Archives of biochemistry and biophysics最新文献

筛选
英文 中文
Knockdown of ERN1 disturbs the expression of phosphoserine aminotransferase 1 and related genes in glioblastoma cells 敲除 ERN1 会干扰胶质母细胞瘤细胞中磷酸丝氨酸氨基转移酶 1 及相关基因的表达。
IF 3.8 3区 生物学
Archives of biochemistry and biophysics Pub Date : 2024-07-24 DOI: 10.1016/j.abb.2024.110104
Oleksandr H. Minchenko, Myroslava Y. Sliusar, Yevgen P. Khikhlo, Oleh V. Halkin, Yuliia M. Viletska, Olena O. Khita, Dmytro O. Minchenko
{"title":"Knockdown of ERN1 disturbs the expression of phosphoserine aminotransferase 1 and related genes in glioblastoma cells","authors":"Oleksandr H. Minchenko,&nbsp;Myroslava Y. Sliusar,&nbsp;Yevgen P. Khikhlo,&nbsp;Oleh V. Halkin,&nbsp;Yuliia M. Viletska,&nbsp;Olena O. Khita,&nbsp;Dmytro O. Minchenko","doi":"10.1016/j.abb.2024.110104","DOIUrl":"10.1016/j.abb.2024.110104","url":null,"abstract":"<div><h3>Background</h3><p>Endoplasmic reticulum stress and synthesis of serine are essential for tumor growth, but the mechanism of their interaction is not clarified yet. The overarching goal of this work was to investigate the impact of ERN1 (endoplasmic reticulum to nucleus signaling 1) inhibition on the expression of serine synthesis genes in U87MG glioblastoma cells concerning the suppression of cell proliferation.</p></div><div><h3>Methods</h3><p>Wild type U87MG glioblastoma cells and their clones with overexpression of transgenes dnERN1 (without cytoplasmic domain of ERN1) and dnrERN1 (with mutation in endoribonuclease of ERN1), and empty vector (as control) were used. The silencing of ERN1 and XBP1 was also used to inhibition of ERN1 and its function. Gene expression was measured by qPCR.</p></div><div><h3>Results</h3><p>We show that the expression of <em>PSAT1</em> and several other related to serine synthesis genes is suppressed in cells with ERN1 inhibition by dissimilar mechanisms: <em>PHGDH</em> gene through ERN1 protein kinase, because its expression was resistant to inhibition of ERN1 endoribonuclease, but <em>ATF4</em> gene via endoribonuclease of ERN1. However, in the control of <em>PSAT1</em> and <em>PSPH</em> genes both enzymatic activities of ERN1 signaling protein are involved. At the same time, ERN1 knockdown strongly increased <em>SHMT1</em> expression, which controls serine metabolism and enhances the proliferation and invasiveness of glioma cells. The level of microRNAs, which have binding sites in PSAT1, SHMT1, and PSPH mRNAs, was also changed in cells harboring dnERN1 transgene. Inhibition of ERN1 suppressed cell proliferation and enzymatic activity of PHGDH, a rate-limiting enzyme for serine synthesis.</p></div><div><h3>Conclusion</h3><p>Changes in the expression of phosphoserine aminotransferase 1 and other genes related to serine synthesis are mediated by diverse ERN1-dependent mechanisms and contributed to suppressed proliferation and enhanced invasiveness of ERN1 knockdown glioblastoma cell.</p></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"759 ","pages":"Article 110104"},"PeriodicalIF":3.8,"publicationDate":"2024-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141765027","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
Protective effect of dimethyl fumarate against ethanol-provoked gastric ulcers in rats via regulation of HMGB1/TLR4/NF-κB, and PPARγ/SIRT1/Nrf2 pathways: Involvement of miR-34a-5p 富马酸二甲酯通过调节 HMGB 1/TLR4/NF-κB 和 PPARγ/SIRT1/Nrf2 通路对乙醇诱发的大鼠胃溃疡的保护作用:miR-34a-5p 的参与。
IF 3.8 3区 生物学
Archives of biochemistry and biophysics Pub Date : 2024-07-23 DOI: 10.1016/j.abb.2024.110103
Eman M. Elbaz , Amina A.S. Abdel Rahman , Amira A. El-Gazar , Bassam Mohamed Ali
