Chemico-biological interactions最新文献

Integrative Structural and Kinetic Analysis of the Molecular Basis for Reduced Carbamate Inhibition in Atypical Butyrylcholinesterase. 氨基甲酸酯对非典型丁基胆碱酯酶抑制降低的分子基础的综合结构和动力学分析。

IF 5.4

Chemico-biological interactions Pub Date : 2026-05-05 DOI: 10.1016/j.cbi.2026.112134

Ana Matošević, Nikola Maraković, Danijela Barić, Alexandre Igert, Xavier Brazzolotto, Zrinka Kovarik, Anita Bosak

{"title":"Integrative Structural and Kinetic Analysis of the Molecular Basis for Reduced Carbamate Inhibition in Atypical Butyrylcholinesterase.","authors":"Ana Matošević, Nikola Maraković, Danijela Barić, Alexandre Igert, Xavier Brazzolotto, Zrinka Kovarik, Anita Bosak","doi":"10.1016/j.cbi.2026.112134","DOIUrl":"https://doi.org/10.1016/j.cbi.2026.112134","url":null,"abstract":"Butyrylcholinesterase (BChE) plays a key role in cholinergic transmission and the metabolism of various drugs, making its regulation a promising therapeutic strategy for several diseases, including Alzheimer's disease. Selective inhibition of BChE helps regulate brain acetylcholine levels. However, genetic polymorphisms in the BCHE gene, particularly the Asp70Gly mutation in atypical BChE, can impact treatment outcomes. This study compares the inhibitory potency of 13 carbamates against atypical and usual BChE. Using molecular docking, quantum chemical cluster calculations, and crystallization of wild-type BChE with the most potent carbamate, we identified key differences in carbamylation mechanisms. Atypical BChE shows a less favorable enzyme-inhibitor complex orientation, lacking the hydrogen bond stabilization of the reactive carbonyl oxygen. Additionally, Asp70 in usual BChE contributes to stabilizing the non-reactive carbamate group, whereas Gly70 in atypical BChE is too distant to form such interactions.","PeriodicalId":93932,"journal":{"name":"Chemico-biological interactions","volume":" ","pages":"112134"},"PeriodicalIF":5.4,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147847537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The protective effects of selenium on mitochondrial quality under exogenous and endogenous stressors. 外源和内源应激条件下硒对线粒体质量的保护作用。

IF 5.4

Chemico-biological interactions Pub Date : 2026-05-05 DOI: 10.1016/j.cbi.2026.112136

Anatoly V Skalny, Michael Aschner, Abel Santamaria, Fernando Barbosa, Joao B T Rocha, Feng Zhang, Xiong Guo, Tatiana V Korobeinikova, Alexey A Tinkov

{"title":"The protective effects of selenium on mitochondrial quality under exogenous and endogenous stressors.","authors":"Anatoly V Skalny, Michael Aschner, Abel Santamaria, Fernando Barbosa, Joao B T Rocha, Feng Zhang, Xiong Guo, Tatiana V Korobeinikova, Alexey A Tinkov","doi":"10.1016/j.cbi.2026.112136","DOIUrl":"https://doi.org/10.1016/j.cbi.2026.112136","url":null,"abstract":"Selenium (Se) and selenoproteins play a significant role in preventing mitochondrial damage. Se regulates mitochondrial dynamics, biogenesis, and mitophagy, but the mechanisms by which it controls mitochondrial quality remain to be fully characterized. Thus, the objective of this review is to address the underlying mechanisms of Se in regulation of mitochondrial quality control upon exposure to endogenous and exogenous stressors. Contemporary data show that Se deficiency is associated with a shift from mitochondrial fusion to fission, inhibition of mitochondrial biogenesis via down-regulation of sirtuin 1 (SIRT1)/peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α)/nuclear respiratory factor 1 and 2 (NRF1/2)/mitochondrial transcription factor A (TFAM) signaling, and alterations in PTEN-induced kinase 1 (PINK1)/Parkin-mediated mitophagy in vitro and in vivo. The role of Se in regulating mitochondrial quality control is mediated by specific selenoproteins, as evidenced from experimental selenoprotein knockout and overexpression models. Correspondingly, treatment with various forms of Se attenuates inhibitory effect of endogenous stressors (oxidative stress, ischemia, etc.), as well as exogenous agents like heavy metals, ammonia, fluoride, mycotoxins, and paraquat, on mitochondrial fusion/fission balance and biogenesis. Administration of Se mitigates the adverse effects of these stressors on mitophagy by recovering impaired mitophagy or by inhibiting mitophagy overactivation. Therefore, Se treatment might be considered a therapeutic approach to mitigate the adverse effects of various stressors on mitochondrial quality control and functioning, leading to prevention of liver, kidney, brain, and intestinal damage. However, the specific mechanisms, as well as dose-response and species-specific effects have yet to be investigated.","PeriodicalId":93932,"journal":{"name":"Chemico-biological interactions","volume":" ","pages":"112136"},"PeriodicalIF":5.4,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147847482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","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 (-)-Loliode isolated from Sargassum horneri against particulate matter-induced skin damage via inhibiting pro-inflammatory cytokines and matrix metalloproteinases expression. 马尾藻(-)- looliode通过抑制促炎细胞因子和基质金属蛋白酶表达对颗粒性皮肤损伤的保护作用

