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Regulatory function of glycolysis-related lncRNAs in tumor progression: Mechanism, facts, and perspectives 糖酵解相关 lncRNA 在肿瘤进展中的调控功能:机制、事实和前景。
IF 5.3 2区 医学 Q1 PHARMACOLOGY & PHARMACY Pub Date : 2024-08-31 DOI: 10.1016/j.bcp.2024.116511
Xinyi Peng , Shuhao Li , Anqi Zeng , Linjiang Song

Altered metabolism is a hallmark of cancer, and reprogramming of energy metabolism, known as the “Warburg effect”, has long been associated with cancer. Cancer cells use the process of glycolysis to quickly manufacture energy from glucose, pyruvic acid, and lactate, which in turn accelerates the growth of cancer and glycolysis becomes a key target for anti-cancer therapies. Recent groundbreaking discoveries regarding long noncoding RNAs (lncRNAs) have opened a new chapter in the mechanism of cancer occurrence. It is widely recognized that lncRNAs regulate energy metabolism through glycolysis in cancer cells. LncRNAs have been demonstrated to engage in several cancer processes such as proliferation, apoptosis, migration, invasion, and chemoresistance, whereas glycolysis is enhanced or inhibited by the dysregulation of lncRNAs. As a result, cancer survival and development are influenced by different signaling pathways. In this review, we summarize the roles of lncRNAs in a variety of cancers and describe the mechanisms underlying their role in glycolysis. Additionally, the predictive potential of glycolysis and lncRNAs in cancer therapy is discussed.

新陈代谢的改变是癌症的标志之一,而能量代谢的重编程(即 "沃伯格效应")与癌症的关系由来已久。癌细胞利用糖酵解过程迅速从葡萄糖、丙酮酸和乳酸中制造能量,这反过来又加速了癌症的生长,糖酵解也成为抗癌疗法的一个关键靶点。最近关于长非编码 RNA(lncRNA)的突破性发现为癌症发生机制揭开了新的篇章。人们普遍认为,lncRNA 通过糖酵解调节癌细胞的能量代谢。研究表明,LncRNAs 参与了多种癌症过程,如增殖、凋亡、迁移、侵袭和化疗抵抗,而糖酵解则会因 lncRNAs 的失调而增强或抑制。因此,癌症的生存和发展受到不同信号通路的影响。在这篇综述中,我们总结了 lncRNA 在多种癌症中的作用,并描述了它们在糖酵解中的作用机制。此外,我们还讨论了糖酵解和 lncRNA 在癌症治疗中的预测潜力。
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引用次数: 0
Exploring the glycation association with dyslipidaemia: Novel approach for diabetic nephropathy 探索糖化与血脂异常的关联:治疗糖尿病肾病的新方法。
IF 5.3 2区 医学 Q1 PHARMACOLOGY & PHARMACY Pub Date : 2024-08-30 DOI: 10.1016/j.bcp.2024.116513
Ashwini D. Jagdale , Mukul M. Angal , Rahul S. Patil , Rashmi S. Tupe

The transcription factor known as sterol regulatory element-binding protein (SREBP) and the glycation pathways, specifically the formation of Advanced Glycation End Products (AGEs), have a significant and deleterious impact on the kidney. They alter renal lipid metabolism and promote glomerulosclerosis, mesangial cell expansion, tubulointerstitial fibrosis, and inflammation, leading to diabetic nephropathy (DN) progression. Although several pieces of scientific evidence are reported for potential causes of glycation and lipotoxicity in DN, the underlying mechanism of renal lipid accumulation still needs to be fully understood. We provide a rationalized view on how AGEs exert multiple effects that cause SREBP activation and inflammation, contributing to DN through Receptor for AGEs (RAGE) signaling, AGE-R1-dependent downregulation of Sirtuin 1 (SIRT-1), and increased SREBP Cleavage Activating Protein (SCAP) glycosylation. This review emphasizes the association between glycation and the SREBP pathway and how it affects the onset of DN associated with obesity. Finally, we discuss the correlation of glycation and the SREBP pathway with insulin resistance (IR), oxidative stress, endoplasmic reticulum stress, inflammation, and existing and emerging therapeutic approaches toward better controlling obesity-related DN.

