PReD-Bench/PRed-Bench huggingface dataset:
Liver protection from apoptosis requires both blockage of initiator caspase activities and inhibition of ASK1/JNK pathway via glutathione S-transferase regulation
Authors: Dominique Lagadic-Gossmann
Anne Corlu
David Gilot
Azeddine Atfi
Denise Glaise
Christiane Guguen-Guillouzo
Hidenori Ichijo
Fabrice Morel
Pascal Loyer
Journal: Journal of Biological Chemistry (2002)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Hepatoprotection; free radical scavenging; dimethyl sulfoxide; apoptosis; caspase-3
Affiliations: INSERM U522, R√©gulation des Equilibres fonctionnels du foie Normal et Pathologique, Avenue de la Bataille Flandre/Dunkerque, H√¥pital Pontchaillou, 35033 Rennes, France. 

Abstract:  Hepatoprotection mediated by free radical scavenging molecules such as dimethyl sulfoxide (Me(2)SO) arose the question as to whether this effect involved one or several anti-apoptotic signals. Here, using primary cultures of rat hepatocytes and in vivo thioacetamide-induced liver failure, we showed that Me(2)SO failed to prevent any cleavage of initiator caspase-8 and -9 but constantly inhibited procaspase-3 maturation and apoptosis execution, pointing to an efficient inhibition of cleaved initiator caspase activities. Evidence was recently provided that apoptosis might require both caspase and ASK1/JNK-p38 activities. We demonstrated that this kinase pathway was strongly inhibited in the presence of Me(2)SO whereas overexpression of ASK1 was able to restore caspase-3 activity and apoptosis. Interestingly, we also found that GST M1/2 and GST Alpha1/2 dropped under apoptotic conditions; furthermore transfection of GST M1, A1, or P1 to cells overexpressing ASK1, abolished caspase-3 activity and restored viability. This role of GSTs was further assessed by showing that their high expression level was tightly associated with inhibition of ASK1 activity in Me(2)SO-protected hepatocytes. Together, these results demonstrate that Me(2)SO-mediated hepatoprotection involves a dual inhibition of cleaved initiator caspase and ASK1/JNK-p38 activities. Furthermore, in highlighting the control of apoptosis by GSTs, these data provide new insights for analyzing the complex mechanisms of hepatoprotection. 

Retracted: No

PubPeer comments:
 In Fig. 6A, JNK panel of Western blot were similar to MKP1 panel only with different bright contrast, and GST M1 2 panel were similar to GST A1 2 panel with different exposure time.  ,
LCAT deficiency does not impair amyloid metabolism in APP/PS1 mice
Authors: Anna Wilkinson
Lita Freeman
Michael Lee
Jeniffer Chan
Veronica Hirsch-Reinshagen
Boris Vaisman
Alice Ossoli
Stephen Demosky
Cheryl L Wellington
Sophie Stukas
Alan T Remaley
Journal: Journal of lipid research (2014)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Alzheimer‚Äôs disease; apolipoproteins; high density lipoprotein metabolism; lecithin:cholesterol acyltransferase.
Affiliations: Department of Pathology and Laboratory Medicine, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada V5Z 4H4., National Institutes of Health, Bethesda, MD 20892-1508.

Abstract:  A key step in plasma HDL maturation from discoidal to spherical particles is the esterification of cholesterol to cholesteryl ester, which is catalyzed by LCAT. HDL-like lipoproteins in cerebrospinal fluid (CSF) are also spherical, whereas nascent lipoprotein particles secreted from astrocytes are discoidal, suggesting that LCAT may play a similar role in the CNS. In plasma, apoA-I is the main LCAT activator, while in the CNS, it is believed to be apoE. apoE is directly involved in the pathological progression of Alzheimer's disease, including facilitating Œ≤-amyloid (AŒ≤) clearance from the brain, a function that requires its lipidation by ABCA1. However, whether apoE particle maturation by LCAT is also required for AŒ≤ clearance is unknown. Here we characterized the impact of LCAT deficiency on CNS lipoprotein metabolism and amyloid pathology. Deletion of LCAT from APP/PS1 mice resulted in a pronounced decrease of apoA-I in plasma that was paralleled by decreased apoA-I levels in CSF and brain tissue, whereas apoE levels were unaffected. Furthermore, LCAT deficiency did not increase AŒ≤ or amyloid in APP/PS1 LCAT(-/-) mice. Finally, LCAT expression and plasma activity were unaffected by age or the onset of Alzheimer's-like pathology in APP/PS1 mice. Taken together, these results suggest that apoE-containing discoidal HDLs do not require LCAT-dependent maturation to mediate efficient AŒ≤ clearance. 