IF 5.4

Chemico-biological interactions Pub Date : 2026-05-04 DOI: 10.1016/j.cbi.2026.112122

Muhammad Faizan, Jun-Geon Je, Jimin Hyun, Kaiqiang Wang, Bomi Ryu, Lei Wang

{"title":"Protective effect of (-)-Loliode isolated from Sargassum horneri against particulate matter-induced skin damage via inhibiting pro-inflammatory cytokines and matrix metalloproteinases expression.","authors":"Muhammad Faizan, Jun-Geon Je, Jimin Hyun, Kaiqiang Wang, Bomi Ryu, Lei Wang","doi":"10.1016/j.cbi.2026.112122","DOIUrl":"https://doi.org/10.1016/j.cbi.2026.112122","url":null,"abstract":"Particulate matter (PM) is a pervasive carcinogen that can exacerbates skin inflammation, oxidative damage with extracellular matrix (ECM) degradation, thereby compromising skin barrier integrity and promoting premature aging. In this study, the protective potential and mechanistic basis of (-)-Loliode separated from Sargassum horneri, used for PM-induced skin injury is investigated. In vitro models demonstrated that PM exposure (400 μg/mL) markedly increased intracellular reactive oxygen species (ROS) by approximately 2 fold, elevated pro-inflammatory cytokines (IL-1β by 176%, TNF-α by 139%, and IL-6 by 366%), up-regulated matrix metalloproteinases (MMP-1 by 310%, MMP-2 by 201%, MMP-8 by 287%, MMP-9 by 176%, and MMP-13 by 139%), and suppressed collagen synthesis to 55% of control levels. Pre-treatment with (-)-Loliode (up to 25 μg/mL) significantly and concentration-dependently attenuated ROS accumulation (reduced to 174% of control), restored collagen content (to 90% of control), and inhibited PM-induced MMP overactivation (reducing MMP-1 to 194%, MMP-8 to 135%, and MMP-9 to 125%) without inducing cytotoxicity (cell viability restored from 66% to 82% in HDFs). Moreover, (-)-Loliode effectively suppressed the secretion of inflammatory cytokines (reducing IL-1β by 29%, TNF-α by 17%, and IL-6 by 41%), indicating robust anti-inflammatory activity. Molecular docking analyses shown favorable binding affinities of (-)-Loliode toward major inflammatory targets, including NF-κB (-6.2 kcal/mol) and COX-2 (-7.2 kcal/mol), suggesting a multi-target mode of action. Collectively, these results demonstrate that (-)-Loliode provides broad protection against PM-induced skin damage by mitigating oxidative stress, inflammation, and ECM degradation, identifying it as a promising seaweed-derived bioactive compound for therapeutic and cosmeceutical applications.","PeriodicalId":93932,"journal":{"name":"Chemico-biological interactions","volume":" ","pages":"112122"},"PeriodicalIF":5.4,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147847509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Discovery of a new function of human butyrylcholinesterase and the catalytic activity of its natural variants toward homocysteine thiolactone hydrolysis. 人丁基胆碱酯酶新功能的发现及其天然变体对同型半胱氨酸硫内酯水解的催化活性。

IF 5.4

Chemico-biological interactions Pub Date : 2025-10-22 Epub Date: 2025-07-29 DOI: 10.1016/j.cbi.2025.111683

Xiabin Chen, Xiaoxuan Li, Huan Liu, Jianzhuang Yao, Yishuang Li, Hualing Li, Zelin Wu, Yun Zhang, Tingjun Hou, Jiye Wang, Shurong Hou