转录因子固醇调节元件结合蛋白(SREBP)和糖化途径,特别是高级糖化终产物(AGEs)的形成,对肾脏有重大的有害影响。它们会改变肾脏脂质代谢,促进肾小球硬化、肾间质细胞扩张、肾小管间质纤维化和炎症,从而导致糖尿病肾病(DN)恶化。尽管有多种科学证据表明 DN 中糖化和脂毒性的潜在原因,但肾脏脂质蓄积的内在机制仍有待全面了解。我们对 AGEs 如何通过 AGEs 受体(RAGE)信号传导、AGE-R1 依赖性下调 Sirtuin 1(SIRT-1)和增加 SREBP 裂解激活蛋白(SCAP)糖基化等多重作用引起 SREBP 激活和炎症,从而导致 DN 的发生提供了合理的观点。本综述强调了糖化与 SREBP 通路之间的关联,以及糖化如何影响与肥胖相关的 DN 的发生。最后,我们将讨论糖化和 SREBP 通路与胰岛素抵抗 (IR)、氧化应激、内质网应激、炎症的相关性,以及现有和新兴的治疗方法,以更好地控制与肥胖相关的 DN。
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引用次数: 0
Ketamine – An Imperfect Wonder Drug? 氯胺酮--一种不完美的神奇药物?
IF 5.3 2区 医学 Q1 PHARMACOLOGY & PHARMACY Pub Date : 2024-08-30 DOI: 10.1016/j.bcp.2024.116516
Tanner Magruder , Marielle Isenhart , Maximillian V. Striepe , Andrew Mannisto , Karry M. Jannie , Jolene Smith , Kenneth E. McCarson , Daniel T. Christian , Vanja Duric

Ketamine is a potent sedative and dissociative anesthetic agent that has been used clinically for over 50 years since it was first developed in the 1960 s as an alternative to phencyclidine (PCP). When compared to PCP, ketamine exhibited a much lower incidence of severe side effects, including hallucinations, leading to its increased popularity in clinical practice. Ketamine was initially used as an anesthetic agent, especially in emergency medicine and in surgical procedures where rapid induction and recovery was necessary. However, over the last few decades, ketamine was found to have additional clinically useful properties making it effective in the treatment of a variety of other conditions. Presently, ketamine has a wide range of clinical uses beyond anesthesia including management of acute and chronic pain, as well as treatment of psychiatric disorders such as major depression. In addition to various clinical uses, ketamine is also recognized as a common drug of abuse sought for its hallucinogenic and sedative effects. This review focuses on exploring the different clinical and non-clinical uses of ketamine and its overall impact on patient care.

氯胺酮是一种强效镇静和解离麻醉剂,自 20 世纪 60 年代作为苯环利定(五氯苯酚)的替代品被首次开发以来,已在临床上使用了 50 多年。与五氯苯酚相比,氯胺酮出现幻觉等严重副作用的几率要低得多,因此在临床上越来越受欢迎。氯胺酮最初被用作麻醉剂,尤其是在急诊和需要快速诱导和恢复的外科手术中。然而,在过去的几十年里,氯胺酮被发现具有更多临床有用的特性,使其在治疗其他各种疾病时也很有效。目前,氯胺酮在麻醉之外还有广泛的临床用途,包括治疗急性和慢性疼痛,以及治疗重度抑郁症等精神疾病。除了各种临床用途外,氯胺酮还因其致幻和镇静作用而被视为一种常见的滥用药物。本综述重点探讨氯胺酮的不同临床和非临床用途及其对病人护理的总体影响。
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引用次数: 0
An introduction to the special issue “Sam Enna legacy of excellence” 萨姆-恩纳的卓越遗产 "特刊导言。
IF 5.3 2区 医学 Q1 PHARMACOLOGY & PHARMACY Pub Date : 2024-08-30 DOI: 10.1016/j.bcp.2024.116510
Jacques Piette, Lynn LeCount
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引用次数: 0
The LAMB3-EGFR signaling pathway mediates synergistic Anti-Cancer effects of berberine and emodin in Pancreatic cancer LAMB3-EGFR信号通路介导小檗碱和大黄素对胰腺癌的协同抗癌作用
IF 5.3 2区 医学 Q1 PHARMACOLOGY & PHARMACY Pub Date : 2024-08-28 DOI: 10.1016/j.bcp.2024.116509
Caiming Xu , Silvia Pascual-Sabater , Cristina Fillat , Ajay Goel

Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy, primarily due to the intrinsic development of chemoresistance. The most apparent histopathological feature associated with chemoresistance is the alterations in extracellular matrix (ECM) proteins. Natural dietary botanicals such as berberine (BBR) and emodin (EMO) have been shown to possess chemo-preventive potential by regulating ECM in various cancers. Herein, we further investigated the potential synergistic effects of BBR and EMO in enhancing anticancer efficacy by targeting ECM proteins in pancreatic cancer. Genomewide transcriptomic profiling identified that LAMB3 was significantly upregulated in PDAC tissue and highly associated with poor overall survival (OS, hazard ratio [HR], 2.99, 95 % confidence interval [CI], 1.46–6.15; p = 0.003) and progress-free survival (PFS, HR, 2.59; 95 % CI, 1.30–5.18; p = 0.007) in PDAC. A systematic series of functional experiments in BxPC-3 and MIA-PaCa-2 cells revealed that the combination of BBR and EMO exhibited synergistic anti-tumor potential, as demonstrated by cell proliferation, clonogenicity, migration, and invasion assays (p < 0.05–0.001). The combination also altered the expression of key proteins involved in apoptosis, EMT, and EGFR/ERK1,2/AKT signaling. These findings were further supported by patient-derived organoids (PDOs), where the combined treatment resulted in fewer and smaller organoids compared to each compound individually (p < 0.05–0.001). Our results suggest that BBR combined with EMO exerts synergistic anti-cancer effects by modulating the EGFR-signaling pathway through interference with LAMB3 in PDAC.

胰腺导管腺癌(PDAC)是一种致命的恶性肿瘤,其主要原因是内在的化疗耐药性。与化疗耐药性相关的最明显的组织病理学特征是细胞外基质(ECM)蛋白的改变。小檗碱(BBR)和大黄素(EMO)等天然植物膳食已被证明可通过调节各种癌症的 ECM 发挥化疗预防潜力。在此,我们进一步研究了小檗碱和大黄素在通过靶向胰腺癌 ECM 蛋白增强抗癌效果方面的潜在协同作用。全基因组转录组分析发现,LAMB3 在 PDAC 组织中显著上调,并与 PDAC 的总生存期(OS,危险比 [HR],2.99,95 % 置信区间 [CI],1.46-6.15;p = 0.003)和无进展生存期(PFS,HR,2.59;95 % CI,1.30-5.18;p = 0.007)不良高度相关。在 BxPC-3 和 MIA-PaCa-2 细胞中进行的一系列系统功能实验表明,BBR 和 EMO 的组合具有协同抗肿瘤潜力,细胞增殖、克隆生成、迁移和侵袭试验均证明了这一点(p=0.003)。
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引用次数: 0
Functional characterisation and modification of a novel Kunitzin peptide for use as an anti-trypsin antimicrobial peptide against drug-resistant Escherichia coli 新型 Kunitzin 肽的功能表征和修饰,以用作抗胰蛋白酶的抗菌肽,对抗耐药大肠杆菌。
IF 5.3 2区 医学 Q1 PHARMACOLOGY & PHARMACY Pub Date : 2024-08-24 DOI: 10.1016/j.bcp.2024.116508
Zhizhong Wang , Wenjing Ding , Daning Shi , Xiaoling Chen , Chengbang Ma , Yangyang Jiang , Tao Wang , Tianbao Chen , Chris Shaw , Lei Wang , Mei Zhou

In recent decades, antimicrobial peptides (AMPs) have emerged as highly promising candidates for the next generation of antibiotic agents, garnering significant attention. Although their potent antimicrobial activities and ability to combat drug resistance make them stand out among alternative agents, their poor stability has presented a great challenge for further development. In this work, we report a novel Kunitzin AMP, Kunitzin-OL, from the frog Odorrana lividia, exhibiting dual antimicrobial and anti-trypsin activities. Through functional screening and comparison with previously reported Kunitzin peptides, we serendipitously discovered a unique motif (−KVKF-) and unveiled its crucial role in the antibacterial functions of Kunitzin-OL by modifying it through motif removal and duplication. Among the designed derivatives, peptides 4 and 8 demonstrated remarkable antimicrobial activities and low cytotoxicity, with high therapeutic index (TI) values (TI4 = 20.8, TI8 = 20.8). Furthermore, they showed potent antibacterial efficacy against drug-resistant Escherichia coli strains and exhibited lipopolysaccharide (LPS)-neutralising activity, effectively alleviating LPS-induced inflammatory responses. Overall, our findings provide a new short motif for designing effective AMP drugs and highlight the potential of the Kunitztin trypsin inhibitory loop as a valuable motif for the design of AMPs with enhancing proteolytic stability.

