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Exploring Chemical Space to Identify Partial Binders Against hMPV Nucleocapsid Protein 探索化学空间以确定 hMPV 核苷酸蛋白的部分结合剂
IF 4 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-17 DOI: 10.1002/jcb.30618
Monika Verma, Nikita S. Panchal, Pramod Kumar Yadav
Human metapneumovirus (hMPV) has gained prominence in recent times as the predominant etiological agent of acute respiratory tract infections. This virus targets children, the elderly, and individuals with compromised immune systems. Given the protracted duration of hMPV transmission, it is probable that the majority of children will have acquired the virus by the age of 5. In individuals with compromised immune systems, recurrence of hMPV infection is possible. As hMPV matures, it remains latent from the time of acquisition. The genome of hMPV encompasses a pivotal protein referred to as the nucleocapsid protein (N). This protein assumes the form of a left‐handed helical nucleocapsid, enveloping the viral RNA genome. The primary function of this structure is to protect nucleases, rendering it a potentially promising target for therapeutic advancements. The present study employs a methodology that involves structure‐based virtual screening, followed by molecular dynamics simulation at a 250‐ns time scale, to identify potential natural molecules or their derivatives from the ZINC Database. These molecules are investigated for their binding properties against the hMPV nucleoprotein. Based on an evaluation of the docking score, binding site interaction, and molecular dynamics studies, it has been found that two naturally occurring molecules, namely M1 (ZINC85629735) and M3 (ZINC85569125), have shown notable docking scores of −9.6 and −10.7 kcal/mol, acceptable RMSD, RMSF, Rg, and so on calculated from molecular dynamics trajectory associated with MMGBSA binding energy of −81.94 and −99.63 kcal/mol, respectively. These molecules have shown the highest binding affinity toward nucleocapsid protein and demonstrated promising attributes as potential binders against hMPV.
近来,人类偏肺病毒(hMPV)作为急性呼吸道感染的主要病原体日益突出。这种病毒主要针对儿童、老人和免疫系统受损的人群。由于 hMPV 的传播时间较长,大多数儿童可能在 5 岁前就感染了病毒。免疫系统受损的人有可能再次感染 hMPV。随着 hMPV 的成熟,它从感染时起就一直处于潜伏状态。hMPV 的基因组包含一种关键蛋白,即核壳蛋白(N)。这种蛋白呈左旋螺旋状核壳,包裹着病毒 RNA 基因组。这种结构的主要功能是保护核酸酶,使其成为一个潜在的治疗目标。本研究采用了一种方法,包括基于结构的虚拟筛选,然后以 250-ns 的时间尺度进行分子动力学模拟,从 ZINC 数据库中识别潜在的天然分子或其衍生物。研究了这些分子与 hMPV 核蛋白的结合特性。根据对对接得分、结合位点相互作用和分子动力学研究的评估,发现两个天然分子,即 M1(ZINC85629735)和 M3(ZINC85569125),显示了显著的对接得分,分别为 -9.6 和 -10.7 kcal/mol,从与 MMGBSA 结合能相关的分子动力学轨迹计算出的可接受 RMSD、RMSF、Rg 等分别为 -81.94 和 -99.63 kcal/mol。这些分子与核壳蛋白的结合亲和力最高,有望成为抗 hMPV 的潜在结合剂。
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引用次数: 0
Cover Image, Volume 125, Number 9, September 2024 封面图片,第 125 卷第 9 期,2024 年 9 月
IF 3 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-17 DOI: 10.1002/jcb.30663
Magdalena M. Bolsinger, Alice Drobny, Sibylle Wilfling, Stephanie Reischl, Florian Krach, Raul Moritz, Denise Balta, Ute Hehr, Elisabeth Sock, Florian Bleibaum, Frank Hanses, Beate Winner, Susy Prieto Huarcaya, Philipp Arnold, Friederike Zunke

Cover Caption: The cover image is based on the article SARS-CoV-2 Spike Protein Induces Time-Dependent CTSL Upregulation in HeLa Cells and Alveolarspheres by Magdalena M. Bolsinger et al., https://doi.org/10.1002/jcb.30627.

