Biochemical and biophysical research communications最新文献

The different functions of V-ATPase subunits in adipocyte differentiation and their expression in obese mice V-ATPase 亚基在脂肪细胞分化中的不同功能及其在肥胖小鼠体内的表达

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2024-09-24 DOI: 10.1016/j.bbrc.2024.150733

{"title":"The different functions of V-ATPase subunits in adipocyte differentiation and their expression in obese mice","authors":"","doi":"10.1016/j.bbrc.2024.150733","DOIUrl":"10.1016/j.bbrc.2024.150733","url":null,"abstract":"<div><h3>Background</h3><div>Obesity is a significant global public health issue linked to numerous chronic diseases, including diabetes, cardiovascular conditions, and various cancers. The vacuolar H + ATPase, a multi-subunit enzyme complex involved in maintaining pH balance, has been implicated in various health conditions, including obesity-related diseases.</div></div><div><h3>Method</h3><div>This study conducts a comprehensive analysis of V-ATPase subunits' roles in adipogenesis within the context of obesity, using knockdown and RNAseq technologies.</div></div><div><h3>Result</h3><div>This study conducts a comprehensive analysis of V-ATPase subunits' roles in adipogenesis, highlighting specific subunits, v0d2 and v1a, which show significant expression alterations. Our findings reveal that v1a plays a crucial role in adipocyte differentiation through pathways related to steroid and cholesterol metabolism.</div></div><div><h3>Conclusion</h3><div>This study provides a comprehensive analysis of the roles played by V-ATPase subunits in adipogenesis and finds the critical role of V-ATPase subunits, particularly v1a, in the differentiation of adipocytes and their potential impact on obesity.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142323423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

3,3′-Diindolylmethane disrupts the endoplasmic reticulum and nuclear envelope in Schizosaccharomyces pombe 3,3′-二吲哚甲烷破坏小鼠内质网和核膜

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2024-09-24 DOI: 10.1016/j.bbrc.2024.150724

引用次数: 0

Unveiling the reaction mechanism of arginine decarboxylase in Aspergillus oryzae: Insights from crystal structure analysis 揭示黑曲霉精氨酸脱羧酶的反应机制：晶体结构分析的启示

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2024-09-21 DOI: 10.1016/j.bbrc.2024.150728

{"title":"Unveiling the reaction mechanism of arginine decarboxylase in Aspergillus oryzae: Insights from crystal structure analysis","authors":"","doi":"10.1016/j.bbrc.2024.150728","DOIUrl":"10.1016/j.bbrc.2024.150728","url":null,"abstract":"<div><div>Agmatine, a natural polyamine also known as 4-aminobutyl-guanidine, is biosynthesized from arginine by decarboxylation. <em>Aspergillus oryzae</em> contains high amounts of agmatine, suggesting highly active arginine decarboxylase (ADC) in this organism. However, genome analysis revealed no ADC homolog in <em>A. oryzae</em>. <em>A. oryzae</em> strain RIB40 has six homologs of phosphatidylserine decarboxylase (PSD), an enzyme that synthesizes phosphatidyl ethanolamine from phosphatidylserine. We previously discovered that one of these homologs, AO090102000327, encodes arginine decarboxylase, which we named ADC1. In the present study, we determined the crystal structures of ligand-free, arginine-treated, and agmatine-treated ADC1 each at 1.9–2.15 Å resolution. Each structure contained four ADC1 molecules (chains A–D) in the asymmetric unit of the cell. Each ADC1 molecule is a heterodimer consisting of the N-terminal region (Asn60–Gly441) and C-terminal region (Ser442–Thr482). In the ligand-free ADC1, the N-terminus of Ser442 was modified to form a pyruvoyl group. In the arginine-treated ADC1, arginine was converted to agmatine, with the pyruvoyl group covalently bound to agmatine by forming a Schiff base. The same structure was observed in agmatine-treated ADC1. These results indicate that ADC1 is a pyruvoyl-dependent decarboxylase and unveils the reaction mechanism of ADC from <em>A. oryzae</em>.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142314840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Activated human Orai1 channel in lipid biolayer may exist as a pentamer 脂质生物层中的活化人 Orai1 通道可能以五聚体形式存在。

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2024-09-21 DOI: 10.1016/j.bbrc.2024.150723

引用次数: 0

CUG repeat RNA-dependent proteasomal degradation of MBNL1 in a cellular model of myotonic dystrophy type 1 1 型肌营养不良症细胞模型中 MBNL1 的 CUG 重复 RNA 依赖性蛋白酶体降解

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2024-09-21 DOI: 10.1016/j.bbrc.2024.150729