{"title":"Protective effect of dimethyl fumarate against ethanol-provoked gastric ulcers in rats via regulation of HMGB1/TLR4/NF-κB, and PPARγ/SIRT1/Nrf2 pathways: Involvement of miR-34a-5p","authors":"Eman M. Elbaz ,&nbsp;Amina A.S. Abdel Rahman ,&nbsp;Amira A. El-Gazar ,&nbsp;Bassam Mohamed Ali","doi":"10.1016/j.abb.2024.110103","DOIUrl":"10.1016/j.abb.2024.110103","url":null,"abstract":"<div><p>Aberration of the gastric mucosal barrier homeostasis circuit is one of the key features linked to the onset of gastric ulcers (GU). This work aimed to inspect the gastroprotective influence of dimethyl fumarate (DMF) on ethanol-induced GU in rats and to decipher the possible mechanisms entailed. Rats were pretreated with either DMF (80 mg/kg) or omeprazole (OMP) (20 mg/kg) by oral gavage for 2 weeks. After 24 h of starvation, ethanol (5 ml/kg, oral) was employed to trigger GU in rats, while carboxymethyl cellulose (CMC) was used as a control. Ethanol notably elevated both macroscopic and microscopic gastric damage. DMF and OMP exhibited similar effects on gastric ulcer healing. DMF intervention led to a substantial improvement in gastric insults. DMF significantly reduced ethanol-triggered gastric lesions, as manifested by decreased gastric secretion, acidity, ulcer surface area percent, reduced leukocyte incursion, and increased mucus percent. DMF upregulated miR-34a-5p expression concomitant with the suppression of high mobility group box1 (HMGB1) and inflammatory responses in gastric mucosal homogenate. DMF improved GU by restoring reduced antioxidant defense mechanisms through the coactivation of nuclear factor erythroid 2-related factor-2 (Nrf2), peroxisome proliferator-activated receptor gamma (PPARγ), and sirtuin1 (SIRT1), indicating the protective role of the PPARγ/SIRT1/Nrf2 pathway. Intriguingly, DMF mitigated apoptosis in ethanol-elicited GU. Taken together, this research implies the potential for the repurposing of DMF as an innovative gastroprotective medication to reestablish the balance of the gastric mucosal barrier via the attenuation of gastric inflammation, oxidative stress, and apoptosis.</p></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"759 ","pages":"Article 110103"},"PeriodicalIF":3.8,"publicationDate":"2024-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141756737","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
Nrf2/FSP1/CoQ10 axis-mediated ferroptosis is involved in sodium aescinate-induced nephrotoxicity Nrf2/FSP1/CoQ10轴介导的铁氧化参与了羊栖菜酸钠诱导的肾毒性
IF 3.8 3区 生物学
Archives of biochemistry and biophysics Pub Date : 2024-07-20 DOI: 10.1016/j.abb.2024.110100
Haiyan Zhu, Yijing Yang, Yenan Duan, Xin Zheng, Zixiong Lin, Jie Zhou
{"title":"Nrf2/FSP1/CoQ10 axis-mediated ferroptosis is involved in sodium aescinate-induced nephrotoxicity","authors":"Haiyan Zhu,&nbsp;Yijing Yang,&nbsp;Yenan Duan,&nbsp;Xin Zheng,&nbsp;Zixiong Lin,&nbsp;Jie Zhou","doi":"10.1016/j.abb.2024.110100","DOIUrl":"10.1016/j.abb.2024.110100","url":null,"abstract":"<div><p>Sodium aescinate (SA), an active compound found in horse chestnut seeds, is widely used in clinical practice. Recently, the incidence of SA-induced adverse events, particularly renal impairment, has increased. Our previous work demonstrated that SA causes severe nephrotoxicity via nephrocyte ferroptosis; however, the underlying mechanism remains to be fully elucidated. In the current study, we investigated additional molecular pathways involved in SA-induced nephrotoxicity. Our results showed that SA inhibited cell viability, disrupted cellular membrane integrity, and enhanced reactive oxygen species (ROS), ferrous iron (Fe<sup>2+</sup>), and malondialdehyde (MDA) levels, as well as lipid peroxidation in rat proximal renal tubular epithelial cell line (NRK-52E) cells. SA also depleted coenzyme Q10 (CoQ10, ubiquinone) and nicotinamide adenine dinucleotide (NADH) and reduced ferroptosis suppressor protein 1 (FSP1) and polyprenyltransferase (coenzyme Q2, COQ2) activity, triggering lipid peroxidation and ROS accumulation in mouse kidneys and NRK-52E cells. The overexpression of COQ2, FSP1, or CoQ10 (ubiquinone) supplementation effectively attenuated SA-induced ferroptosis, whereas iFSP1 or 4-formylbenzoic acid (4-CBA) pretreatment exacerbated SA-induced nephrotoxicity. Additionally, SA decreased nuclear factor-erythroid-2-related factor 2 (Nrf2) levels and inhibited Nrf2 binding to the −1170/-1180 bp ARE site in FSP1 promoter, resulting in FSP1 suppression. Overexpression of Nrf2 or its agonist dimethyl fumarate (DMF) promoted FSP1 expression, thereby improving cellular antioxidant capacity and alleviating SA-induced ferroptosis. These results suggest that SA-triggers renal injury through oxidative stress and ferroptosis, driven by the suppression of the Nrf2/FSP1/CoQ10 axis.</p></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"759 ","pages":"Article 110100"},"PeriodicalIF":3.8,"publicationDate":"2024-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141732190","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
Simultaneous induction of systemic hyperglycaemia and stress impairs brain redox homeostasis in the adult zebrafish 同时诱导全身性高血糖和应激会损害成年斑马鱼大脑的氧化还原平衡
IF 3.8 3区 生物学
Archives of biochemistry and biophysics Pub Date : 2024-07-18 DOI: 10.1016/j.abb.2024.110101
Rhea Subba , Gianluca Fasciolo , Eugenio Geremia , Maria Teresa Muscari Tomajoli , Adriana Petito , Sabrina Carrella , Amal Chandra Mondal , Gaetana Napolitano , Paola Venditti
{"title":"Simultaneous induction of systemic hyperglycaemia and stress impairs brain redox homeostasis in the adult zebrafish","authors":"Rhea Subba ,&nbsp;Gianluca Fasciolo ,&nbsp;Eugenio Geremia ,&nbsp;Maria Teresa Muscari Tomajoli ,&nbsp;Adriana Petito ,&nbsp;Sabrina Carrella ,&nbsp;Amal Chandra Mondal ,&nbsp;Gaetana Napolitano ,&nbsp;Paola Venditti","doi":"10.1016/j.abb.2024.110101","DOIUrl":"10.1016/j.abb.2024.110101","url":null,"abstract":"<div><p>For diabetic patients it is crucial to constantly monitor blood glucose levels to mitigate complications due to hyperglycaemia, including neurological issues and cognitive impairments. This activity leads to psychological stress, called “diabetes distress,” a problem for most patients living with diabetes. Diabetes distress can exacerbate the hyperglycaemia effects on brain and negatively impact the quality of life, but the underlying mechanisms remain poorly explored. We simulated diabetes distress in adult zebrafish by modelling hyperglycaemia, through exposure to dextrose solution, along with chronic unpredictable mild stress (CUMS), and evaluated brain redox homeostasis by assessing reactive oxygen species (ROS) content, the antioxidant system, and effects on mitochondrial biogenesis and fission/fusion processes. We also evaluated the total, cytosolic and nuclear content of nuclear factor erythroid 2-related factor 2 (NRF2), a critical regulator of redox balance, in the whole brain and total NRF2 in specific brain emotional areas. The combined CUMS + Dextrose challenge, but not the individual treatments, reduced total NRF2 levels in the entire brain, but strongly increased its levels in the nuclear fraction. Compensatory upregulation of antioxidant genes appeared inadequate to combat elevated levels of ROS, leading to lowering of the reduced glutathione content and total antioxidant capacity. CUMS + Dextrose treatment also upregulated transcription factors implicated in mitochondrial biogenesis and dynamics with a predominance of fission, which is consistent with increased oxidative stress. In conclusion, this study highlights the close interplay between hyperglycaemia and psychological distress causing overriding oxidative stress in the brain, rendering the organism vulnerable to the development of disease complications.