封面标题:封面图片来自 Magdalena M. Bolsinger 等人撰写的文章《SARS-CoV-2 Spike Protein Induces Time-Dependent CTSL Upregulation in HeLa Cells and Alveolarspheres》(SARS-CoV-2 Spike Protein Induces Time-Dependent CTSL Upregulation in HeLa Cells and Alveolarspheres),https://doi.org/10.1002/jcb.30627。
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引用次数: 0
RETRACTION: Identification of Nrf2/STAT3 Axis in Induction of Apoptosis Through Sub-G1 Cell Cycle Arrest Mechanism in HT-29 Colon Cancer Cells 回归:识别 Nrf2/STAT3 轴在 HT-29 结肠癌细胞中通过亚 G1 细胞周期停滞机制诱导凋亡的作用
IF 3 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-12 DOI: 10.1002/jcb.30647

RETRACTION: I. Tajmohammadi, J. Mohammadian, M. Sabzichi, S. Mahmuodi, M. Ramezani, M. Aghajani, and F. Ramezani, “Identification of Nrf2/STAT3 Axis in Induction of Apoptosis Through Sub-G1 Cell Cycle Arrest Mechanism in HT-29 Colon Cancer Cells,” Journal of Cellular Biochemistry 120, no. 8 (2019): 14035–14043, https://doi.org/10.1002/jcb.28678.

The above article, published online on 16 April 2019 in Wiley Online Library (wileyonlinelibrary.com) has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals, LLC. The retraction has been agreed due to concerns raised by a third party on the data presented in the article. Specifically, some image elements in Figure 4, where found to have been published elsewhere in a different scientific context. The authors did not provide a satisfactory explanation to address the concerns. For these reasons, the editors have lost trust in the accuracy and integrity of the full body of data presented in the article and consider its conclusions invalid.

All authors have been informed of the decision of retraction. The corresponding author Fatemeh Ramezani, first author Issa Tajmohammadi, and Coauthor Mehdi Sabzichi disagree with the decision of retraction. Coauthor Marjan Aghajani has stated that she did not directly participate in the experiments conducted for the study, and that her role was limited to manuscript editing and language polishing; she neither agreed nor disagreed with the decision of retraction. No confirmation was obtained by the remaining co-authors.

撤回:I. Tajmohammadi, J. Mohammadian, M. Sabzichi, S. Mahmuodi, M. Ramezani, M. Aghajani, and F. Ramezani, "Identification of Nrf2/STAT3 Axis in Induction of Apoptosis Through Sub-G1 Cell Cycle Arrest Mechanism in HT-29 Coloner Cancer Cells," Journal of Cellular Biochemistry 120, no:14035-14043, https://doi.org/10.1002/jcb.28678.The 上述文章于 2019 年 4 月 16 日在线发表于 Wiley Online Library (wileyonlinelibrary.com),经期刊主编 Christian Behl 和 Wiley Periodicals, LLC 协议,已被撤回。同意撤稿的原因是第三方对文章中提供的数据提出了疑虑。特别是图 4 中的一些图像元素被发现已在不同的科学背景下发表在其他地方。作者没有提供令人满意的解释来解决这些问题。由于这些原因,编辑们对文章中提供的全部数据的准确性和完整性失去了信任,并认为其结论无效。通讯作者 Fatemeh Ramezani、第一作者 Issa Tajmohammadi 和共同作者 Mehdi Sabzichi 不同意撤稿决定。共同作者 Marjan Aghajani 表示,她没有直接参与为该研究进行的实验,她的作用仅限于手稿编辑和语言润色;她既不同意也不反对撤稿决定。其余合著者也未予以证实。
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引用次数: 0
Correction to “The Oncolytic Virus H101 Combined with Gnaq Sirna-Mediated Knockdown Reduces Uveal Melanoma Cell Viability” 对 "溶瘤病毒 H101 与 Gnaq Sirna 基因敲除相结合可降低葡萄膜黑色素瘤细胞活力 "的更正。
IF 3 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-06 DOI: 10.1002/jcb.30648

Li Y, He J, Qiu C, et al. The oncolytic virus H101 combined with GNAQ siRNA-mediated knockdown reduces uveal melanoma cell viability. J Cell Biochem. 2019;120:5766-5776. https://doi.org/10.1002/jcb.27863.