Retracted: No

PubPeer comments:
 Fig 3A B use the same actin loading controls, but different GAPDH loading controls. The apo-A1 blot in the first panel appears to have an undeclared splice. Some of the p values, error bars and histograms in 3A do not seem to be consistent with each other or the blots. For example, from the histograms, the Hp samples look much more significantly different than the Cx samples, whereas the p values seem to indicate the opposite.  ,
Generation of a human iPSC line from a Bardet-Biedl syndrome patient compound heterozygous for the BBS7 variants c.849¬†+¬†1G¬†>¬†C/c.754G¬†>¬†A
Authors: Nan Zhou
Yeping Jiang
Lan Mi
Fan Duan
Qian Fu
Hui Wang
Ying Liang
Journal: Stem Cell Research (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Bardet-Biedl syndrome; BBS; iPSC line; patient; compound heterozygous
Affiliations: Department 2 of Nephrology, Beijing Children's Hospital Affiliated to Capital Medical University, Beijing Key Laboratory for Chronic Renal Disease and Blood Purification, Key Laboratory of Major Diseases in Children, Ministry of Education, National Center for Children's Health, China., Department 2 of Nephrology, Beijing Children's Hospital Affiliated to Capital Medical University, Beijing Key Laboratory for Chronic Renal Disease and Blood Purification, Key Laboratory of Major Diseases in Children, Ministry of Education, National Center for Children's Health, China. Electronic address: ., School of Pediatrics, Capital Medical University, China.

Abstract:  Bardet-Biedl syndrome (BBS) is primarily a multisystem nonmotile ciliopathy. In this study, we describe the successful establishment and characterization of an iPSC line from a patient diagnosed with BBS who was compound heterozygous for the BBS7 variants c.849 + 1G &gt; C (splicing) and c.754G &gt; A (p.D252N). 

Retracted: No

PubPeer comments:
 The authors of this paper have named their iPSC cell line BCHI001-A, which conflict with another iPSC cell lune which was attributed that name by hPSCreg using the standardized nomenclature for stem cell lines. See: https: web.expasy.org cellosaurus CVCL_A7JZ and https: hpscreg.eu cell-line BCHi001-A This is due to the fact that the authors did not register their cell line in hPSCreg. This is one of the steps indicated in the instruction to authors of the  Lab resources section of this journal. In the last 6 months this has happened very frequently. Elsevier seems to not really car about the quality of this section and are much more interested in generating profits than correcting mistakes or inconsistencies. There is not a single paper from the  Lab resource section that does not contain an error, some minor, other more important. If Stem Cell Research does not start to do some QC on their paper I will start to PubPer all these errors. , 
 Thank you for your comment. BCHi001-A is the alternative name of our cell line. We have finished the registration of our cell line in hPSCreg. The hPSCreg Name is BCHNi001-A. Seeuff1ahttps: hpscreg.eu cell-line BCHNi001-A Thank you again. We will be more rigorous in future research. , 
 #2 Thank you very much for having registered your cell line in hPSCreg, thus making it easier to distinguish it from the previously published BCHi001-A cell line. Best regards Amos ,
Long Noncoding RNA ATB Promotes Proliferation, Migration, and Invasion in Bladder Cancer by Suppressing MicroRNA-126
Authors: Xingquan Zhai
Wei Xu
Journal: Oncology research (2018)
Discipline: CLINICAL MEDICINE
Keywords: lncRNA-ATB; miR-126; KRAS; bladder cancer; cell viability
Affiliations: Department of Urology, Zoucheng People‚Äôs Hospital, Zoucheng, Shandong, P.R. China

Abstract:  This study aimed to explore the biological functions of long noncoding RNA activated by transforming growth factor-Œ≤ (lncRNA-ATB) in bladder cancer cells. For the expressions of lncRNA-ATB, miR-126, and KRAS, T24 cells were transfected with their specific vectors/shRNA or mimic/inhibitor. Then cell viability, migration, invasion, and apoptosis as well as the protein levels of apoptosis-related factors and PI3K/AKT and mTOR signal pathways were measured. The relationships of lncRNA-ATB and miR-126 or miR-126 and KRAS were analyzed by Dual-Luciferase Reporter assay. Functional experiments showed that lncRNA-ATB overexpression significantly promoted cell viability, migration, and invasion in T24 cells. lncRNA-ATB was a molecular sponge of miR-126 and exerted tumor-promoting effects by downregulation of miR-126. Moreover, KRAS was a direct target of miR-126 and was negatively regulated by miR-126. Finally, overexpression of KRAS increased cell viability, migration, and invasion, as well as activated PI3K/AKT and mTOR signaling pathways in T24 cells. The results revealed that lncRNA-ATB was an oncogene, which promoted cell proliferation, migration, and invasion by regulating miR-126 in bladder cancer. These findings may provide a potential prognostic biomarker and a therapeutic target for bladder cancer. 

