Journal of biochemistry最新文献_第2页

Activation of platelet-derived growth factor receptors regulate connective tissue growth factor protein levels via the AKT pathway in malignant mesothelioma cells. 激活血小板衍生生长因子受体可通过 AKT 途径调节恶性间皮瘤细胞中的结缔组织生长因子蛋白水平。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2024-10-23 DOI: 10.1093/jb/mvae068

Tomoya Suehiro, Khoja Mouhand Ahmad, Nguyen Truong Duc Hoang, Bingwen Xu, Honoka Komatsu, Komei Kurachi, Hiroki Nikawa, Yuichi Mine, Tohru Matsuki, Katsura Asano, Makiko Fujii

{"title":"Activation of platelet-derived growth factor receptors regulate connective tissue growth factor protein levels via the AKT pathway in malignant mesothelioma cells.","authors":"Tomoya Suehiro, Khoja Mouhand Ahmad, Nguyen Truong Duc Hoang, Bingwen Xu, Honoka Komatsu, Komei Kurachi, Hiroki Nikawa, Yuichi Mine, Tohru Matsuki, Katsura Asano, Makiko Fujii","doi":"10.1093/jb/mvae068","DOIUrl":"https://doi.org/10.1093/jb/mvae068","url":null,"abstract":"The incidence of malignant mesothelioma (MM), a disease linked to refractory asbestos exposure, continues to increase globally, and remains largely resistant to various treatments. Our previous studies have identified a strong correlation between connective tissue growth factor (CTGF) protein expression and MM malignancy, underscoring the importance of understanding CTGF regulation in MM cells. In this study, we demonstrate for the first time that stimulation with platelet-derived growth factor receptor (PDGFR) ligand, PDGF-BB, increases CTGF protein expression levels without affecting CTGF mRNA levels. Inhibition of PDGFR resulted in a reduction of CTGF protein expression, indicating that PDGFR activation is essential in regulating CTGF protein expression in MM cells. PDGF-BB also activated the protein kinase B (AKT) pathway, and inhibition of AKT phosphorylation abolished the PDGFR-induced CTGF protein expression, suggesting that PDGFR acts upstream of CTGF via the AKT pathway. This reinforces the role of CTGF protein as a key regulator of MM malignancy. Additionally, PDGFR activation led to the phosphorylation of mTOR and 4E-BP1, critical regulators of protein synthesis downstream of AKT, suggesting that PDGFR controls CTGF protein expression through the regulation of CTGF mRNA translation.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142501135","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

Open and closed structures of L-arginine oxidase by cryo-electron microscopy and X-ray crystallography. 通过冷冻电镜和 X 射线晶体学研究 L-精氨酸氧化酶的开放和封闭结构。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2024-10-18 DOI: 10.1093/jb/mvae070

Hiroki Yamaguchi, Kazutoshi Takahashi, Nobutaka Numoto, Hiroshi Suzuki, Moemi Tatsumi, Akiko Kamegawa, Kouki Nishikawa, Yasuhisa Asano, Toshimi Mizukoshi, Hiroshi Miyano, Yoshinori Fujiyoshi, Masayuki Sugiki

{"title":"Open and closed structures of L-arginine oxidase by cryo-electron microscopy and X-ray crystallography.","authors":"Hiroki Yamaguchi, Kazutoshi Takahashi, Nobutaka Numoto, Hiroshi Suzuki, Moemi Tatsumi, Akiko Kamegawa, Kouki Nishikawa, Yasuhisa Asano, Toshimi Mizukoshi, Hiroshi Miyano, Yoshinori Fujiyoshi, Masayuki Sugiki","doi":"10.1093/jb/mvae070","DOIUrl":"https://doi.org/10.1093/jb/mvae070","url":null,"abstract":"L-arginine oxidase (AROD, EC 1.4.3.25) is an oxidoreductase that catalyzes the deamination of L-arginine, with flavin adenine dinucleotide (FAD) as a cofactor. Recently identified AROD from Pseudomonas sp. TPU 7192 (PT-AROD) demonstrates high selectivity for L-arginine. This enzyme is useful for accurate assays of L-arginine in biological samples. The structural characteristics of the FAD-dependent AROD, however, remain unknown. Here, we report the structure of PT-AROD at a resolution of 2.3 Å by cryo-electron microscopy. PT-AROD adopts an octameric structure with D4 symmetry, which is consistent with its molecular weight in solution, estimated by mass photometry. Comparative analysis of this structure with that determined using X-ray crystallography reveals open and closed forms of the lid-like loop at the entrance to the substrate pocket. Furthermore, mutation of Glu493, located at the substrate binding site, diminishes substrate selectivity, suggesting that this residue contributes significantly to the high selectivity of PT-AROD.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142466392","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