In the original version of this article, the authors mistakenly duplicated panels in Figure 2A showing the morphological changes of OMM2.3 cells treated with “H101” and “H101+siNC,” as well as in Figure 3A, showing the flow cytometric analysis of OMM2.3 cells in the “NC” and “siGNAQ” groups. In the corrected Figures 2A and 3A below, the authors have replaced the duplicated “H101+siNC” and “siGNAQ” panels with the correct ones, respectively. Additionally, in the correct Figure 3 below, the axis labels have been corrected from “PMT4 Log” to “PI” (Propidium Iodide) and from “PMT2 Log” to “Annexin V-FITC”.

The legend for Figure 3 is corrected as per below (changes in bold):

Figure 3. Apoptosis was modulated by cotreatment with H101 and siGNAQ. A, Apoptosis of the OMM2.3, 92.1, and OCM1 cell lines was detected with an annexin-V kit and a flow-cytometric analysis. B, At 48 h after transfection, the proportion of early apoptotic cells (Annexin V+ PI-) was calculated. When H101 was combined with siGNAQ, the apoptosis of UM cells was enhanced relative to that induced by H101 alone. The results are presented as the means and standard error of the mean; *P < 0.05. UM, uveal melanoma.

Additionally, there is a typographical error in the sequence of the reverse primer for GADPH amplification. The correct sequence is “CAAAGTTGTCATGGATGACC”.

Finally, the author omitted to mention that the bands for GNAQ and β-actin in Figure 5A are referenced from Figure 1C.

The authors apologize for these mistakes and for any inconvenience these may have caused.

Li Y, He J, Qiu C, et al.溶瘤病毒H101结合GNAQ siRNA介导的基因敲除降低了葡萄膜黑色素瘤细胞的存活率。J Cell Biochem.2019;120:5766-5776。 https://doi.org/10.1002/jcb.27863.In 在本文的原始版本中,作者错误地重复了图2A中显示经 "H101 "和 "H101+siNC "处理的OMM2.3细胞形态变化的面板,以及图3A中显示 "NC "和 "siGNAQ "组OMM2.3细胞流式细胞分析的面板。在更正后的图 2A 和图 3A 中,作者分别用正确的面板替换了重复的 "H101+siNC "和 "siGNAQ "面板。此外,在下面正确的图 3 中,坐标轴标签已从 "PMT4 Log "更正为 "PI"(碘化丙啶),从 "PMT2 Log "更正为 "Annexin V-FITC"。H101 和 siGNAQ 共处理调节细胞凋亡。A、用附件素-V试剂盒和流式细胞仪检测 OMM2.3、92.1 和 OCM1 细胞系的细胞凋亡。B、转染 48 小时后,计算早期凋亡细胞(Annexin V+ PI-)的比例。当 H101 与 siGNAQ 联用时,UM 细胞的凋亡相对于 H101 单独诱导的凋亡更强。结果以平均值和平均值的标准误表示;*P < 0.05。UM,葡萄膜黑色素瘤。此外,用于 GADPH 扩增的反向引物序列存在印刷错误。最后,作者没有提到图 5A 中 GNAQ 和 β-actin 的条带是从图 1C 中引用的。作者对这些错误和可能造成的不便表示歉意。
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引用次数: 0
Synthesis of Pyrazolo[3,4-b]pyridine Derivatives and Their In-Vitro and In-Silico Antidiabetic Activities 吡唑并[3,4-b]吡啶衍生物的合成及其体外和体内抗糖尿病活性。
IF 3 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-06 DOI: 10.1002/jcb.30646
Iqra Rafique, Tahir Maqbool, Muhammad Salman Javed

In the current study, new pyrazolo[3,4-b]pyridine esters, hydrazides, and Schiff bases have been synthesized starting from 3-methyl-1-phenyl-1H-pyrazol-5-amine. The first step involved solvent-free synthesis of pyrazolo[3,4-b]pyridine-6-carboxylate derivatives (2ad) with 55%–70% yield in the minimum time frame compared with the conventional refluxing method, which was followed by the synthesis of corresponding hydrazides (3a–d) and hydrazones (4a–e). The structures of the synthesized derivatives were confirmed using element analysis, FT-IR, 1H NMR, 13C NMR, and LC-MS techniques. Synthesized hydrazides (3a–d) and hydrazones (4a–e) were also tested for their in-vitro antidiabetic activity and found that all the compounds exhibited significant antidiabetic activity, while 3c (IC50 = 9.6 ± 0.5 μM) among the hydrazides and 4c (IC50 = 13.9 ± 0.7 μM) among the hydrazones were found to be more active in comparison to other synthesized derivatives. These in-vitro results were further validated via docking studies against the α-amylase enzyme using the reference drug acarbose (200.1 ± 10.0 μM). The results were greatly in agreement with their in-vitro studies and these derivatives can be encouraging candidates for further in-vivo studies in mice models.