近几十年来,抗菌肽(AMPs)已成为下一代抗生素制剂中极具潜力的候选药物,备受关注。虽然 AMPs 强大的抗菌活性和对抗耐药性的能力使其在众多替代药物中脱颖而出,但其较差的稳定性给进一步开发带来了巨大挑战。在这项研究中,我们报道了一种新型的昆氮蛋白 AMP--昆氮蛋白-OL,它来自于青蛙 Odorrana lividia,具有抗菌和抗胰蛋白酶的双重活性。通过功能筛选以及与之前报道的 Kunitzin 肽的比较,我们偶然发现了一个独特的基团(-KVKF-),并通过基团的去除和复制对其进行修饰,揭示了它在 Kunitzin-OL 的抗菌功能中的关键作用。在所设计的衍生物中,肽 4 和肽 8 具有显著的抗菌活性和较低的细胞毒性,治疗指数(TI)值较高(TI4 = 20.8,TI8 = 20.8)。此外,它们还对耐药大肠杆菌菌株显示出强大的抗菌功效,并具有中和脂多糖(LPS)的活性,能有效缓解 LPS 引起的炎症反应。总之,我们的研究结果为设计有效的 AMP 药物提供了一个新的短基团,并突出了 Kunitztin 胰蛋白酶抑制环作为设计具有增强蛋白水解稳定性的 AMP 的重要基团的潜力。
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引用次数: 0
Therapeutic potential of relaxin or relaxin mimetics in managing cardiovascular complications of diabetes 松弛素或松弛素模拟物在控制糖尿病心血管并发症方面的治疗潜力。
IF 5.3 2区 医学 Q1 PHARMACOLOGY & PHARMACY Pub Date : 2024-08-23 DOI: 10.1016/j.bcp.2024.116507
Arun George Devasia , Meyammai Shanmugham , Adaikalavan Ramasamy , Sophie Bellanger , Laura J. Parry , Chen Huei Leo

Diabetes mellitus is a metabolic disease with an escalating global prevalence. Despite the abundance and relative efficacies of current therapeutic approaches, they primarily focus on attaining the intended glycaemic targets, but patients ultimately still suffer from various diabetes-associated complications such as retinopathy, nephropathy, cardiomyopathy, and atherosclerosis. There is a need to explore innovative and effective diabetic treatment strategies that not only address the condition itself but also combat its complications. One promising option is the reproductive hormone relaxin, an endogenous ligand of the RXFP1 receptor. Relaxin is known to exert beneficial actions on the cardiovascular system through its vasoprotective, anti-inflammatory and anti-fibrotic effects. Nevertheless, the native relaxin peptide exhibits a short biological half-life, limiting its therapeutic potential. Recently, several relaxin mimetics and innovative delivery technologies have been developed to extend its biological half-life and efficacy. The current review provides a comprehensive landscape of the cardiovascular effects of relaxin, focusing on its potential therapeutic applications in managing complications associated with diabetes. The latest advancements in the development of relaxin mimetics and delivery methods for the treatment of cardiometabolic disorders are also discussed.