{"title":"CUG repeat RNA-dependent proteasomal degradation of MBNL1 in a cellular model of myotonic dystrophy type 1","authors":"","doi":"10.1016/j.bbrc.2024.150729","DOIUrl":"10.1016/j.bbrc.2024.150729","url":null,"abstract":"<div><div>Myotonic dystrophy type 1 (DM1) is caused by the expansion of a non-coding CTG repeat in <em>DMPK</em>. CUG-repeat-containing transcripts sequester the splicing regulator MBNL1 into nuclear RNA foci, causing aberrant splicing of many genes. Although the mislocalization of MBNL1 represents a causal event in DM1 pathogenesis, the effect of CUG repeat RNA on the protein level of MBNL1 remains unclear. Using a DM1 model cell line, we found that CUG repeat RNA caused a significant decrease in the protein, but not mRNA levels, of MBNL1. As CUG repeats did not decrease MBNL1 translation, we investigated protein degradation pathways. Although autophagy-related reagents induced little change, proteasome inhibitors partially recovered MBNL1 protein expression levels under conditions of CUG repeat expression and induced a slight, but significant, reversal of splicing dysregulation. MBNL1 was detected in the polyubiquitinated protein fraction, but MBNL1 polyubiquitination was not detected. Moreover, inhibition of the ubiquitin-activating enzyme E1 did not increase MBNL1 levels, suggesting that MBNL1 is a substrate of polyubiquitin-independent proteasomal degradation. These results suggest that CUG-repeat-induced proteasomal degradation partially contributes to the functional decline of MBNL1.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0006291X24012658/pdfft?md5=85fc757b2b410ffa2fd7c6d7a5cc6d20&pid=1-s2.0-S0006291X24012658-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142314842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Nuclear interactions between the Pseudo-Response Regulator clock proteins and the Multi-Step Phosphorelay mediator Histidine-containing phosphotransfers in the moss Physcomitrium patens 藓类中伪响应调节器时钟蛋白与多步磷转运介质含组氨酸磷转运蛋白之间的核相互作用

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2024-09-21 DOI: 10.1016/j.bbrc.2024.150734

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Non-associative potentiation of proximal excitatory inputs to layer 2/3 pyramidal cells in rat visual cortex 大鼠视觉皮层第 2/3 层锥体细胞近端兴奋性输入的非关联性电位增强

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2024-09-21 DOI: 10.1016/j.bbrc.2024.150736

{"title":"Non-associative potentiation of proximal excitatory inputs to layer 2/3 pyramidal cells in rat visual cortex","authors":"","doi":"10.1016/j.bbrc.2024.150736","DOIUrl":"10.1016/j.bbrc.2024.150736","url":null,"abstract":"<div><div>Long-term changes of synaptic transmission can be induced by Hebbian-type homosynaptic mechanisms which require activation of both pre- and postsynapse and mediate associative learning, as well as by heterosynaptic mechanisms which do not require activation of the presynapse and are non-associative. The rules for induction of homosynaptic plasticity depend on the distance of the synapse from the soma. Does induction of heterosynaptic plasticity also depend on synaptic location? Here, we investigated heterosynaptic changes in pharmacologically isolated glutamatergic inputs arriving at either the proximal or the distal segments of the apical dendrite of layer 2/3 pyramidal neurons in rat visual cortex. We show that bursts of action potentials evoked without presynaptic stimulation induced potentiation of proximal inputs while having little effect on distal inputs. Such gradient of plasticity could be related to the attenuation of backpropagating action potentials along the dendrites. Thus, the location of the synapse on the dendritic tree is a determinant not only for homosynaptic but also for heterosynaptic plasticity.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142323424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

MicroRNA miR-199a-3p alleviates liver fibrosis by targeting CDK17 in activated hepatic stellate cells 微RNA miR-199a-3p通过靶向激活的肝星状细胞中的CDK17减轻肝纤维化

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2024-09-20 DOI: 10.1016/j.bbrc.2024.150727

{"title":"MicroRNA miR-199a-3p alleviates liver fibrosis by targeting CDK17 in activated hepatic stellate cells","authors":"","doi":"10.1016/j.bbrc.2024.150727","DOIUrl":"10.1016/j.bbrc.2024.150727","url":null,"abstract":"<div><div>Liver fibrosis, a common feature of most chronic liver diseases, poses significant health risks and results from various etiologies. While microRNAs (miRNAs) have demonstrated promising anti-fibrotic potential through the direct regulation of target genes, their therapeutic mechanisms remain incompletely understood. In this study, we identified miR-199a, initially discovered in anti-liver fibrotic exosomes, as a key modulator that alleviates thioacetamide-induced liver fibrosis in a mouse model. Consistent with its <em>in vivo</em> effects, treatment with an miR-199a mimic effectively inhibited the activation and function of human hepatic stellate cells (HSCs)-central drivers of liver fibrosis-as well as HSC proliferation and viability <em>in vitro</em>. Notably, miR-199a-3p exerted these anti-fibrotic effects by directly downregulating its biologically relevant target, <em>cyclin-dependent kinase 17</em> (<em>CDK17</em>). Depletion of CDK17 alone in activated HSCs was sufficient to suppress their activation, function, proliferation, and viability, mirroring the effects of miR-199a mimic treatment. Conversely, overexpression of <em>CDK17</em> reversed all cellular effects induced by miR-199a mimic treatment. Our findings highlight the miR-199a-3p-<em>CDK17</em> regulatory axis and suggest that targeting CDK17 in activated HSCs could be a promising therapeutic strategy for liver fibrosis.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142314841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Junctophilin-2 is a double-stranded RNA-binding protein that regulates cardiomyocyte-autonomous innate immune response Junctophilin-2 是一种双链 RNA 结合蛋白，能调节心肌细胞自主的先天性免疫反应