本研究以 3-甲基-1-苯基-1H-吡唑-5-胺为起点,合成了新的吡唑并[3,4-b]吡啶酯、酰肼和希夫碱。第一步是无溶剂合成吡唑并[3,4-b]吡啶-6-羧酸酯衍生物(2a-d),与传统的回流法相比,在最短的时间内获得了 55%-70% 的产率,随后合成了相应的酰肼(3a-d)和酰肼酮(4a-e)。利用元素分析、傅立叶变换红外光谱、1H NMR、13C NMR 和 LC-MS 技术确认了合成衍生物的结构。还对合成的酰肼(3a-d)和酰肼(4a-e)进行了体外抗糖尿病活性测试,结果发现所有化合物都具有显著的抗糖尿病活性,而与其他合成衍生物相比,酰肼中的 3c(IC50 = 9.6 ± 0.5 μM)和酰肼中的 4c(IC50 = 13.9 ± 0.7 μM)活性更高。这些体外研究结果通过使用参考药物阿卡波糖(200.1 ± 10.0 μM)与α-淀粉酶的对接研究得到了进一步验证。研究结果与体外研究结果十分吻合,这些衍生物有望在小鼠模型中进行进一步的体内研究。
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引用次数: 0
RETRACTION: Cryptotanshinone Inhibits RANKL-induced Osteoclastogenesis by Regulating ERK and NF-κB Signaling Pathways 回归:隐丹参酮通过调节ERK和NF-κB信号通路抑制RANKL诱导的破骨细胞生成
IF 3 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-30 DOI: 10.1002/jcb.30636

RETRACTION: W. Wang, M. Huang, Y. Hui, P. Yuan, X. Guo, and K. Wang, “Cryptotanshinone Inhibits RANKL-induced Osteoclastogenesis by Regulating ERK and NF-κB Signaling Pathways,” Journal of Cellular Biochemistry 120, no. 5 (2019): 7333-7340, https://doi.org/10.1002/jcb.28008.

The above article, published online on 2 December 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Specifically, several image elements in Figure 1 C were found to have been sourced from a previously published article by a different author group and inappropriately edited. Finally, inappropriate post-acquisition splicing has been detected in the Western Blot experiment depicted in Figure 5 A. The article has been retracted as the editors have lost trust in the overall accuracy of the presented data, and consider the conclusions to be invalid. The authors agree with the decision of retraction and apologize for any inconvenience caused.

退稿:W. Wang, M. Huang, Y. Hui, P. Yuan, X. Guo, and K. Wang, "Cryptotanshinone Inhibits RANKL-induced Osteoclastogenesis by Regulating ERK and NF-κB Signaling Pathways," Journal of Cellular Biochemistry 120, no.5 (2019): 7333-7340, https://doi.org/10.1002/jcb.28008.The 上述文章于 2018 年 12 月 2 日在线发表于 Wiley Online Library (wileyonlinelibrary.com),经作者、期刊主编 Christian Behl 和 Wiley Periodicals LLC 协议,已被撤回。之所以同意撤稿,是因为第三方对文章中的数据提出了质疑。具体来说,图 1 C 中的几个图像元素被发现来自另一作者小组之前发表的一篇文章,并经过了不恰当的编辑。最后,在图 5 A 中描述的 Western Blot 实验中发现了不恰当的采集后拼接。由于编辑对所提供数据的整体准确性失去了信任,并认为结论无效,文章已被撤回。作者同意撤稿决定,并对造成的不便表示歉意。
{"title":"RETRACTION: Cryptotanshinone Inhibits RANKL-induced Osteoclastogenesis by Regulating ERK and NF-κB Signaling Pathways","authors":"","doi":"10.1002/jcb.30636","DOIUrl":"10.1002/jcb.30636","url":null,"abstract":"<p><b>RETRACTION:</b> W. Wang, M. Huang, Y. Hui, P. Yuan, X. Guo, and K. Wang, “Cryptotanshinone Inhibits RANKL-induced Osteoclastogenesis by Regulating ERK and NF-κB Signaling Pathways,” <i>Journal of Cellular Biochemistry</i> 120, no. 5 (2019): 7333-7340, https://doi.org/10.1002/jcb.28008.</p><p>The above article, published online on 2 December 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Specifically, several image elements in Figure 1 C were found to have been sourced from a previously published article by a different author group and inappropriately edited. Finally, inappropriate post-acquisition splicing has been detected in the Western Blot experiment depicted in Figure 5 A. The article has been retracted as the editors have lost trust in the overall accuracy of the presented data, and consider the conclusions to be invalid. The authors agree with the decision of retraction and apologize for any inconvenience caused.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 10","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30636","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142107818","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
RETRACTION: Posttreatment of Melatonin With CCl4 Better Reduces Fibrogenic and Oxidative Changes in Liver Than Melatonin Co-treatment 回放:褪黑素与四氯化碳联合治疗比褪黑素联合治疗更能减轻肝脏的纤维化和氧化变化。
IF 3 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-27 DOI: 10.1002/jcb.30635