{"title":"Discovery of a new function of human butyrylcholinesterase and the catalytic activity of its natural variants toward homocysteine thiolactone hydrolysis.","authors":"Xiabin Chen, Xiaoxuan Li, Huan Liu, Jianzhuang Yao, Yishuang Li, Hualing Li, Zelin Wu, Yun Zhang, Tingjun Hou, Jiye Wang, Shurong Hou","doi":"10.1016/j.cbi.2025.111683","DOIUrl":"10.1016/j.cbi.2025.111683","url":null,"abstract":"Abnormal activity level of human butyrylcholinesterase (BChE) was detected in patients with cardiovascular disease and neurodegenerative disorders, however, the specific role of BChE in the pathology of these diseases are not known yet. Homocysteine thiolactone (HTL) is a toxic thioester metabolite of homocysteine in conditions of hyperhomocysteinemia (HHcy). Experimental evidences suggest that HTL and resultant N-Hcy proteins that disrupt normal protein function, are associated with the pathology of HHcy-related complications such as cardiovascular diseases. Given the abundance of BChE in the blood and its esterase capacity, it is worthy to investigate the hydrolytic ability of BChE and its genetic polymorphism effects towards the endogenous toxic HTL in order to delineate its function in the complex disease network. In this study, human BChE and acetylcholinesterase were examined for their ability in HTL hydrolysis, and BChE demonstrates higher catalytic efficiency than reported serum paraoxonase 1. Furthermore, the catalytic mechanism uncovered by Quantum mechanics/Molecular mechanics molecular dynamics method helps to understand and substantiate the function of BChE in HTL metabolism. Six frequent BChE nonsynonymous coding single nucleotide polymorphisms (SNPs) variants were recombinantly produced and their catalytic activity was assessed. Differential catalytic efficiency toward HTL was observed among these variants, suggesting their distinct metabolic capability in vivo. These findings highlight the potential protection role of BChE against HTL-induced toxicity, and pave a way for future investigation into BChE's contribution in HTL metabolism and the possible correlation between specific BChE SNPs and susceptibility for developing HTL-associated diseases.","PeriodicalId":93932,"journal":{"name":"Chemico-biological interactions","volume":" ","pages":"111683"},"PeriodicalIF":5.4,"publicationDate":"2025-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144762677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cigarette smoke-induced glycerophospholipid DLPC promotes macrophage ferroptosis through the USP7/GPX4 regulatory axis in chronic obstructive pulmonary disease. 香烟烟雾诱导的甘油磷脂DLPC通过USP7/GPX4调节轴促进慢性阻塞性肺疾病的巨噬细胞铁凋亡。

IF 5.4

Chemico-biological interactions Pub Date : 2025-10-22 Epub Date: 2025-08-05 DOI: 10.1016/j.cbi.2025.111697

Weibin Ruan, Zhimin Peng, Mingsi Huang, Hui Zhang, Xiaohua Li, Tingting Ma, Jiehua Deng, Mianluan Pan, Ziqing Mai, Xia Meng, Jianquan Zhang