</p></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"759 ","pages":"Article 110101"},"PeriodicalIF":3.8,"publicationDate":"2024-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0003986124002236/pdfft?md5=43e172b5020f6d8878c4d3d3f6ad44cc&pid=1-s2.0-S0003986124002236-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141726724","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
GSDMB involvement in the pathogenesis of abdominal aortic aneurysm through regulation of macrophage non-canonical pyroptosis GSDMB 通过调控巨噬细胞的非典型热解参与腹主动脉瘤的发病机制。
IF 3.8 3区 生物学
Archives of biochemistry and biophysics Pub Date : 2024-07-17 DOI: 10.1016/j.abb.2024.110102
Xiaoping Xie , Xiaoyan Shen , Yi Liu , Yifan Zuo , Su Wang , Yang Zhou , Xu li , Kexin Wang , Bowen Li , Zhiwei Wang
{"title":"GSDMB involvement in the pathogenesis of abdominal aortic aneurysm through regulation of macrophage non-canonical pyroptosis","authors":"Xiaoping Xie ,&nbsp;Xiaoyan Shen ,&nbsp;Yi Liu ,&nbsp;Yifan Zuo ,&nbsp;Su Wang ,&nbsp;Yang Zhou ,&nbsp;Xu li ,&nbsp;Kexin Wang ,&nbsp;Bowen Li ,&nbsp;Zhiwei Wang","doi":"10.1016/j.abb.2024.110102","DOIUrl":"10.1016/j.abb.2024.110102","url":null,"abstract":"<div><p>Abdominal aortic aneurysm (AAA) is a dangerous condition affecting the aorta. Macrophage pyroptosis, phenotypic transformation, and apoptosis of aortic smooth muscle cells (ASMCs) are pivotal mechanisms in AAA pathogenesis. This study explores how Gasdermin B (GSDMB) regulates macrophage non-canonical pyroptosis and its impact on the phenotypic transformation and apoptosis of ASMCs, thereby unveiling the role of GSDMB in AAA pathogenesis. Immunofluorescence analysis was used to assess the expression levels and localization of GSDMB, cysteinyl aspartate-specific protease-4 (Caspase-4), and N-terminal of cleaved GSDMD (N-GSDMD) in AAA tissues. A cell model that mimics macrophage non-canonical pyroptosis was established by treating THP-1 cells with lipopolysaccharide (LPS). THP-1 cells with reduced or increased GSDMB were generated using small interfering RNA (siRNA) or plasmids. Co-culture experiments involving THP-1 cells and HASMCs were conducted to explore the impact of GSDMB on HASMCs. The mitochondrial reactive oxygen species (mtROS) scavenger Mito-TEMPO lowered mtROS levels in THP-1 cells. Our findings revealed that GSDMB was significantly upregulated in AAA macrophages, which was accompanied by robust non-canonical pyroptosis. THP-1 cells showed non-canonical pyroptosis in response to LPS, which was accompanied by an increase in GSDMB. Further research demonstrated that altering GSDMB, either by knockdown or overexpression, can affect macrophage non-canonical pyroptosis as well as the phenotypic transformation and apoptosis of HASMCs. LPS-induced non-canonical pyroptosis in THP-1 cells was associated with an increase in mtROS, whereas Mito-TEMPO effectively decreased non-canonical pyroptosis and the expression of GSDMB. These findings suggest that GSDMB plays a role in AAA macrophage non-canonical pyroptosis, which influences the phenotypic transformation and apoptosis of HASMCs. The mtROS-Dynamin-Related Protein 1 (Drp1) axis is likely to regulate the GSDMB-mediated non-canonical pyroptosis.</p></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"759 ","pages":"Article 110102"},"PeriodicalIF":3.8,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141726723","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
Dynamics of small molecule-enzyme interactions: Novel benzenesulfonamides as multi-target agents endowed with inhibitory effects against some metabolic enzymes 小分子与酶相互作用的动力学:新型苯磺酰胺类药物作为多靶点药物对某些代谢酶具有抑制作用。