RETRACTION: K. Mortezaee, J. Majidpoor, E. Daneshi, M. Abouzaripour, and M. Abdi, “Posttreatment of Melatonin With CCl4 Better Reduces Fibrogenic and Oxidative Changes in Liver Than Melatonin Co-treatment,” Journal of Cellular Biochemistry 119, no. 2 (2018): 1716-1725, https://doi.org/10.1002/jcb.26331.

The above article, published online on 7 August 2017 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed upon due to concerns about the accuracy of the data presented in the article. The authors informed the journal of significant errors in the compilation of Figure 2. Subsequent investigation by the publisher revealed that several image elements in Figure 2 had been previously published by the same author group to illustrate different staining and/or treatment. The authors acknowledged that these mistakes may have resulted from problems in data management while performing similar experiments for different research projects. Therefore, due to the concerns on data accuracy, the editors consider the conclusions of this article to be invalid.

撤回:K. Mortezaee, J. Majidpoor, E. Daneshi, M. Abouzaripour, and M. Abdi, "Posttreatment of Melatonin With CCl4 Better Reduces Fibrogenic and Oxidative Changes in Liver Than Melatonin Co-treatment," Journal of Cellular Biochemistry 119, no:1716-1725, https://doi.org/10.1002/jcb.26331.The 上述文章于2017年8月7日在线发表于Wiley Online Library (wileyonlinelibrary.com),经期刊主编Christian Behl和Wiley Periodicals LLC协议,已被撤回。同意撤稿的原因是对文章中数据准确性的担忧。作者告知期刊,图 2 的编制存在重大错误。出版商随后的调查显示,图 2 中的几个图像元素曾由同一作者小组发表过,用来说明不同的染色和/或处理方法。作者承认,这些错误可能是在不同研究项目中进行类似实验时数据管理出现问题所致。因此,出于对数据准确性的考虑,编辑认为这篇文章的结论无效。
{"title":"RETRACTION: Posttreatment of Melatonin With CCl4 Better Reduces Fibrogenic and Oxidative Changes in Liver Than Melatonin Co-treatment","authors":"","doi":"10.1002/jcb.30635","DOIUrl":"10.1002/jcb.30635","url":null,"abstract":"<p><b>RETRACTION:</b> K. Mortezaee, J. Majidpoor, E. Daneshi, M. Abouzaripour, and M. Abdi, “Posttreatment of Melatonin With CCl4 Better Reduces Fibrogenic and Oxidative Changes in Liver Than Melatonin Co-treatment,” <i>Journal of Cellular Biochemistry</i> 119, no. 2 (2018): 1716-1725, https://doi.org/10.1002/jcb.26331.</p><p>The above article, published online on 7 August 2017 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed upon due to concerns about the accuracy of the data presented in the article. The authors informed the journal of significant errors in the compilation of Figure 2. Subsequent investigation by the publisher revealed that several image elements in Figure 2 had been previously published by the same author group to illustrate different staining and/or treatment. The authors acknowledged that these mistakes may have resulted from problems in data management while performing similar experiments for different research projects. Therefore, due to the concerns on data accuracy, the editors consider the conclusions of this article to be invalid.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 10","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30635","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142072941","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
RETRACTION: FV-429 Induced Apoptosis Through ROS-Mediated ERK2 Nuclear Translocation and p53 Activation in Gastric Cancer Cells 回归:FV-429 通过 ROS 介导的 ERK2 核转移和 p53 激活诱导胃癌细胞凋亡
IF 3 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-27 DOI: 10.1002/jcb.30640

