Journal of biochemistry最新文献_第2页

Biomechanical regulation of Ca2+ dynamics during muscle stem cell activation. 肌肉干细胞活化过程中Ca2+动力学的生物力学调控。

IF 2.4 4区生物学

Journal of biochemistry Pub Date : 2026-09-09 DOI: 10.1093/jb/mvag062

Kotaro Hirano, Yudai Ishikawa, Norio Motohashi, Yujiro Kobata, Hiroto Watanabe, Mao Sasaki, Takuya Yokoyama, Yuto Yamada, Yuta Aoyagi, Kanako Takakura, Akira Murakami, Masaki Tsuchiya, Yusuke Ono, Keiko Nonomura, Yoshitsugu Aoki, Yuji Hara

{"title":"Biomechanical regulation of Ca2+ dynamics during muscle stem cell activation.","authors":"Kotaro Hirano, Yudai Ishikawa, Norio Motohashi, Yujiro Kobata, Hiroto Watanabe, Mao Sasaki, Takuya Yokoyama, Yuto Yamada, Yuta Aoyagi, Kanako Takakura, Akira Murakami, Masaki Tsuchiya, Yusuke Ono, Keiko Nonomura, Yoshitsugu Aoki, Yuji Hara","doi":"10.1093/jb/mvag062","DOIUrl":"https://doi.org/10.1093/jb/mvag062","url":null,"abstract":"Muscle satellite cells (MuSCs) are muscle-resident stem cells that are responsible for myofiber regeneration. Although the importance of calcium ions (Ca 2+) in muscle physiology has been well established, the mechanism by which Ca 2+ mobilization governs MuSC function remains poorly understood. In this study, we aimed to systematically characterize Ca2+ dynamics in MuSCs and to define the mechanisms regulating these signals during muscle regeneration. By employing modified protocols for mouse MuSC isolation and Ca2+ measurement, we observed spontaneous Ca2+ fluctuations in MuSCs isolated from regenerating muscle after cardiotoxin-induced myofiber injury. Our detailed analysis using chemical Ca2+ indicators and a genetically encoded Ca2+ indicator revealed that the frequency and amplitude of Ca2+ fluctuations increased significantly during the activated and proliferative stages of MuSCs. This effect was more pronounced in MuSCs isolated from dystrophic and aged mice. Mechanistically, these Ca2+ fluctuations were at least partially mediated by mechanosensitive ion channels, including PIEZO1 and TRPM7, which promote MuSC migration. Collectively, our findings demonstrate that Ca2+ fluctuations through mechanosensitive ion channels act as a key regulator of MuSC activation during muscle regeneration and may provide new insights into the role of Ca2+ influx in muscle biology and the pathogenesis of muscle diseases.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148912202","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

Revitalizing Science-Japan's New Strategy for Research and Innovation. 振兴科学——日本的研究创新新战略。

IF 2.4 4区生物学

Journal of biochemistry Pub Date : 2026-09-09 DOI: 10.1093/jb/mvag063

Kohei Miyazono

引用次数: 0

MARK4 regulates GLUT3 surface expression and neuronal glucose uptake. MARK4调节GLUT3表面表达和神经元葡萄糖摄取。

IF 2.4 4区生物学

Journal of biochemistry Pub Date : 2026-08-19 DOI: 10.1093/jb/mvag061

Sophia Jobien M Limlingan, Ambika Krishnankutty, Akiko Asada, Kanae Ando, Taro Saito