{"title":"Cigarette smoke-induced glycerophospholipid DLPC promotes macrophage ferroptosis through the USP7/GPX4 regulatory axis in chronic obstructive pulmonary disease.","authors":"Weibin Ruan, Zhimin Peng, Mingsi Huang, Hui Zhang, Xiaohua Li, Tingting Ma, Jiehua Deng, Mianluan Pan, Ziqing Mai, Xia Meng, Jianquan Zhang","doi":"10.1016/j.cbi.2025.111697","DOIUrl":"10.1016/j.cbi.2025.111697","url":null,"abstract":"Chronic obstructive pulmonary disease (COPD), a smoking-associated chronic inflammatory disorder, involves macrophage-mediated inflammation and cell death, yet the mechanisms linking cigarette smoke (CS) to macrophage ferroptosis remain unclear. Through integrated transcriptomic and metabolomic analyses of CS-exposed macrophages, we identified activation of the ferroptosis pathway accompanied by dysregulated glycerophospholipid metabolism. Notably, phosphatidylcholine species enriched in polyunsaturated fatty acids (PUFA-PC), particularly 1,2-dilinoleoyl-sn-glycero-3-phosphocholine (DLPC), were markedly elevated. Functional studies revealed that DLPC exacerbated lipid peroxidation and triggered ferroptosis in macrophages. Mechanistically, DLPC downregulated the deubiquitinase ubiquitin-specific peptidase 7 (USP7), which normally stabilizes glutathione peroxidase 4 (GPX4) through TRAF/CAT domain-mediated binding and deubiquitination activity. This suppression accelerated GPX4 ubiquitination and subsequent proteasomal degradation. Furthermore, CS upregulated glycerol-3-phosphate acyltransferase 3 (GPAT3), whose genetic ablation diminished PUFA-PC (including DLPC) synthesis, attenuated lipid reactive oxygen species (ROS) accumulation, and inhibited ferroptosis in CS-stimulated macrophages. In vivo, adeno-associated virus-mediated GPAT3 knockdown in murine lung tissues mitigated ROS production, ferroptosis, and emphysema in an experimental emphysema murine model. Collectively, our findings delineate a CS-GPAT3-DLPC axis that drives macrophage ferroptosis via USP7/GPX4 dysregulation, offering novel mechanistic insights into COPD pathogenesis and identifying DLPC and GPAT3 as potential therapeutic targets.","PeriodicalId":93932,"journal":{"name":"Chemico-biological interactions","volume":" ","pages":"111697"},"PeriodicalIF":5.4,"publicationDate":"2025-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144796334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The effects of Co-exposure of tobacco smoke with Dibenzo[a,l]pyrene diol epoxide on molecular targets and immune cells in the mouse oral cavity. 烟草烟雾与二苯并[a， 1]芘二醇环氧化物共暴露对小鼠口腔分子靶点和免疫细胞的影响

IF 5.4

Chemico-biological interactions Pub Date : 2025-10-22 Epub Date: 2025-08-05 DOI: 10.1016/j.cbi.2025.111694

Todd D Schell, Zachary T Bitzer, Kun-Ming Chen, Cesar Aliaga, Yuan-Wan Sun, Dhimant Desai, Matthew Lanza, Jiafen Hu, Neil Christensen, Karam El-Bayoumy

{"title":"The effects of Co-exposure of tobacco smoke with Dibenzo[a,l]pyrene diol epoxide on molecular targets and immune cells in the mouse oral cavity.","authors":"Todd D Schell, Zachary T Bitzer, Kun-Ming Chen, Cesar Aliaga, Yuan-Wan Sun, Dhimant Desai, Matthew Lanza, Jiafen Hu, Neil Christensen, Karam El-Bayoumy","doi":"10.1016/j.cbi.2025.111694","DOIUrl":"10.1016/j.cbi.2025.111694","url":null,"abstract":"Tobacco smoking (TS) is an established etiological factor in the development of head and neck squamous cell carcinoma (HNSCC). We previously developed a mouse model using a select tobacco carcinogen, dibenzo[a,l]pyrene (DB[a,l]P, and its ultimate carcinogenic metabolite diol-epoxide (DB[a,l]PDE) to induce oral squamous cell carcinoma (OSCC) in mice; the molecular characteristics and histological changes observed in the mouse oral cavity mimic those found in human HNSCC. In the present study, using our mouse model, we examined for the first time the co-carcinogenic effects of TS with DB[a,l]PDE on DNA damage, histology, molecular targets, and immune cell regulation. We observed a non-significant increase of the levels of DB[a,l]PDE-DNA adduct in the oral cavity of mice exposed to TS as compared to those exposed to compressed air. Histologically, we observed significant increases in epithelial hyperplasia and epithelial single cell necrosis in TS treated mice. TS significantly enhanced protein expression of NF-κB and Ki67 while the enhancement of COX-2 did not reach significance but p53 expression was significantly decreased. We analyzed immune cell regulation in both spleen and tongue (target organ). No significant changes were observed in the spleen; however, in the tongue, we observed a significantly reduced frequency of CD3+T cells that included reductions of both CD4 and CD8 T cells and a corresponding increase was observed for multiple myeloid cell populations. While preliminary, our results offer the foundation for future research using this mouse model to explore the impact of co-carcinogens/tumor promotors other than TS on critical factors involved in the development of HNSCC.","PeriodicalId":93932,"journal":{"name":"Chemico-biological interactions","volume":" ","pages":"111694"},"PeriodicalIF":5.4,"publicationDate":"2025-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12392687/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144777259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Copper exposure induces inflammation and PANoptosis through the TLR4/NF-κB signaling pathway, leading to testicular damage and impaired spermatogenesis in Wilson disease. 铜暴露会通过 TLR4/NF-κB 信号通路诱发炎症和 PAN 细胞凋亡，导致威尔逊氏病患者的睾丸损伤和精子发生障碍。