IF 3.8 3区 生物学
Archives of biochemistry and biophysics Pub Date : 2024-07-14 DOI: 10.1016/j.abb.2024.110099
Özcan Güleç , Cüneyt Türkeş , Mustafa Arslan , Mesut Işık , Yeliz Demir , Hatice Esra Duran , Muhammet Fırat , Ömer İrfan Küfrevioğlu , Şükrü Beydemir
{"title":"Dynamics of small molecule-enzyme interactions: Novel benzenesulfonamides as multi-target agents endowed with inhibitory effects against some metabolic enzymes","authors":"Özcan Güleç ,&nbsp;Cüneyt Türkeş ,&nbsp;Mustafa Arslan ,&nbsp;Mesut Işık ,&nbsp;Yeliz Demir ,&nbsp;Hatice Esra Duran ,&nbsp;Muhammet Fırat ,&nbsp;Ömer İrfan Küfrevioğlu ,&nbsp;Şükrü Beydemir","doi":"10.1016/j.abb.2024.110099","DOIUrl":"10.1016/j.abb.2024.110099","url":null,"abstract":"<div><p>In contemporary medicinal chemistry, employing a singular small molecule to concurrently multi-target disparate molecular entities is emerging as a potent strategy in the ongoing battle against metabolic disease. In this study, we present the meticulous design, synthesis, and comprehensive biological evaluation of a novel series of 1,2,3-triazolylmethylthio-1,3,4-oxadiazolylbenzenesulfonamide derivatives (<strong>8a-m</strong>) as potential multi-target inhibitors against human carbonic anhydrase (EC.4.2.1.1, <em>h</em>CA I/II), α-glycosidase (EC.3.2.1.20, α-GLY), and α-amylase (EC.3.2.1.1, α-AMY). Each synthesized sulfonamide underwent rigorous assessment for inhibitory effects against four distinct enzymes, revealing varying degrees of <em>h</em>CA I/II, a-GLY, and a-AMY inhibition across the tested compounds. <em>h</em>CA I was notably susceptible to inhibition by all compounds, demonstrating remarkably low inhibition constants (<em>K</em><sub>I</sub>) ranging from 42.20 ± 3.90 nM to 217.90 ± 11.81 nM compared to the reference standard AAZ (<em>K</em><sub>I</sub> of 439.17 ± 9.30 nM). The evaluation against <em>h</em>CA II showed that most of the synthesized compounds exhibited potent inhibition effects with <em>K</em><sub>I</sub> values spanning the nanomolar range 16.44 ± 1.53–70.82 ± 4.51 nM, while three specific compounds, namely <strong>8a-b</strong> and <strong>8d</strong>, showcased lower inhibitory potency than other derivatives that did not exceed that of the reference drug AAZ (with a <em>K</em><sub>I</sub> of 98.28 ± 1.69 nM). Moreover, across the spectrum of synthesized compounds, potent inhibition profiles were observed against diabetes mellitus-associated α-GLY (<em>K</em><sub>I</sub> values spanning from 0.54 ± 0.06 μM to 5.48 ± 0.50 μM), while significant inhibition effects were noted against α-AMY, with <em>IC</em><sub>50</sub> values ranging between 0.16 ± 0.04 μM and 7.81 ± 0.51 μM) compared to reference standard ACR (<em>K</em><sub>I</sub> of 23.53 ± 2.72 μM and <em>IC</em><sub>50</sub> of 48.17 ± 2.34 μM, respectively). Subsequently, these inhibitors were evaluated for their DPPH· and ABTS<sup>+</sup>· radical scavenging activity. Moreover, molecular docking investigations were meticulously conducted within the active sites of <em>h</em>CA I/II, α-GLY, and α-AMY to provide comprehensive elucidation and rationale for the observed inhibitory outcomes.</p></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"759 ","pages":"Article 110099"},"PeriodicalIF":3.8,"publicationDate":"2024-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141619175","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
Retraction notice to “Inhibiting microRNA-424 in bone marrow mesenchymal stem cells-derived exosomes suppresses tumor growth in colorectal cancer by upregulating TGFBR3” [Archiv. Biochem. Biophys. 709 (2021) 108965] 骨髓间充质干细胞衍生的外泌体中的microRNA-424通过上调TGFBR3抑制结直肠癌的肿瘤生长》的撤稿通知[Archiv.