{"title":"MARK4 regulates GLUT3 surface expression and neuronal glucose uptake.","authors":"Sophia Jobien M Limlingan, Ambika Krishnankutty, Akiko Asada, Kanae Ando, Taro Saito","doi":"10.1093/jb/mvag061","DOIUrl":"https://doi.org/10.1093/jb/mvag061","url":null,"abstract":"Brain neurons rely predominantly on glucose as an energy source and express glucose transporter 3 (GLUT3) as their principal glucose transporter. Unlike GLUT4, which undergoes insulin-stimulated membrane translocation in peripheral tissues, GLUT3 mediates largely constitutive and relatively insulin-independent glucose uptake in neurons. Although GLUT3 is essential for neuronal functions, its regulatory mechanisms are not fully understood. Microtubule affinity-regulating kinase 4 (MARK4), a member of the AMP-activated protein kinase-related kinase family, has been implicated in Alzheimer's disease and metabolic regulation in peripheral tissues. Here, we show that MARK4 knockdown in primary neurons reduces GLUT3 surface expression and consequently decreases glucose uptake. While MARK4 knockdown did not alter the intracellular distribution of GLUT3 or mitochondria, it reduced mitochondrial abundance. We further found that MARK4 activity is negatively regulated by the insulin/IGF-1-GSK3β signaling axis in primary neurons. Despite these acute metabolic effects in cultured neurons, Mark4-null mice exhibited no overt morphological abnormalities in the brain. Together, these findings identify MARK4 as a regulator of neuronal glucose uptake by modulating GLUT3 surface expression and suggest that MARK4 functions as a modulatory rather than essential component of neuronal metabolic homeostasis.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148793647","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

DISCUSSING CHROMATIN DYNAMICS AND FUNCTION. 讨论染色质动力学和功能。

IF 2.4 4区生物学

Journal of biochemistry Pub Date : 2026-08-12 DOI: 10.1093/jb/mvag060

Nabanita Das, Rohini Bhatt, Tapas K Kundu

引用次数: 0

Time to rethink circadian rhythms beyond the transcriptome. 是时候重新思考转录组之外的昼夜节律了。

IF 2.4 4区生物学

Journal of biochemistry Pub Date : 2026-08-03 DOI: 10.1093/jb/mvag031

Yuta Otobe, Hikari Yoshitane

{"title":"Time to rethink circadian rhythms beyond the transcriptome.","authors":"Yuta Otobe, Hikari Yoshitane","doi":"10.1093/jb/mvag031","DOIUrl":"10.1093/jb/mvag031","url":null,"abstract":"The circadian clock generates ~24-hour rhythms in physiology by coordinating gene expression programs, but temporal mRNA profiles often fail to predict their protein function rhythms. This gap reflects regulatory layers beyond transcription, including rhythmic translation, protein stability, subcellular localization and post-translational modifications that collectively determine the circadian rhythms of protein abundance and activity. Here, we summarize evidence supporting a shift from RNA-level descriptions to protein-level frameworks and readouts of the circadian rhythms. Here, we highlight three topics: (i) protein abundance rhythms as informative but incomplete readouts, (ii) widespread circadian control of nuclear localization and phosphorylation that can occur without changes in total protein levels, and (iii) multi-tissue proteomic comparisons that reveal how circadian rhythms are organized differently across tissues. We then discuss how recent data-independent acquisition-based, high-throughput mass spectrometry accelerates cross-study reuse and hypothesis generation, as illustrated by a mouse circadian proteome atlas and an interactive portal enabled by Orbitrap Astral mass spectrometer. Together, these advances motivate 'functional chronobiology', linking proteome dynamics to mechanism and disease-relevant physiology.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":"93-99"},"PeriodicalIF":2.4,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13384777/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148360966","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

A two-tiered epigenetic mechanism ensures imprint stability after fertilization: insights from the Igf2/H19 locus. 一个双层的表观遗传机制确保受精后的印记稳定性：来自Igf2/H19位点的见解。

IF 2.4 4区生物学

Journal of biochemistry Pub Date : 2026-08-03 DOI: 10.1093/jb/mvag030

Hitomi Matsuzaki, Teruhito Ishihara, Keiji Tanimoto

{"title":"A two-tiered epigenetic mechanism ensures imprint stability after fertilization: insights from the Igf2/H19 locus.","authors":"Hitomi Matsuzaki, Teruhito Ishihara, Keiji Tanimoto","doi":"10.1093/jb/mvag030","DOIUrl":"10.1093/jb/mvag030","url":null,"abstract":"Genomic imprinting is a crucial epigenetic mechanism directing parent-of-origin-specific gene expression in mammals, and it is regulated by allele-specific DNA methylation at imprinting control regions (ICRs). In this canonical imprinting mechanism, maintenance factors preserve germline-derived DNA methylation at ICRs during genome-wide demethylation after fertilization. However, our studies of the Igf2/H19 locus reveal that allele-specific de novo DNA methylation after fertilization, termed 'post-fertilization imprinted methylation', also contributes to imprint maintenance. In this process, epigenetic imprints other than DNA methylation are thought to guide the recognition of parental alleles by de novo methyltransferases in the next generation, acting in concert with maintenance factors to ensure stable DNA methylation at canonical imprinted loci. Recently identified non-canonical imprinting, in contrast, relies on non-DNA methylation marks that are converted into DNA methylation only after implantation. Despite differences in the timing of this conversion, post-fertilization imprinted methylation may share similarities with non-canonical imprinting. Collectively, these findings suggest that the robustness of canonical imprinting is supported by a two-tiered regulatory system.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":"83-92"},"PeriodicalIF":2.4,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147698858","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