Retracted: No

PubPeer comments:
 This paper belongs to a set of over 400 papers (as per February 2020) that share very similar Western blots with tadpole-like shaped bands, the same background pattern, and striking similarities in title structures, paper layout, bar graph design, and - in a subset - flow cytometry panels. Despite these similarities, these papers are authored by researchers from different departments and institutes, with almost no overlap in authors. The list of these papers is available here: https: docs.google.com spreadsheets d 1KXqTAyl4j-jVorFPMD2XRpr76LcIKJ0CVyIvRj0exYQ edit?usp=sharing A more detailed description of this set of papers, suspected to all be generated by a common source, a paper mill , can be found here: * https: forbetterscience.com 2020 01 24 the-full-service-paper-mill-and-its-chinese-customers (January 2020) * https: scienceintegritydigest.com 2020 02 21 the-tadpole-paper-mill (February 2020) The same paper mill has been described in these papers: * Jana Christopher - Systematic fabrication of scientific images revealed - FEBS Letters (2018) - https: febs.onlinelibrary.wiley.com doi full 10.1002 1873-3468.13201 * Jennifer A Byrne and Jana Christopher - Digital magic, or the dark arts of the 21st centuryu2014how can journals and peer reviewers detect manuscripts and publications from paper mills? - FEBS Letters (2020) - https: febs.onlinelibrary.wiley.com doi full 10.1002 1873-3468.13747 ,
Integrin-mediated signaling induced by simian virus 40 leads to transient uncoupling of cortical actin and the plasma membrane
Authors: Manuel Bauer
Ariella Oppenheim
Waltraud Mair
Lilli Stergiou
Nir Drayman
Damaris Bausch-Fluck
Bernd Wollscheid
Lucas Pelkmans
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: Simian Virus 40; GM1; integrins; ILK; PDK1
Affiliations: Institute of Molecular Systems Biology, ETH Zurich, Zurich, Switzerland.

Abstract:  Simian Virus 40 (SV40) is a paradigm pathogen with multivalent binding sites for the sphingolipid GM1, via which it induces its endocytosis for infection. Here we report that SV40 also utilizes cell surface integrins to activate signaling networks required for infection, even in the absence of the previously implicated glycosphingolipids. We identify ILK, PDK1, the RhoGAP GRAF1 and RhoA as core nodes of the signaling network activated upon SV40 engagement of integrins. We show that integrin-mediated signaling through host SV40 engagement induces the de-phosphorylation of Ezrin leading to uncoupling of the plasma membrane and cortical actin. Our results provide functional evidence for a mechanism by which SV40 activates signal transduction in human epithelial cells via integrins in the context of clathrin-independent endocytosis. 

Retracted: No

PubPeer comments:
 Figure 2D. * Blue arrows: sharp vertical background transitions appear to be visible between lanes * Orange boxes: The top VP1 panel looks similar to the bottom VP1 panel * Purple boxes: The top tubulin panel looks similar to the bottom tubulin panel It is not clear what the difference between these 2 sets of panels is, however, since the labels appear to be the same. Could the authors perhaps clarify?  , 
 Figure 2E. * Blue arrows: sharp vertical background transitions appear to be visible between lanes * In the tubulin panel, two adjacent lanes look similar. Image made darker to bring out details.  ,
Bazedoxifene enhances paclitaxel efficacy to suppress glioblastoma via altering Hippo/YAP pathway
Authors: Jie Wu
Xuejun Liu
Haiyang Fu
Yingchao Liu
Peng Zhao
Hong Li
Weiwei Fu
Journal: Journal of Cancer (2020)
Discipline: CLINICAL MEDICINE
Keywords: Bazedoxifene; Glioblastoma; Paclitaxel; YAP.
Affiliations: Department of Pathology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P. R. China., Department of Radiology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P. R. China., Department of Neurosurgery, Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250006, P. R. China.