RETRACTION: Y. Zhou, L. Wei, H. Zhang, Q. Dai, Z. Li, B. Yu, et al., “FV-429 Induced Apoptosis Through ROS-Mediated ERK2 Nuclear Translocation and p53 Activation in Gastric Cancer Cells,” Journal of Cellular Biochemistry 116, no. 8 (2015): 1624–1637, https://doi.org/10.1002/jcb.25118.

The above article, published online on 3 February 2015 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties related to the data presented in the article. Specifically, duplication of Western Blot images has been detected across Figures 5D and 6A; and 5B, 6B and 6I. Furthermore, inappropriate post-acquisition modifications have been detected within Figure 4B and 4F, and image elements in Figure 4B and 4E were found to have been previously published by the same author group in a different scientific context. The authors were unable to provide the relative raw data upon request. Finally, the cell lines used in this study (BGC-823 and MGC-803) have been reported as contaminated [1-4]. Therefore, retraction has been agreed upon as the editors consider the conclusions of this article to be invalid. The authors have been informed of the decision of retraction but unavailable for a final confirmation.

撤回:Y. Zhou, L. Wei, H. Zhang, Q. Dai, Z. Li, B. Yu, et al., "FV-429 Induced Apoptosis Through ROS-Mediated ERK2 Nuclear Translocation and p53 Activation in Gastric Cancer Cells," Journal of Cellular Biochemistry 116, no. 8 (2015): 1624-1637, https://doi.org/10.1002/jcb.25118.上述文章于 2015 年 2 月 3 日在线发表于 Wiley Online Library (wileyonlinelibrary.com),经期刊主编 Christian Behl 和 Wiley Periodicals LLC 协议,该文章已被撤回。同意撤稿的原因是第三方对文章中提供的数据提出了疑虑。具体来说,在图 5D 和 6A 以及图 5B、6B 和 6I 中发现了 Western Blot 图像的重复。此外,在图 4B 和图 4F 中发现了不恰当的采集后修改,图 4B 和图 4E 中的图像元素被发现之前已由同一作者小组在不同的科学背景下发表过。作者无法应要求提供相关原始数据。最后,本研究中使用的细胞系(BGC-823 和 MGC-803)已被报道为受到污染[1-4]。因此,由于编辑认为这篇文章的结论无效,同意撤回。作者已被告知撤稿决定,但尚未得到最终确认。
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引用次数: 0
FOXO3 Activates MFN2 Expression to Maintain the Autophagy Response in Cancer Cells Under Amino Acid Deprivation. FOXO3 激活 MFN2 表达以维持氨基酸匮乏条件下癌细胞的自噬反应
IF 3 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-22 DOI: 10.1002/jcb.30641
Xu Jiang, Jing Wang, Fang Ma, Yuyun Li

The lack of amino acids triggers the autophagic response. Some studies have shown such starvation conditions also induce mitochondrial fusion, revealing a close correlation between the two processes. Although Mitofusin-2 (MFN2) has been demonstrated to play a role in fusion regulation, its role in the autophagic response and the variables that activate MFN2 under stress remain unknown. In this investigation, we screened and confirmed that forkhead box protein O3 (FOXO3) participates in MFN2's expression during short periods of starvation. Luciferase reporter test proved that FOXO3 facilitates MFN2's transcription by binding to its promoter region, and FOXO3 downregulation directly depresses MFN2's expression. Consequently, inhibiting the FOXO3-MFN2 axis results in the loss of mitochondrial fusion, disrupting the normal morphology of mitochondria, impairing the degradation of substrates, and reducing autophagosome accumulation, ultimately leading to the blockage of the autophagy. In conclusion, our work demonstrates that the FOXO3-MFN2 pathway is essential for adaptive changes in mitochondrial morphology and cellular autophagy response under nutritional constraints.

