asymmetry is crucial for animal development, particularly in Drosophila where LR-asymmetric morphogenesis of organs hinges on cellular-level chirality, termed cell chirality. In this species, two class I myosins, Myosin1D (Myo1D), and Myosin1C (Myo1C), respectively determine dextral (wild type) and sinistral (mirror image) cell chirality. Previous studies demonstrated Myo1D's ability to propel F-actin in leftward circles during in vitro gliding assays, suggesting its mechanochemical role in defining dextral chirality. Conversely, Myo1C propels F-actin without exhibiting LR-directional preference in this assay, suggesting at other properties governing sinistral chirality. Given the interaction of Myo1D and Myo1C with the membrane, we hypothesized that differences in their membrane behaviors might be critical in dictating their dextral or sinistral activities. In this study, employing single-molecule imaging analyses, we investigated the dynamic behaviors of Myo1D and Myo1C on the plasma membrane. Our findings revealed that Myo1C exhibits a significantly greater proportion of slow-diffusing population compared to Myo1D. Importantly, this characteristic was contingent upon both head and tail domains of Myo1C. The distinct diffusion patterns of Myo1D and Myo1C did not exert mutual influence on each other. This divergence in membrane diffusion between Myo1D and Myo1C may be crucial for dictating cell and organ chirality.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.13110","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140059126","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

Mode of SUV420H2 heterochromatin localization through multiple HP1 binding motifs in the heterochromatic targeting module 通过异染色质靶向模块中的多个 HP1 结合基序实现 SUV420H2 异染色质定位的模式

IF 2.1 4区生物学

Genes to Cells Pub Date : 2024-02-25 DOI: 10.1111/gtc.13109

Masaru Nakao, Yuko Sato, Arisa Aizawa, Hiroshi Kimura

{"title":"Mode of SUV420H2 heterochromatin localization through multiple HP1 binding motifs in the heterochromatic targeting module","authors":"Masaru Nakao, Yuko Sato, Arisa Aizawa, Hiroshi Kimura","doi":"10.1111/gtc.13109","DOIUrl":"10.1111/gtc.13109","url":null,"abstract":"Constitutive heterochromatin is transcriptionally repressed and densely packed chromatin, typically harboring histone H3 Lys9 trimethylation (H3K9me3) and heterochromatin protein 1 (HP1). SUV420H2, a histone H4 Lys20 methyltransferase, is recruited to heterochromatin by binding to HP1 through its Heterochromatic Targeting Module (HTM). Here, we have identified three HP1 binding motifs within the HTM. Both the full-length HTM and its N-terminal region (HTM-N), which contains the first and second motifs, stabilized HP1 on heterochromatin. The intervening region between the first and second HP1 binding motifs in HTM-N was also crucial for HP1 binding. In contrast, the C-terminal region of HTM (HTM-C), containing the third motif, destabilized HP1 on chromatin. An HTM V374D mutant, featuring a Val374 to Asp substitution in the second HP1 binding motif, localizes to heterochromatin without affecting HP1 stability. These data suggest that the second HP1 binding motif in the SUV420H2 HTM is critical for locking HP1 on H3K9me3-enriched heterochromatin. HTM V374D, tagged with a fluorescent protein, can serve as a live-cell probe to visualize HP1-bound heterochromatin.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.13109","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139968905","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

Self-recognition through Dectin-1 exacerbates liver inflammation 通过 Dectin-1 进行自我识别会加剧肝脏炎症。

IF 2.1 4区生物学

Genes to Cells Pub Date : 2024-02-22 DOI: 10.1111/gtc.13106

Shota Torigoe, Douglas W. Lowman, Toshihiko Sugiki, David L. Williams, Sho Yamasaki

{"title":"Self-recognition through Dectin-1 exacerbates liver inflammation","authors":"Shota Torigoe, Douglas W. Lowman, Toshihiko Sugiki, David L. Williams, Sho Yamasaki","doi":"10.1111/gtc.13106","DOIUrl":"10.1111/gtc.13106","url":null,"abstract":"Dectin-1 is a well-characterized C-type lectin receptor involved in anti-fungal immunity through the recognition of polysaccharides; however, molecular mechanisms and outcomes initiated through self-recognition have not been fully understood. Here, we purified a water-soluble fraction from mouse liver that acts as a Dectin-1 agonist. To address the physiological relevance of this recognition, we utilized sterile liver inflammation models. The CCl4-induced hepatitis model showed that Dectin-1 deficiency led to reduced inflammation through decreased inflammatory cell infiltration and lower pro-inflammatory cytokine levels. Moreover, in a NASH model induced by streptozotocin and a high-fat diet, hepatic inflammation and fibrosis were ameliorated in Dectin-1-deficient mice. The Dectin-1 agonist activity was increased in the water-soluble fraction from NASH mice, suggesting a potential pathogenic cycle between Dectin-1 activation and hepatitis progression. In vivo administration of the fraction into mice induced hepatic inflammation. These results highlight a role of self-recognition through Dectin-1 that triggers hepatic innate immune responses and contributes to the exacerbation of inflammation in pathogenic settings. Thus, the blockade of this axis may provide a therapeutic option for liver inflammatory diseases.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139930817","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

Premature gray hair development in the interbrow region owing to the loss of maxillary first molars in young mice 幼鼠上颌第一臼齿脱落导致眉间区灰白毛发过早生长。

IF 2.1 4区生物学

Genes to Cells Pub Date : 2024-02-20 DOI: 10.1111/gtc.13107

Masae Furukawa, Haruna Yokoi, Jingshu Wang, Yoriko Ikuyo, Hirobumi Tada, Mitsuyoshi Yamada, Yosuke Shikama, Kenji Matsushita

引用次数: 0

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":null,"pages":null},"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":null,"pages":null},"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