糖尿病是一种代谢性疾病,在全球的发病率不断攀升。尽管目前的治疗方法很多,而且相对有效,但这些方法主要侧重于实现预期的血糖目标,但患者最终仍会患上各种糖尿病相关并发症,如视网膜病变、肾病、心肌病和动脉粥样硬化。因此,有必要探索创新而有效的糖尿病治疗策略,不仅要解决糖尿病本身的问题,还要防治其并发症。其中一个很有前景的选择是生殖激素松弛素,它是 RXFP1 受体的内源性配体。众所周知,松弛素具有保护血管、抗炎和抗纤维化的作用,对心血管系统有益。然而,原生松弛素肽的生物半衰期较短,限制了其治疗潜力。最近,为了延长弛缓素肽的生物半衰期和疗效,人们开发出了多种弛缓素模拟物和创新给药技术。本综述全面介绍了弛缓素对心血管的影响,重点关注其在控制糖尿病相关并发症方面的潜在治疗应用。此外,还讨论了用于治疗心血管代谢疾病的弛缓素模拟物和给药方法的最新进展。
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引用次数: 0
Dietary sodium modulates mTORC1-dependent trained immunity in macrophages to accelerate CKD development 饮食中的钠会调节巨噬细胞中依赖于 mTORC1 的训练有素的免疫力,从而加速慢性肾脏病的发展
IF 5.3 2区 医学 Q1 PHARMACOLOGY & PHARMACY Pub Date : 2024-08-23 DOI: 10.1016/j.bcp.2024.116505
Huihui Chen , Jie Song , Li Zeng , Jie Zha , Jiefu Zhu , Anqun Chen , Yu Liu , Zheng Dong , Guochun Chen

Chronic Kidney Disease (CKD) is a significant global health issue linked to dietary habits, especially high salt intake. However, the precise mechanisms driving this progression remain incompletely understood. This study reveals that a high-salt diet intensifies macrophage trained immunity, leading to a marked pro-inflammatory response upon repeated pathogenic exposures, as evidenced by increased renal damage and fibrosis. Under high-salt conditions, there was an induction of CD45+F4/80+ macrophage infiltration into the renal tissue, accompanied by heightened production of inflammatory cytokines. Distinct responses were observed between circulating and resident renal macrophages to a high-salt diet, with a notable upsurge in the migration of pro-inflammatory macrophages, driven by CCL2-CCR2 signaling and aberrant mTORC1 pathway activation. Treatment with rapamycin-liposome effectively reduced this inflammatory cascade by mitigating mTORC1 signaling. Transplantation of monocytes from CKD mice with a high-salt diet significantly exacerbates renal inflammatory damage in the host mice, showing increased migratory tendency and inflammatory activity. The cell co-culture experiment further confirmed that macrophages derived from CKD mice, particularly those under conditions of high salt exposure, significantly induced apoptosis and inflammatory responses in renal tubular cells. Taken together, recurrent exposure to LPS elicits the activation of trained immunity, consequently augmenting inflammatory response of monocytes/macrophages in the involved kidneys. The high-salt diet exacerbates this phenomenon, attributable at least in part to the overactivation of the mTORC1 pathway. This research emphasizes the importance of dietary modulation and targeted immunological interventions in slowing CKD progression, providing new insights into mTORC1-mediated pathophysiological mechanisms and potential management strategies for CKD.

慢性肾脏病(CKD)是与饮食习惯,尤其是高盐摄入量有关的全球重大健康问题。然而,人们对这一疾病进展的确切机制仍不甚了解。这项研究揭示了高盐饮食会增强巨噬细胞训练有素的免疫力,从而在反复接触致病因素时导致明显的促炎反应,肾脏损伤和纤维化的加剧就是证明。在高盐条件下,诱导 CD45+F4/80+ 巨噬细胞浸润肾组织,并伴随着炎症细胞因子分泌的增加。在 CCL2-CCR2 信号和异常 mTORC1 通路激活的驱动下,促炎巨噬细胞的迁移显著增加。使用雷帕霉素脂质体治疗可通过减轻 mTORC1 信号传导有效减少这种炎症级联反应。移植高盐饮食的 CKD 小鼠的单核细胞会明显加重宿主小鼠的肾脏炎症损伤,表现出更强的迁移倾向和炎症活性。细胞共培养实验进一步证实,来自 CKD 小鼠的巨噬细胞,尤其是在高盐暴露条件下的巨噬细胞,能明显诱导肾小管细胞的凋亡和炎症反应。综上所述,反复暴露于 LPS 会激活训练有素的免疫系统,从而增强受累肾脏中单核细胞/巨噬细胞的炎症反应。高盐饮食加剧了这一现象,这至少部分归因于 mTORC1 通路的过度激活。这项研究强调了饮食调节和有针对性的免疫学干预在延缓慢性肾脏病进展方面的重要性,为 mTORC1 介导的病理生理机制和潜在的慢性肾脏病管理策略提供了新的见解。
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引用次数: 0
Chronic post-ischemic pain (CPIP) a model of complex regional pain syndrome (CRPS-I): Role of oxidative stress and inflammation 复杂区域性疼痛综合征(CRPS-I)的慢性缺血后疼痛(CPIP)模型:氧化应激和炎症的作用
IF 5.3 2区 医学 Q1 PHARMACOLOGY & PHARMACY Pub Date : 2024-08-23 DOI: 10.1016/j.bcp.2024.116506
Julia Maria Frare , Patrícia Rodrigues , Náthaly Andrighetto Ruviaro , Gabriela Trevisan