Abstract:  Glioblastoma multiform (GBM) is an aggressive type of brain tumor originated from astrocytes. Owing to the limited therapeutic options, intensive efforts are still being made to find novel treatments for GBM. In this study, we first identified that bazedoxifene bore the ability to reduce cell survival and cell invasion of glioblastoma cells. Furthermore, our results also revealed that bazedoxifene combining with paclitaxel had better efficacy to suppress glioblastoma progression by promoting apoptosis and reducing EMT. Combination of bazedoxifene and paclitaxel also accelerated YAP phosphorylation and inactivation. Importantly, preclinical animal model also verified our in vitro findings. Together, our data not only define the underlying mechanism responsible for action of bazedoxifene on glioblastoma cells but also build strong rational to develop bazedoxifene for the treatment of GBM patients. 

Retracted: No

PubPeer comments:
 Figure 2B. * Red boxes: two colony formation assay panels appear to look similar.  ,
Improvement of carbon tetrachloride-induced acute hepatic failure by transplantation of induced pluripotent stem cells without reprogramming factor c-Myc
Authors: Szu-Yu Chen
Shaw-Yeu Jeng
Yuh-Lih Chang
Chih-Hung Chiang
Yueh Chien
Jung-Hung Hsieh
Hsin-Yang Li
Yi-Wen Liao
Liang-Kung Chen
Ying-Hsiu Lai
Hen-Li Chen
Chi-Hsien Peng
Yi-Jen Chen
Hua-Ming Chang
Teh-Ia Huo
Journal: International Journal of Molecular Sciences (2012)
Discipline: CHEMISTRY
Keywords: c-Myc; carbon tetrachloride; hepatic encephalopathy; hepatic failure; induced pluripotent stem cell.
Affiliations: Department of Optics and Photonics, National Central University, Chung-Li, Taiwan; E-Mails:    (H.-M.C.);    (S.-Y.C.).

Abstract:  The only curative treatment for hepatic failure is liver transplantation. Unfortunately, this treatment has several major limitations, as for example donor organ shortage. A previous report demonstrated that transplantation of induced pluripotent stem cells without reprogramming factor c-Myc (3-genes iPSCs) attenuates thioacetamide-induced hepatic failure with minimal incidence of tumorigenicity. In this study, we investigated whether 3-genes iPSC transplantation is capable of rescuing carbon tetrachloride (CCl(4))-induced fulminant hepatic failure and hepatic encephalopathy in mice. Firstly, we demonstrated that 3-genes iPSCs possess the capacity to differentiate into hepatocyte-like cells (iPSC-Heps) that exhibit biological functions and express various hepatic specific markers. 3-genes iPSCs also exhibited several antioxidant enzymes that prevented CCl(4)-induced reactive oxygen species production and cell death. Intraperitoneal transplantation of either 3-genes iPSCs or 3-genes iPSC-Heps significantly reduced hepatic necrotic areas, improved hepatic functions, and survival rate in CCl(4)-treated mice. CCl(4)-induced hepatic encephalopathy was also improved by 3-genes iPSC transplantation. Hoechst staining confirmed the successful engraftment of both 3-genes iPSCs and 3-genes iPSC-Heps, indicating the homing properties of these cells. The most pronounced hepatoprotective effect of iPSCs appeared to originate from the highest antioxidant activity of 3-gene iPSCs among all transplanted cells. In summary, our findings demonstrated that 3-genes iPSCs serve as an available cell source for the treatment of an experimental model of acute liver diseases. 

Retracted: No

PubPeer comments:
 image duplication  Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
Down-regulation of long non-coding RNA HOTAIR sensitizes breast cancer to trastuzumab
Authors: Tianwen Chen
Tao Huang
Wen Zeng
Zeming Liu
Journal: Scientific Reports (2019)
Discipline: Multidisciplinary
Keywords: HOTAIR; breast cancer; trastuzumab resistance; EMT; TGF-Œ≤
Affiliations: Department of Breast and Thyroid Surgery, Nanshan Hospital affiliated to Shenzhen University, Shenzhen, China., Department of Breast and Thyroid Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China., Department of Ophthalmology, Zhongnan Hospital, Wuhan University, Wuhan, Hubei, China., Department of Breast and Thyroid Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. .