IF 3.8 3区 生物学
Archives of biochemistry and biophysics Pub Date : 2024-07-14 DOI: 10.1016/j.abb.2024.110089
Ning Zhang , Ling Li , Jun Luo , Jiahua Tan , Wanfu Hu , Zihui Li , Xinxin Wang , Tao Ye
{"title":"Retraction notice to “Inhibiting microRNA-424 in bone marrow mesenchymal stem cells-derived exosomes suppresses tumor growth in colorectal cancer by upregulating TGFBR3” [Archiv. Biochem. Biophys. 709 (2021) 108965]","authors":"Ning Zhang ,&nbsp;Ling Li ,&nbsp;Jun Luo ,&nbsp;Jiahua Tan ,&nbsp;Wanfu Hu ,&nbsp;Zihui Li ,&nbsp;Xinxin Wang ,&nbsp;Tao Ye","doi":"10.1016/j.abb.2024.110089","DOIUrl":"10.1016/j.abb.2024.110089","url":null,"abstract":"","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"759 ","pages":"Article 110089"},"PeriodicalIF":3.8,"publicationDate":"2024-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S000398612400211X/pdfft?md5=350fba5ffca8302ef7bb6d07f75b8ae5&pid=1-s2.0-S000398612400211X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141603167","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
Naked mole-rat TMEM2 lacks physiological hyaluronan-degrading activity 裸鼠 TMEM2 缺乏生理性透明质酸降解活性。
IF 3.8 3区 生物学
Archives of biochemistry and biophysics Pub Date : 2024-07-14 DOI: 10.1016/j.abb.2024.110098
Shinya Sato , Yukiko Mizutani , Minori Abe , Shinji Fukuda , Shigeki Higashiyama , Shintaro Inoue
{"title":"Naked mole-rat TMEM2 lacks physiological hyaluronan-degrading activity","authors":"Shinya Sato ,&nbsp;Yukiko Mizutani ,&nbsp;Minori Abe ,&nbsp;Shinji Fukuda ,&nbsp;Shigeki Higashiyama ,&nbsp;Shintaro Inoue","doi":"10.1016/j.abb.2024.110098","DOIUrl":"10.1016/j.abb.2024.110098","url":null,"abstract":"<div><p>Mouse transmembrane protein 2 (mTMEM2) has been identified as a hyaluronidase, which has extracellularly G8 and GG domains and PbH1 repeats; however, our previously study showed that human TMEM2 (hTMEM2) is not a catalytic hyaluronidase due to the absence of the critical amino acid residues (His248/Ala303) in the GG domain. Naked mole-rats (NMRs) accumulate abundant high-molecular weight hyaluronan (HA) in their tissues, suggesting decreased HA degradation. Therefore, we aimed to evaluate the HA-degrading activity of NMR TMEM2 (nmrTMEM2) and compare it with those of mTMEM2 and hTMEM2. The amino acid residues of nmrTMEM2 (Asn247/Val302) are similar to Asn248/Phe303 of hTMEM2, and nmrTMEM2-expressing HEK293T cells showed negligible activity. We confirmed the significance of these amino acid residues using an inactive chimeric TMEM2 with the human GG domain, which acquired catalytic activity when Asn248/Phe303 was substituted with His248/Ala303. Semi-quantitative comparison of the activities of the membrane-fractions derived from m/h/nmrTMEM2-expressing HEK293T cells revealed that at least 20- and 14-fold higher amounts of nmr/hTMEM2 were required to degrade HA to the same extent as by mTMEM2. Thus, unlike mTMEM2, nmrTMEM2 is not a physiological hyaluronidase. The inability of nmrTMEM2 to degrade HA might partially account for the high-molecular-weight HA accumulation in NMR tissues.</p></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"759 ","pages":"Article 110098"},"PeriodicalIF":3.8,"publicationDate":"2024-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0003986124002200/pdfft?md5=e5ecc6f8498bf45c2059976ca7d3a048&pid=1-s2.0-S0003986124002200-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141619185","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
Corrigendum to “Building on a theme: The redox hierarchy of pyridine nucleotide-disulfide oxidoreductases” [Arch. Biochem. Biophys. 755 (2024) 109966] 以主题为基础:吡啶核苷酸-二硫氧化还原酶的氧化还原层次"[Arch. Biochem:吡啶核苷酸-二硫氧化还原酶的氧化还原层次" [Arch.
