Journal of biochemistry最新文献

UNC5B is an isoform-dependent target for ectodomain shedding. UNC5B是胞外结构域脱落的同工异构体依赖性靶标。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2025-07-09 DOI: 10.1093/jb/mvaf043

Kotaro Sugimoto, Eichi Watabe, Mio Takuma, Kaname Nagahara, Toshinori Sawano, Mihoko Kajita, Junichi Takagi, Hidehito Kuroyanagi, Kyoko Shirakabe

引用次数: 0

Repressive S-adenosylmethionine biosynthesis status inhibits transcription of HeT-A retrotransposon in the germline of Drosophila. 抑制s -腺苷蛋氨酸生物合成状态抑制果蝇种系HeT-A反转录转座子的转录。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2025-07-02 DOI: 10.1093/jb/mvaf041

Yoshiki Hayashi, Shinjiro Hino, Tetsuya Sato, Soshiro Kashio, Kiito Otsubo, Kuniaki Saito, Ban Sato, Natsuko Kawano, Daisuke Saito, Masayuki Miura, Mikita Suyama, Mitsuyoshi Nakao, Satoru Kobayashi

{"title":"Repressive S-adenosylmethionine biosynthesis status inhibits transcription of HeT-A retrotransposon in the germline of Drosophila.","authors":"Yoshiki Hayashi, Shinjiro Hino, Tetsuya Sato, Soshiro Kashio, Kiito Otsubo, Kuniaki Saito, Ban Sato, Natsuko Kawano, Daisuke Saito, Masayuki Miura, Mikita Suyama, Mitsuyoshi Nakao, Satoru Kobayashi","doi":"10.1093/jb/mvaf041","DOIUrl":"https://doi.org/10.1093/jb/mvaf041","url":null,"abstract":"S-adenosylmethionine (SAM) is the major cellular methyl donor and regulates gene expression through epigenetic and other methylation-related processes. While SAM biosynthesis influences a variety of biological phenomena including aging and disease, its cell type-specific regulation and functional implications remain poorly understood. In this study, we report that the Drosophila germline exhibits a uniquely repressive SAM biosynthesis status during gametogenesis, as indicated by low expression of SAM synthetase (Sam-S), a key enzyme for SAM production. Experimentally enhancing SAM biosynthesis in the germline led to increased expression of retrotransposons, with HeT-A, a telomere-specific element, showing the most pronounced response. We also observed increased promoter activity of HeT-A under high SAM conditions, along with accumulation of N6-methyladenine (6mA), the major form of DNA methylation in the Drosophila genome. Although a direct causal link between 6mA levels and transcription was not broadly observed across other retrotransposons or genes, these results raise the possibility that SAM levels modulate HeT-A expression at least in part through DNA methylation. Our findings highlight a previously underexplored metabolic feature of the Drosophila germline and suggest that SAM availability contributes to the regulation of retrotransposon activity in a lineage-specific manner.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540355","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

NMR analysis of interaction between RNA structure elements and small molecules. RNA结构元件与小分子相互作用的核磁共振分析。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2025-07-01 DOI: 10.1093/jb/mvaf020

Megumi Tomemori, Rika Ichijo, Yoko Shinohara, Kaori Hatta, Kazuhiko Nakatani, Gota Kawai

引用次数: 0

Inhibition of autophagy by Atg7 knockdown enhances chemosensitivity in gemcitabine/paclitaxel-resistant pancreatic cancer MIAPaCa2 cells. Atg7敲低抑制自噬增强吉西他滨/紫杉醇耐药胰腺癌MIAPaCa2细胞的化疗敏感性。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2025-07-01 DOI: 10.1093/jb/mvaf022

Yudai Kudo, Kotaro Hirota, Honoka Tsuzuki, Shinya Kawano, Tomofumi Saka, Riri Hayashi, Yuta Yoshino, Akira Ikari, Satoshi Endo