Zinc-mediated structural and functional regulation of ERp44 and ERGIC-53 in protein quality control. 锌介导ERp44和ERGIC-53在蛋白质量控制中的结构和功能调控。

IF 2.4 4区生物学

Journal of biochemistry Pub Date : 2026-08-03 DOI: 10.1093/jb/mvag033

Satoshi Watanabe, Kenji Inaba

引用次数: 0

FGF21-inducing rare sugars for addressing obesity and alcoholism. 诱导fgf21的稀有糖用于解决肥胖和酗酒问题。

IF 2.4 4区生物学

Journal of biochemistry Pub Date : 2026-07-24 DOI: 10.1093/jb/mvag059

Tsutomu Sasaki

引用次数: 0

Lysosomes and Supersulfides: Emerging Links in Cellular Metabolism and Homeostasis. 溶酶体和超硫化物：细胞代谢和体内平衡的新联系。

IF 2.4 4区生物学

Journal of biochemistry Pub Date : 2026-07-24 DOI: 10.1093/jb/mvag058

Natsumi Sakata, Takaaki Akaike, Hozumi Motohashi

引用次数: 0

Establishment of prohaptoglobin-specific antibody and haptoglobin detection systems as biomarkers for pancreatic diseases. 建立亲珠蛋白特异性抗体和亲珠蛋白检测系统作为胰腺疾病的生物标志物。

IF 2.4 4区生物学

Journal of biochemistry Pub Date : 2026-07-23 DOI: 10.1093/jb/mvag057

Daisuke Sakon, Jumpei Kondo, Kayoko Shimizu, Takuma Otsubo, Muya Matsumoto, Ayusa Kuroda, Shinji Takamatsu, Takeshi Kumada, Toshifumi Ito, Hirofumi Akita, Hidetoshi Eguchi, Eiji Miyoshi

{"title":"Establishment of prohaptoglobin-specific antibody and haptoglobin detection systems as biomarkers for pancreatic diseases.","authors":"Daisuke Sakon, Jumpei Kondo, Kayoko Shimizu, Takuma Otsubo, Muya Matsumoto, Ayusa Kuroda, Shinji Takamatsu, Takeshi Kumada, Toshifumi Ito, Hirofumi Akita, Hidetoshi Eguchi, Eiji Miyoshi","doi":"10.1093/jb/mvag057","DOIUrl":"https://doi.org/10.1093/jb/mvag057","url":null,"abstract":"Fucosylated haptoglobin (Fuc-Hp) has been recognized as a cancer-associated glycoform. We previously established a monoclonal antibody, 10-7G mAb, which detects both Fuc-Hp and its precursor prohaptoglobin (proHp). Recent studies have suggested that proHp itself may serve as a cancer-associated biomarker with clinical implications distinct from those of Fuc-Hp. Importantly, proHp is produced during inflammation and cancer progression and may exert biological activities different from mature haptoglobin. These observations highlight the need for a reagent that can specifically detect proHp. However, to date, no antibody strictly specific to proHp has been available. In this study, we generated a monoclonal antibody, 21-4F mAb, that specifically recognizes human proHp without cross-reactivity to mature Hp. Using 21-4F mAb, we developed a proHp-specific ELISA and integrated it with assays for several types of Hp, enabling independent quantification of three Hp-related isoforms. Serum analyses of healthy volunteers and patients with chronic pancreatitis or pancreatic cancer revealed distinct alterations among these isoforms, and their combined use provided the highest diagnostic performance. Taken together, 21-4F mAb offers a novel analytical tool for investigating the pathophysiological significance of proHp and may contribute to the development of refined biomarker panels for cancer diagnosis and disease monitoring.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148562197","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