Abstract:  This study aimed to investigate the roles and possible molecular mechanisms of long non-coding RNA HOTAIR in regulating resistance to trastuzumab in breast cancer. Trastuzumab-resistant breast cancer cell line SK-BR-3-TR was assayed for the expression of HOX antisense intergenic RNA (HOTAIR), epithelial-mesenchymal transition (EMT)-related proteins or genes. Methylation levels of TGF- Œ≤, PTEN and cyclin-dependent kinase inhibitor 1B (or P27) were determined. In trastuzumab-resistant cell line, the mRNA level of HOTAIR was significantly up-regulated; in addition, the expression of TGF-Œ≤, Snail and Vimentin was also up-regulated, E-cadherin was down-regulated while the expression of HER2, PI3K, AKT, mTOR and MAPK in the HER2 receptor pathway and phosphorylation level of HER2 receptor remained unchanged, the methylation levels of the PTEN gene and TGF-Œ≤ were increased and decreased, respectively. RNA interference downregulated the HOTAIR level and sensitized the cells to trastuzumab. It also resulted in down-regulation of TGF-Œ≤, Snail, Vimentin, p-AKT, p-APK and CyclinD1 and up-regulation of E-cadherin, PTEN and P27. Besides, the methylation levels of the PTEN gene and TGF-Œ≤ were reduced and increased, respectively. Mouse models grafted with SK-BR-3-TR grew faster than with SK-BR-3-TS and siHOTAIR-SK-BR-3-TR. 

Retracted: No

PubPeer comments:
 Figures 1G and 1H. A7M3 and A7M8 panels much more similar than you would expect. https: imgur.com 9B9xHKx , 
 #1 For full clarity, we here provide the original figure sent for publication in 2007. This high resolution figure as well as magnifications clearly reveal differences between each of the indicated western blot frames:  In parallel to marked differences on both intensity and morphological level, the light blue frames display also similar elements between construct overexpression. Only the original full Rx films would enable us to provide further proof for these frames, and we highly regret that these original Rx films from 2007 are now not available anymore. Without these, we can only further underline that even in the presence of similarities in the light blue frames, morphological differences cannot occur if data would have been derived from the same western blot scan. ,
Multi-method approach for characterizing the interaction between Fusarium verticillioides and Bacillus thuringiensis subsp. Kurstaki
Authors: Sabina Moser Tralamazza
Cynara B Barbosa
Leon Rabinovitch
Gabriela M Reis
Benedito Corr√™a
Liliana O Rocha
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: Bacterial antagonists; biocontrol agent; Bacillus thuringiensis; Fusarium; microscopy
Affiliations: Department of Microbiology, Laboratory of Mycotoxins and Toxigenic Fungi, University of S√£o Paulo, S√£o Paulo, S√£o Paulo, Brazil., Department of Bacteriology, Laboratory of Bacterial Physiology, Oswaldo Cruz Institute, FIOCRUZ, Rio de Janeiro, Rio de Janeiro, Brazil.

Abstract:  Bacterial antagonists used as biocontrol agents represent part of an integrated management program to reduce pesticides in the environment. Bacillus thuringiensis is considered a good alternative as a biocontrol agent for suppressing plant pathogens such as Fusarium. In this study, we used microscopy, flow cytometry, indirect immunofluorescence, and high performance liquid chromatography to determine the interaction between B. thuringiensis subsp. kurstaki LFB-FIOCRUZ (CCGB) 257 and F. verticillioides MRC 826, an important plant pathogen frequently associated with maize. B. thuringiensis showed a strong in vitro suppressive effect on F. verticillioides growth and inhibited fumonisin production. Flow cytometry analysis was found to be adequate for characterizing the fungal cell oscillations and death during these interactions. Further studies of the antagonistic effect of this isolate against other fungi and in vivo testing are necessary to determine the efficacy of B. thuringiensis subsp. kurstaki in controlling plant pathogens. This is the first report on the use of flow cytometry for quantifying living and apoptotic F. verticillioides cells and the B. thuringiensis Cry 1Ab toxin. 

Retracted: No

PubPeer comments:
 Three corrections for this paper, in August 2014 , October 2015 , and May 2019 . It appears the last correction addresses the concerns shared with the journal in April 2014. * Red boxes: Two panels in Figure 2B appear to look the same * Blue boxes: Two panels in Figure 3 appear to look the same (the authors wrote in the third correction that these represent the same sample). I thank the authors for their three corrections.  ,
Intracellular Delivery of DNA and Protein by a Novel Cell-Permeable Peptide Derived from DOT1L
Authors: Fengqin Wang
Changbai Liu
Jingping Geng
Richard Q Nguyen
Lidan Wang
Hu Wang
Xiangli Guo
Journal: Biomolecules (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: cell-permeable peptides (CPPs); plasmid; protein delivery; transfection.
Affiliations: Department of Pathology and Immunology, Medical School, China Three Gorges University, Yichang 443002, China., Hubei Key Laboratory of Tumor Microenvironment and Immunotherapy, China Three Gorges University, Yichang 443002, China., Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