{"title":"Inhibition of autophagy by Atg7 knockdown enhances chemosensitivity in gemcitabine/paclitaxel-resistant pancreatic cancer MIAPaCa2 cells.","authors":"Yudai Kudo, Kotaro Hirota, Honoka Tsuzuki, Shinya Kawano, Tomofumi Saka, Riri Hayashi, Yuta Yoshino, Akira Ikari, Satoshi Endo","doi":"10.1093/jb/mvaf022","DOIUrl":"10.1093/jb/mvaf022","url":null,"abstract":"The 5-year survival rate for pancreatic cancer is extremely low, at ~12%, primarily because most patients present with advanced and unresectable tumours. Chemotherapy regimens, such as gemcitabine (GEM) plus paclitaxel (PTX) and FOLFIRINOX, are standard treatments; however, resistance to these therapies remains a major challenge. Autophagy has been implicated in this resistance. Both the Atg8 and Atg12 conjugation systems are essential for autophagosome maturation, and the ubiquitin-like protein activator Atg7 plays an essential role in these systems. This study investigated the effects of Atg7 knockdown on GEM/PTX sensitivity in GEM/PTX-resistant pancreatic cancer MIAPaCa2 (GP-R) cells. GP-R cells exhibited reduced sensitivity to GEM/PTX, increased expression of autophagy-related factors, and elevated basal autophagy compared to parental cells. Atg7 knockdown in GP-R cells effectively inhibited both basal and GEM/PTX-induced autophagy, significantly increased total and mitochondrial reactive oxygen species (ROS), and led to the induction of apoptotic cell death. These findings suggest that autophagy inhibition via Atg7 knockdown enhances GEM/PTX sensitivity in GP-R cells. In conclusion, targeting Atg7 to inhibit autophagy may be a promising approach to improving the efficacy of GEM/PTX therapy in pancreatic cancer.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":"11-24"},"PeriodicalIF":2.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144019870","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

ZNRF1-dependent regulation of AKT activity modulates Nav subcellular localization and AIS position in neurons to regulate fear-related behaviour. 依赖znrf1的AKT活性调节神经元中Nav亚细胞定位和AIS位置，从而调节恐惧相关行为。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2025-07-01 DOI: 10.1093/jb/mvaf024

Moeka Ohno, Shuji Wakatsuki, Hiroshi Kuniishi, Masayuki Sekiguchi, Eri Takeuchi, Keizo Takao, Megumi Watase, Takaya Abe, Toshiyuki Araki

引用次数: 0

The tumor promoter 12-O-tetradecanoylphorbol-13-acetate suppresses cell proliferation in metastatic melanoma through TC-PTP/PTPN2 and SH-PTP2/PTPN11. 肿瘤启动子12- o - tetradecanoylphorol -13-acetate通过TC-PTP/PTPN2和SH-PTP2/PTPN11抑制转移性黑色素瘤细胞增殖。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2025-07-01 DOI: 10.1093/jb/mvaf040

Yuki Akamatsu, Mami Onishi, Taiki Nagano, Masahiro Oka, Shinji Kamada, Tetsushi Iwasaki

{"title":"The tumor promoter 12-O-tetradecanoylphorbol-13-acetate suppresses cell proliferation in metastatic melanoma through TC-PTP/PTPN2 and SH-PTP2/PTPN11.","authors":"Yuki Akamatsu, Mami Onishi, Taiki Nagano, Masahiro Oka, Shinji Kamada, Tetsushi Iwasaki","doi":"10.1093/jb/mvaf040","DOIUrl":"https://doi.org/10.1093/jb/mvaf040","url":null,"abstract":"Despite being a carcinogen, the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) inhibits metastatic melanoma growth by downregulating signal transducer and activator of transcription 3 (STAT3). However, the molecular mechanisms remain unclear. The aim of this study was to identify tyrosine phosphatases that are involved in TPA-induced inhibition of cell proliferation in metastatic melanoma cells. We screened protein tyrosine phosphatases (PTPs) required for TPA-mediated inhibition of cell proliferation. We identified two PTPs, SH2 domain-containing protein tyrosine phosphatase2 (SH-PTP2/PTPN11) and T-cell protein tyrosine phosphatase (TC-PTP/PTPN2), which play key roles in TPA-mediated inhibition of metastatic melanoma cell growth. Transient expression of SH-PTP2 and TC-PTP induced G0/G1 cell cycle arrest in a phosphatase-dependent manner. Furthermore, SH-PTP2 was translocated to the cell membrane upon TPA treatment, resulting in a decrease in Janus kinase 2 (JAK2) activity. TC-PTP is localized in the nucleus together with the adapter protein ubiquitin-like protein 4A (UBL4A/GdX); TC-PTP was translocated to the nuclear periphery upon TPA stimulation. These two signaling pathways, involving SH-PTP2 and TC-PTP, are distinct from those observed in normal melanocytes and benign melanoma cells. These pathways represent previously unknown responses to TPA specific to metastatic melanoma cells. Overall, these findings may contribute to the development of new anticancer agents.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528140","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

Valosin-containing protein mediates DNA-dependent protein kinase activation in response to DNA topoisomerase II-associated DNA double-strand breaks. 在DNA拓扑异构酶ii相关DNA双链断裂的反应中，含缬草苷蛋白介导DNA依赖性蛋白激酶激活。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2025-07-01 DOI: 10.1093/jb/mvaf025