IF 3.8 3区 生物学
Archives of biochemistry and biophysics Pub Date : 2024-07-12 DOI: 10.1016/j.abb.2024.110081
{"title":"Corrigendum to “Building on a theme: The redox hierarchy of pyridine nucleotide-disulfide oxidoreductases” [Arch. Biochem. Biophys. 755 (2024) 109966]","authors":"","doi":"10.1016/j.abb.2024.110081","DOIUrl":"10.1016/j.abb.2024.110081","url":null,"abstract":"","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"759 ","pages":"Article 110081"},"PeriodicalIF":3.8,"publicationDate":"2024-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0003986124002029/pdfft?md5=f0bc610e4b0fd249ad0add9ba561c32c&pid=1-s2.0-S0003986124002029-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141598328","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
Modulation of aryl hydrocarbon receptor activity by tyrosine kinase inhibitors (ponatinib and tofacitinib) 酪氨酸激酶抑制剂(泊纳替尼和托法替尼)对芳香烃受体活性的调节作用
IF 3.8 3区 生物学
Archives of biochemistry and biophysics Pub Date : 2024-07-09 DOI: 10.1016/j.abb.2024.110088
Farag E.S. Mosa , Mohammed A. Alqahtani , Mahmoud A. El-Ghiaty, Sara R. El-Mahrouk, Khaled Barakat, Ayman O.S. El-Kadi
{"title":"Modulation of aryl hydrocarbon receptor activity by tyrosine kinase inhibitors (ponatinib and tofacitinib)","authors":"Farag E.S. Mosa ,&nbsp;Mohammed A. Alqahtani ,&nbsp;Mahmoud A. El-Ghiaty,&nbsp;Sara R. El-Mahrouk,&nbsp;Khaled Barakat,&nbsp;Ayman O.S. El-Kadi","doi":"10.1016/j.abb.2024.110088","DOIUrl":"10.1016/j.abb.2024.110088","url":null,"abstract":"<div><p>Ponatinib and tofacitinib, established kinase inhibitors and FDA-approved for chronic myeloid leukemia and rheumatoid arthritis, are recently undergoing investigation in diverse clinical trials for potential repurposing. The aryl hydrocarbon receptor (AhR), a transcription factor influencing a spectrum of physiological and pathophysiological activities, stands as a therapeutic target for numerous diseases. This study employs molecular modelling tools and in vitro assays to identify ponatinib and tofacitinib as AhR ligands, elucidating their binding and molecular interactions in the AhR PAS-B domain. Molecular docking analyses revealed that ponatinib and tofacitinib occupy the central pocket within the primary cavity, similar to AhR agonists 2,3,7,8-tetrachlorodibenzodioxin (TCDD) and (benzo[a]pyrene) B[a]P. Our simulations also showed that these compounds exhibit good stability, stabilizing many hot spots within the PAS-B domain, including the Dα-Eα loop, which serves as a regulatory element for the binding pocket. Binding energy calculations highlighted ponatinib's superior predicted affinity, revealing F295 as a crucial residue in maintaining strong interaction with the two compounds. Our in vitro data suggest that ponatinib functions as an AhR antagonist, blocking the downstream signaling of AhR pathway induced by TCDD and B[a]P. Additionally, both tofacitinib and ponatinib cause impairment in AhR-regulated CYP1A1 enzyme activity induced by potent AhR agonists. This study unveils ponatinib and tofacitinib as potential modulators of AhR, providing valuable insights into their therapeutic roles in AhR-associated diseases and enhancing our understanding of the intricate relationship between kinase inhibitors and AhR.</p></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"759 ","pages":"Article 110088"},"PeriodicalIF":3.8,"publicationDate":"2024-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0003986124002108/pdfft?md5=5d42136d5373c5943398de4f49988939&pid=1-s2.0-S0003986124002108-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141589510","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
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信