Complex regional pain syndrome (CRPS) presents as a persistent and distressing pain condition often stemming from limb trauma or ischemia, manifesting as either CRPS-I (without initial nerve injury) or CRPS-II (accompanied by nerve injury). Despite its prevalence and significant impact on functionality and emotional well-being, standard treatments for CRPS remain elusive. The multifaceted nature of CRPS complicates the identification of its underlying mechanisms. In efforts to elucidate these mechanisms, researchers have turned to animal models such as chronic post-ischemic pain (CPIP), which mirrors the symptoms of CRPS-I. Various mechanisms have been proposed to underlie the acute and chronic pain experienced in CRPS-I, including oxidative stress and inflammation. Traditional treatment approaches often involve antidepressants, non-steroidal anti-inflammatory drugs (NSAIDs), and opioids. However, these methods frequently fall short of providing adequate relief. Accordingly, there is a growing interest in exploring alternative treatments, such as antioxidant supplementation, anti-inflammatory agents, and non-pharmacological interventions. Future research directions should focus on optimizing treatment strategies and addressing remaining gaps in knowledge to improve patient outcomes. This review aims to delve into the pathophysiological mechanisms implicated in the CPIP model, specifically focusing on oxidative stress and inflammation, with the ultimate goal of proposing innovative therapeutic strategies for alleviating the symptoms of CRPS-I.

复杂性区域疼痛综合征(CRPS)是一种持续性、令人痛苦的疼痛症状,通常源于肢体创伤或缺血,表现为 CRPS-I(最初无神经损伤)或 CRPS-II(伴有神经损伤)。尽管 CRPS 的发病率很高,而且对患者的功能和情绪有很大影响,但标准的 CRPS 治疗方法仍然难以捉摸。CRPS 的多面性使其潜在机制的确定变得复杂。在努力阐明这些机制的过程中,研究人员转向了动物模型,如慢性缺血后疼痛(CPIP),它反映了 CRPS-I 的症状。研究人员提出了多种机制,包括氧化应激和炎症,来解释 CRPS-I 所经历的急性和慢性疼痛。传统的治疗方法通常包括抗抑郁药、非甾体抗炎药(NSAIDs)和阿片类药物。然而,这些方法往往无法提供充分的缓解。因此,人们对探索替代疗法的兴趣日益浓厚,如补充抗氧化剂、消炎药和非药物干预。未来的研究方向应侧重于优化治疗策略和解决知识上的不足,以改善患者的治疗效果。本综述旨在深入探讨 CPIP 模型所涉及的病理生理机制,特别关注氧化应激和炎症,最终目的是提出创新的治疗策略,缓解 CRPS-I 的症状。
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引用次数: 0
Corrigendum to “Tankyrase1/2 inhibitor XAV-939 reverts EMT and suggests that PARylation partially regulates aerobic activities in human hepatocytes and HepG2 cells” [Biochem. Pharmacol. 227 (2024) 116445] Tankyrase1/2 抑制剂 XAV-939 可逆转 EMT 并表明 PARylation 部分调节人肝细胞和 HepG2 细胞的有氧活动》[《生物化学。 药理学》227 (2024) 116445]更正
IF 5.3 2区 医学 Q1 PHARMACOLOGY & PHARMACY Pub Date : 2024-08-22 DOI: 10.1016/j.bcp.2024.116497
Kristof De Vos , Adamantios Mavrogiannis , Justina Clarinda Wolters , Susan Schlenner , Keimpe Wierda , Álvaro Cortés Calabuig , Reena Chinnaraj , Vera Dermesrobian , Yeghig Armoudjian , Maarten Jacquemyn , Nikky Corthout , Dirk Daelemans , Pieter Annaert
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引用次数: 0
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Biochemical pharmacology
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