Chemico-biological interactions Pub Date : 2024-06-01 Epub Date: 2024-05-17 DOI: 10.1016/j.cbi.2024.111060

Dan Zhao, Limin Wu, Xinru Fang, Luyao Wang, Qianzhuo Liu, Pengyu Jiang, Zhihui Ji, Nian Zhang, Miaozhu Yin, Hui Han

{"title":"Copper exposure induces inflammation and PANoptosis through the TLR4/NF-κB signaling pathway, leading to testicular damage and impaired spermatogenesis in Wilson disease.","authors":"Dan Zhao, Limin Wu, Xinru Fang, Luyao Wang, Qianzhuo Liu, Pengyu Jiang, Zhihui Ji, Nian Zhang, Miaozhu Yin, Hui Han","doi":"10.1016/j.cbi.2024.111060","DOIUrl":"10.1016/j.cbi.2024.111060","url":null,"abstract":"Copper is a toxic heavy metal that causes various damage when it accumulates in the body beyond the physiological threshold. Wilson disease (WD) is an inherited disorder characterized by impaired copper metabolism. Reproductive damage in male patients with WD is gradually attracting attention. However, the underlying mechanisms of copper toxicity are unclear. In this study, we investigated the role of inflammation and PANoptosis in testicular damage and impaired spermatogenesis caused by copper deposition using the WD model toxic milk (TX) mice. Copper chelator-penicillamine and toll-like receptor 4 (TLR4) inhibitor-eritoran were used to intervene in TX mice in our animal experiment methods. Testis samples were collected from mice for further analysis. The results showed that the morphology and ultrastructure of the testis and epididymis in TX mice were damaged, and the sperm counts decreased significantly. The TLR4/nuclear factor kappa-B (NF-κB) signaling pathway was activated by copper deposition, which led to the upregulation of serum and testicular inflammatory factors in TX mice. Meanwhile, pyroptosis, apoptosis, and necroptosis were significant in the testis of TX mice. Both chelated copper or inhibited TLR4 expression markedly suppressed the TLR4/NF-κB signaling pathway, thereby reducing the expression of inflammatory factors. PANoptosis in the testis of TX mice was also reversed. Our study indicated that pathological copper exposure induces inflammation and PANoptosis through the TLR4/NF-κB signaling pathway, leading to toxic testicular damage and impaired spermatogenesis in WD.","PeriodicalId":93932,"journal":{"name":"Chemico-biological interactions","volume":" ","pages":"111060"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140961149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Elucidating the Molecular Mechanisms of Pterostilbene Against Cervical Cancer Through an Integrated Bioinformatics and Network Pharmacology Approach 通过综合生物信息学和网络药理学方法阐明紫檀芪抗宫颈癌的分子机制

Chemico-biological interactions Pub Date : 2024-05-01 DOI: 10.1016/j.cbi.2024.111058

Xiang Li, Dequan Yu, Qiming Wang, Yating Chen, Hanbing Jiang

引用次数: 0

Assessment of anti-hyperglycemic and anti-hyperlipidemic effects of thiazolidine-2,4-dione derivatives in HFD-STZ diabetic animal model 评估噻唑烷-2,4-二酮衍生物在 HFD-STZ 糖尿病动物模型中的降血糖和降血脂作用

Chemico-biological interactions Pub Date : 2024-02-01 DOI: 10.1016/j.cbi.2024.110902

S. Fettach, Fatima Zahra Thari, Khalid Karrouchi, Laila Benbacer, Learn-Han Lee, Abdelhakim Bouyahya, Y. Cherrah, Hassan Sefrioui, Khalid Bougrin, M. El Abbes Faouzi

引用次数: 0

Loss of VRK1 alters the nuclear phosphoproteome in the DNA damage response to doxorubicin VRK1缺失会改变DNA损伤对多柔比星反应的核磷酸蛋白组

Chemico-biological interactions Pub Date : 2024-02-01 DOI: 10.1016/j.cbi.2024.110908

Elena Navarro-Carrasco, Aurora Campos-Díaz, Eva Monte-Serrano, F. Rolfs, Richard de Goeij-de Haas, T. Pham, S. Piersma, Connie R. Jimenez, Pedro A. Lazo

引用次数: 0