氨基酸的缺乏会引发自噬反应。一些研究表明,这种饥饿条件也会诱导线粒体融合,揭示了这两个过程之间的密切联系。虽然已证实 Mitofusin-2(MFN2)在融合调控中发挥作用,但它在自噬反应中的作用以及在应激状态下激活 MFN2 的变量仍然未知。在这项研究中,我们筛选并证实叉头盒蛋白 O3(FOXO3)在短时间饥饿时参与了 MFN2 的表达。荧光素酶报告试验证明,FOXO3通过与其启动子区域结合促进MFN2的转录,而FOXO3的下调会直接抑制MFN2的表达。因此,抑制 FOXO3-MFN2 轴会导致线粒体融合的丧失,破坏线粒体的正常形态,影响底物的降解,减少自噬体的积累,最终导致自噬受阻。总之,我们的研究表明,FOXO3-MFN2 通路对于营养限制下线粒体形态的适应性变化和细胞自噬反应至关重要。
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引用次数: 0
PLM-T3SE: Accurate Prediction of Type III Secretion Effectors Using Protein Language Model Embeddings. PLM-T3SE:利用蛋白质语言模型嵌入精确预测 III 型分泌效应因子。
IF 3 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-20 DOI: 10.1002/jcb.30642
Mengru Gao, Chen Song, Taigang Liu

The Type III secretion effectors (T3SEs) are bacterial proteins synthesized by Gram-negative pathogens and delivered into host cells via the Type III secretion system (T3SS). These effectors usually play a pivotal role in the interactions between bacteria and hosts. Hence, the precise identification of T3SEs aids researchers in exploring the pathogenic mechanisms of bacterial infections. Since the diversity and complexity of T3SE sequences often make traditional experimental methods time-consuming, it is imperative to explore more efficient and convenient computational approaches for T3SE prediction. Inspired by the promising potential exhibited by pre-trained language models in protein recognition tasks, we proposed a method called PLM-T3SE that utilizes protein language models (PLMs) for effective recognition of T3SEs. First, we utilized PLM embeddings and evolutionary features from the position-specific scoring matrix (PSSM) profiles to transform protein sequences into fixed-length vectors for model training. Second, we employed the extreme gradient boosting (XGBoost) algorithm to rank these features based on their importance. Finally, a MLP neural network model was used to predict T3SEs based on the selected optimal feature set. Experimental results from the cross-validation and independent test demonstrated that our model exhibited superior performance compared to the existing models. Specifically, our model achieved an accuracy of 98.1%, which is 1.8%-42.4% higher than the state-of-the-art predictors based on the same independent data set test. These findings highlight the superiority of the PLM-T3SE and the remarkable characterization ability of PLM embeddings for T3SE prediction.

III 型分泌效应物(T3SE)是革兰氏阴性病原体合成的细菌蛋白质,通过 III 型分泌系统(T3SS)输送到宿主细胞。这些效应物通常在细菌与宿主的相互作用中发挥关键作用。因此,精确鉴定 T3SE 有助于研究人员探索细菌感染的致病机制。由于 T3SE 序列的多样性和复杂性,传统的实验方法往往费时费力,因此探索更高效、更便捷的 T3SE 预测计算方法势在必行。受到预训练语言模型在蛋白质识别任务中展现出的巨大潜力的启发,我们提出了一种名为 PLM-T3SE 的方法,利用蛋白质语言模型(PLM)来有效识别 T3SE。首先,我们利用蛋白质语言模型嵌入和来自特定位置评分矩阵(PSSM)剖面的进化特征,将蛋白质序列转换成固定长度的向量,用于模型训练。其次,我们采用极端梯度提升(XGBoost)算法,根据这些特征的重要性对其进行排序。最后,我们使用 MLP 神经网络模型,根据选定的最优特征集预测 T3SE。交叉验证和独立测试的实验结果表明,与现有模型相比,我们的模型表现出更优越的性能。具体来说,基于相同的独立数据集测试,我们的模型达到了 98.1%的准确率,比最先进的预测器高出 1.8%-42.4%。这些发现凸显了 PLM-T3SE 的优越性,以及 PLM 嵌入对 T3SE 预测的显著表征能力。
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Journal of cellular biochemistry
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