Mitochondria-giant lipid droplet proximity and autophagy suppression in nitrogen-depleted oleaginous yeast Lipomyces starkeyi cells. 缺氮油脂酵母星酵母细胞中线粒体-巨脂滴的接近和自噬抑制。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2024-10-15 DOI: 10.1093/jb/mvae069

Lan Duan, Akinobu Togou, Keisuke Ohta, Koji Okamoto

{"title":"Mitochondria-giant lipid droplet proximity and autophagy suppression in nitrogen-depleted oleaginous yeast Lipomyces starkeyi cells.","authors":"Lan Duan, Akinobu Togou, Keisuke Ohta, Koji Okamoto","doi":"10.1093/jb/mvae069","DOIUrl":"https://doi.org/10.1093/jb/mvae069","url":null,"abstract":"Balancing energy production and storage is a fundamental process critical for cellular homeostasis in most eukaryotes that relies on the intimate interplay between mitochondria and lipid droplets. In the oleaginous yeast Lipomyces starkeyi under nitrogen starvation, lipid droplet forms a single giant spherical structure that is easily visible under a light microscope. Currently, how mitochondria behave in L. starkeyi cells undergoing giant lipid droplet formation remains unknown. Here we show that mitochondria transition from fragments to elongated tubules and sheet-like structures that are in close proximity to a giant lipid droplet in nitrogen-depleted L. starkeyi cells. Under the same conditions, mitochondrial degradation and autophagy are strongly suppressed, suggesting that these catabolic events are not required for giant lipid droplet formation. Conversely, carbon-depleted cells suppress mitochondrial elongation and lipid droplet expansion, whereas they promote mitochondrial degradation and autophagy. We propose a potential link of mitochondrial proximity and autophagic suppression to giant lipid droplet formation.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142466391","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

Molecular mechanisms of mechanosensing and plasticity of tendons and ligaments. "肌腱和韧带机械感应和可塑性的分子机制"。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2024-09-30 DOI: 10.1093/jb/mvae039

Takahide Matsushima, Asahara Hiroshi

引用次数: 0

Dyslipidemia and hyperglycemia induce overexpression of Syndecan-3 in erythrocytes and modulate erythrocyte adhesion. 血脂异常和高血糖会诱导红细胞中的Syndecan-3过度表达，并调节红细胞的粘附性。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2024-09-30 DOI: 10.1093/jb/mvae050

Smitha Honnalagere Mallanna, Rajesh K Thimmulappa, Nandini D Chilkunda

{"title":"Dyslipidemia and hyperglycemia induce overexpression of Syndecan-3 in erythrocytes and modulate erythrocyte adhesion.","authors":"Smitha Honnalagere Mallanna, Rajesh K Thimmulappa, Nandini D Chilkunda","doi":"10.1093/jb/mvae050","DOIUrl":"10.1093/jb/mvae050","url":null,"abstract":"Erythrocytes are important vascular components that play vital roles in maintaining vascular homeostasis, in addition to carrying oxygen. Previously, we reported that the changes in the internal milieu (e.g. hyperglycemia or hypercholesterolemia) increase erythrocyte adhesion to various extracellular matrix components, potentially through altering glycosaminoglycans (GAGs). In this study, we have investigated the expression of syndecan (Sdc) family members that could be involved in mediating cytoadherence under conditions of dyslipidemia and hyperglycemia. Among the Sdc family members analysed, we found significant overexpression of Sdc-3 in erythrocyte membranes harvested from high-fat-fed control and diabetic animals. Animal studies revealed a positive correlation between Sdc-3 expression, blood sugar levels and erythrocyte adhesion. In the human study, diabetic cohorts with body mass index >24.9 showed significantly increased expression of Sdc-3. Interestingly, blocking the Sdc-3 moiety with an anti-Sdc-3 antibody revealed that the core protein might not be directly involved in erythrocyte adhesion to fibronectin despite the GAGs bringing about adhesion. Lastly, Nano liquid chromatography-mass spectrometry/MS verified the presence of Sdc-3 in erythrocyte membranes. In conclusion, the high-fat diet and diabetes modulated Sdc-3 expression in the erythrocyte membrane, which may alter its adhesive properties and promote vascular complications.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141498151","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

Spatial heterogeneity and functional zonation of living tissues and organs in situ. 活体组织和器官在原位的空间异质性和功能分区。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2024-09-30 DOI: 10.1093/jb/mvae049

Yu Miyamoto, Masaru Ishii

引用次数: 0

CRABP2 promotes cell migration and invasion by activating PI3K/AKT and MAPK signalling pathways via upregulating LAMB3 in prostate cancer. CRABP2 在前列腺癌中通过上调 LAMB3 激活 PI3K/AKT 和 MAPK 信号通路，从而促进细胞迁移和侵袭。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2024-09-30 DOI: 10.1093/jb/mvae052