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2024-09-20 DOI: 10.1016/j.bbrc.2024.150725

{"title":"Junctophilin-2 is a double-stranded RNA-binding protein that regulates cardiomyocyte-autonomous innate immune response","authors":"","doi":"10.1016/j.bbrc.2024.150725","DOIUrl":"10.1016/j.bbrc.2024.150725","url":null,"abstract":"<div><div>Junctophilin-2 (JPH2) is traditionally recognized as a cardiomyocyte-enriched structural protein that anchors the junction between the plasma membrane and the endo/sarcoplasmic reticulum, facilitating excitation-induced cardiac contraction. In this study, we uncover a novel function of JPH2 as a double-stranded RNA (dsRNA)-binding protein, which forms complexes with dsRNA both in vitro and in cells. Stimulation by cytosolic dsRNA enhances the interaction of JPH2 with the dsRNA sensor MDA5. Notably, JPH2 inhibits MDA5's binding to its dsRNA ligand, likely by sequestering the dsRNA. Silencing JPH2 in cardiomyocytes increased the interaction between MDA5 and its dsRNA ligands, activated the MAVS/TBK1 signaling, and triggered spontaneous interferon-beta (IFNb1) production in the absence of foreign pathogen. Mouse hearts deficient in JPH2 exhibited upregulation of innate immune signaling cascade. Collectively, these findings identify JPH2 as a regulator of dsRNA sensing and highlight its role in suppressing the automatic activation of innate immune responses in cardiomyocytes, suggesting the cytosolic surface of the endo/sarcoplasmic reticulum as a hub for dsRNA sequestration.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142314837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Comprehensive evaluation of pathogenic protein accumulation in fibroblasts from all subtypes of Sanfilippo disease patients 全面评估桑菲利波病患者所有亚型成纤维细胞中致病蛋白的积累情况

IF 2.5 3区生物学

Biochemical and biophysical research communications Pub Date : 2024-09-19 DOI: 10.1016/j.bbrc.2024.150718

{"title":"Comprehensive evaluation of pathogenic protein accumulation in fibroblasts from all subtypes of Sanfilippo disease patients","authors":"","doi":"10.1016/j.bbrc.2024.150718","DOIUrl":"10.1016/j.bbrc.2024.150718","url":null,"abstract":"<div><p>Sanfilippo disease is a lysosomal storage disorder from the group of mucopolysaccharidoses (MPS), characterized by storage of glycosaminoglycans (GAGs); thus, it is also called MPS type III. The syndrome is divided into 4 subtypes (MPS III A, B, C and D). Despite the storage of the same GAG, heparan sulfate (HS), the course of these subtypes can vary considerably. Here, we comprehensively evaluated the levels of protein aggregates (APP, β-amyloid, p-tau, α-synuclein, TDP43) in fibroblasts derived from patients with all MPS III subtypes, and tested whether lowering GAG levels results in a decrease in the levels of the investigated proteins and the number of aggregates they form. Elevated levels of APP, β-amyloid, tau, and TDP43 proteins were evident in all MPS III subtypes, and elevated levels of p-tau and α-synuclein were demonstrated in all subtypes except MPS IIIC. These findings were confirmed in the neural tissue of MPS IIIB mice. Fluorescence microscopy studies also indicated a high number of protein aggregates formed by β-amyloid and tau in all cell lines tested, and a high number of aggregates of p-tau, TDP43, and α-synuclein in all lines except MPS IIIC. Reduction of GAG levels by genistein led to the decrease of levels of all tested proteins and their aggregates except α-synuclein, indicating a relationship between GAG levels and those of some protein aggregates. This work describes for the first time the problem of deposited protein aggregates in all subtypes of Sanfilippo disease and suggests that GAGs are partly responsible for the formation of protein aggregates.</p></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0006291X24012543/pdfft?md5=018d26cd984cead61249bcb1d7a2ed5b&pid=1-s2.0-S0006291X24012543-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142274191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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