Ryo Sakasai, Yumi Sunatani, Tadashi Matsui, Kuniyoshi Iwabuchi

{"title":"Valosin-containing protein mediates DNA-dependent protein kinase activation in response to DNA topoisomerase II-associated DNA double-strand breaks.","authors":"Ryo Sakasai, Yumi Sunatani, Tadashi Matsui, Kuniyoshi Iwabuchi","doi":"10.1093/jb/mvaf025","DOIUrl":"10.1093/jb/mvaf025","url":null,"abstract":"DNA topoisomerase II (Top2) induces DNA double-strand breaks (DSBs) to relieve the torsional stress associated with DNA replication and transcription. Etoposide (ETP), a Top2 poison in clinical use as an anticancer drug, traps Top2 reactive intermediates, resulting in the accumulation of DSBs, coupled with the formation of Top2-DNA protein crosslinks (Top2-DPC) at the ends of DSBs. Proteasome-dependent processing of trapped Top2 is necessary for some cellular responses to ETP-induced DSBs; however, the effect of suppressing Top2 removal on DSB repair is not well understood. In this study, we focused on valosin-containing protein (VCP), a proteasome mediator, to analyse the effect of the suppression of Top2-DPC resolution on the repair of ETP-induced DSBs. ETP-induced activation of DNA-dependent protein kinase (DNA-PK), a non-homologous end-joining (NHEJ) factor, was suppressed by VCP inhibitors, similar to the effects observed in proteasome-inhibited cells. Consistent with this finding, VCP inhibition suppressed repair activity in response to ETP-induced DSBs. Additionally, VCP inhibition delayed the resolution of ETP-induced Top2-DPC. These results suggest that the processing of trapped Top2 via the VCP-proteasome pathway is important for efficient DNA-PK activation and subsequent repair in response to ETP-induced DSBs.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":"51-60"},"PeriodicalIF":2.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144063977","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

Improvement of a FRET-based redox probe Redoxfluor through circular permutation and effects of substitution of cysteine residues on its redox properties. 基于fret的氧化还原探针Redoxfluor的循环置换改进及半胱氨酸残基取代对其氧化还原性能的影响。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2025-07-01 DOI: 10.1093/jb/mvaf023

Kosuke Shiraishi, Banri Kitamura, Kaho Aramaki, Yasuyoshi Sakai, Jun Hoseki

{"title":"Improvement of a FRET-based redox probe Redoxfluor through circular permutation and effects of substitution of cysteine residues on its redox properties.","authors":"Kosuke Shiraishi, Banri Kitamura, Kaho Aramaki, Yasuyoshi Sakai, Jun Hoseki","doi":"10.1093/jb/mvaf023","DOIUrl":"10.1093/jb/mvaf023","url":null,"abstract":"The properties of a FRET-based redox probe Redoxfluor have been improved for its sensitivity and dynamic range. Substitution of the Citrine portion of Redoxfluor with circular permutated (cp) Citrine improved the dynamic range without affecting the redox potential. The cp158 mutant, referred to as Redoxfluor 2, possessed the most extended dynamic range and detected intracellular redox changes in yeast and bacteria, while the original did not. Investigation of the glutathione-redox dependency of the FRET ratio of various cysteine-substituted mutants revealed that Cys230 in the linker between Cerulean and the C-terminal cysteine-rich domain (CRD) and Cys385 in Citrine are essential for glutathione redox sensing. Although neither cysteine residues in CRD is essential for glutathione redox sensing, substitution of the CRD cysteine residues prominently affected the dynamic range of redox sensing and the redox potential titrated with glutathione. One of the CRD cysteine-substituted mutants (C259A) showed a greatly extended dynamic range and a substantially reducing redox potential compared to the original Redoxfluor. Redoxfluor 2 and the C259A mutant are suitable for versatile uses including sensitive detection of aberrant redox states, redox visualization in the more reducing intracellular compartments and high-throughput screening of redox modulators active against pathologically abnormal redox states.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":"25-38"},"PeriodicalIF":2.1,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144078323","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

Interaction between a fluoroquinolone derivative KG022 and RNAs: effect of the bulged residues. 氟喹诺酮衍生物KG022与rna的相互作用：凸起残基的作用。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2025-06-26 DOI: 10.1093/jb/mvaf039

Rika Ichijo, Gota Kawai

引用次数: 0

Correction to: Innate immune signals triggered on organelle membranes. 修正：先天免疫信号触发细胞器膜。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2025-06-24 DOI: 10.1093/jb/mvaf035

引用次数: 0