Rui Wang, Zhaoping Liao, Chunhua Liu, Shifang Yu, Kaihua Xiang, Ting Wu, Jie Feng, Senjuan Ding, Tingao Yu, Gang Cheng, Sanlian Li

{"title":"CRABP2 promotes cell migration and invasion by activating PI3K/AKT and MAPK signalling pathways via upregulating LAMB3 in prostate cancer.","authors":"Rui Wang, Zhaoping Liao, Chunhua Liu, Shifang Yu, Kaihua Xiang, Ting Wu, Jie Feng, Senjuan Ding, Tingao Yu, Gang Cheng, Sanlian Li","doi":"10.1093/jb/mvae052","DOIUrl":"10.1093/jb/mvae052","url":null,"abstract":"Prostate cancer (PCa) has become a worldwide health burden among men. Previous studies have suggested that cellular retinoic acid binding protein 2 (CRABP2) significantly affects the regulation of cell proliferation, motility and apoptosis in multiple cancers; however, the effect of CRABP2 on PCa is poorly reported. CRABP2 expression in different PCa cell lines and its effect on different cellular functions varied. While CRABP2 promotes cell migration and invasion, it appears to inhibit cell proliferation specifically in PC-3 cells. However, the proliferation of DU145 and 22RV1 cells did not appear to be significantly affected by CRABP2. Additionally, CRABP2 had no influence on the cell cycle distribution of PCa cells. The RNA-seq assay showed that overexpressing CRABP2 upregulated laminin subunit beta-3 (LAMB3) mRNA expression, and the enrichment analyses revealed that the differentially expressed genes were enriched in the phosphoinositide 3-kinase (PI3K)/activated protein kinase B (AKT) and mitogen-activated protein kinase (MAPK) signalling pathways. The following western blot experiments also confirmed the upregulated LAMB3 protein level and the activation of the PI3K/AKT and MAPK signalling pathways. Moreover, overexpressing CRABP2 significantly inhibited tumour growth in vivo. In conclusion, CRABP2 facilitates cell migration and invasion by activating PI3K/AKT and MAPK signalling pathways through upregulating LAMB3 in PCa.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141748309","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

The Hox-based positional memory in muscle stem cells. 肌肉干细胞中基于 Hox 的位置记忆。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2024-09-30 DOI: 10.1093/jb/mvae059

Ryosuke Okino, Yuki Goda, Yusuke Ono

引用次数: 0

Cutting-edge skin ageing research on tissue stem cell. 关于组织干细胞的尖端皮肤老化研究。

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2024-09-30 DOI: 10.1093/jb/mvae022

Ryo Ichijo

引用次数: 0

Cardiac remodeling: novel pathophysiological mechanisms and therapeutic strategies. 心脏重塑：新的病理生理学机制和治疗策略

IF 2.1 4区生物学

Journal of biochemistry Pub Date : 2024-09-30 DOI: 10.1093/jb/mvae031

Motohiro Nishida, Xinya Mi, Yukina Ishii, Yuri Kato, Akiyuki Nishimura

{"title":"Cardiac remodeling: novel pathophysiological mechanisms and therapeutic strategies.","authors":"Motohiro Nishida, Xinya Mi, Yukina Ishii, Yuri Kato, Akiyuki Nishimura","doi":"10.1093/jb/mvae031","DOIUrl":"10.1093/jb/mvae031","url":null,"abstract":"Morphological and structural remodeling of the heart, including cardiac hypertrophy and fibrosis, has been considered as a therapeutic target for heart failure for approximately three decades. Groundbreaking heart failure medications demonstrating reverse remodeling effects have contributed significantly to medical advancements. However, nearly 50% of heart failure patients still exhibit drug resistance, posing a challenge to the healthcare system. Recently, characteristics of heart failure resistant to ARBs and β-blockers have been defined, highlighting preserved systolic function despite impaired diastolic function, leading to the classification of heart failure with preserved ejection fraction (HFpEF). The pathogenesis and aetiology of HFpEF may be related to metabolic abnormalities, as evidenced by its mimicry through endothelial dysfunction and excessive intake of high-fat diets. Our recent findings indicate a significant involvement of mitochondrial hyper-fission in the progression of heart failure. This mitochondrial pathological remodeling is associated with redox imbalance, especially hydrogen sulphide accumulation due to abnormal electron leak in myocardium. In this review, we also introduce a novel therapeutic strategy for heart failure from the current perspective of mitochondrial redox-metabolic remodeling.","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140174872","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