Abstract:  Cellular uptake and intracellular release efficiency of biomacromolecules is low because of hurdles in the cell membrane that result in limited access to intra-cellular targets with few functional effects. Cell-penetrating peptides (CPPs) act as cargo delivery vehicles to promote therapeutic molecule translocation. Here, we describe the novel CPP-Dot1l that not only penetrates by itself, but also mediates cargo translocation in cultured cells, as confirmed by fluorescence microscopy and fluorescence spectrophotometry. We conducted cytotoxicity assays and safety evaluations, and determined peptide-membrane interactions to understand the possible pathway for cargo translocation. Additional nucleic acid and covalently conjugated green fluorescence protein (GFP) studies mediated by CPP-Dot1l were conducted to show functional delivery potential. Results indicate that CPP-Dot1l is a novel and effective CPP due to its good penetrating properties in different cell lines and its ability to enter cells in a concentration-dependent manner. Its penetration efficiency can be prompted by DMSO pretreatment. In addition, not only can it mediate plasmid delivery, but CPP-Dot1l can also deliver GFP protein into cytosol. In conclusion, the findings of this study showed CPP-Dot1l is an attractive pharmaceutical and biochemical tool for future drug, regenerative medicine, cell therapy, gene therapy, and gene editing-based therapy development. 

Retracted: No

PubPeer comments:
 Fig 2A and FIg 3A have duplicates. Please make comments. Thanks!  , 
 Dear Paraburkholderia Caffeinilytica, This is Hu Wang, co-corresponding author of this paper. We appreciate that you brought this to our attention, and we have immediately checked our paper and raw data, we found that this duplicated panel in figure 3A (37 u00b0C group) with figure 2A (5 u00b5M group) was a unconscious mistake during figure processing. We have already contacted journal editorial to correct the mistake. This comment is valuable for us to improve our paper and guiding significance to our research. Thank you again for your attention! Kindly regards, Hu Wang. ,
Human nonsense-mediated RNA decay regulates EMT by targeting the TGF-√ü signaling pathway in lung adenocarcinoma
Authors: Bin Meng
Wenfeng Cao
Wangzhao Song
Baocun Sun
Lingmei Li
Lisha Qi
Cong Xu
Changxu Liu
Lingyi Yang
Lin Zhang
Lu Cao
Yue Yu
Bin Zhang
Yalei Wang
Qiujuan Huang
Yuhong Guo
Journal: Cancer letters (2017)
Discipline: CLINICAL MEDICINE
Keywords: EMT; Lung adenocarcinoma; Nonsense-mediated mRNA decay; TGF-√ü; UPF1.
Affiliations: Department of Pathology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin Medical University, Ministry of Education, Tianjin 300060, China., Department of Pathology, Tianjin Central Hospital of Gynecology Obstetrics, Tianjin 300060, China., Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Breast Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin Medical University, Ministry of Education, Tianjin 300060, China., Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Breast Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin Medical University, Ministry of Education, Tianjin 300060, China. Electronic address: ., Department of Pathology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin Medical University, Ministry of Education, Tianjin 300060, China. Electronic address: .

Abstract:  Nonsense-mediated mRNA decay (NMD) is a highly conserved pathway that selectively degrades aberrant RNA transcripts. In this study, we proved that NMD regulates the epithelial-mesenchymal transition (EMT) of lung adenocarcinoma (ADC). Moreover, we found that NMD core factor UP-frameshift 1 tends to be expressed at lower levels in human ADC tissues than in normal lung tissues, thereby raising the possibility that NMD may be downregulated to permit ADC oncogenesis. Our experiments in human ADC cell lines showed that downregulating NMD can promote EMT. Moreover, EMT can be inhibited by upregulating NMD. We tested the role of TGF-√ü signaling and found that NMD influences EMT by targeting the TGF-√ü signaling pathway. Our findings reveal that NMD is a potential tumor regulatory mechanism and may be a potential therapeutic target for ADC. 

Retracted: No

PubPeer comments:
 In Figure 2C, three of the Western immunoblots (UPF1, Vimenting and Zeb1) contain discontinuities, but they not not seen in the other blots and not the control blot (actin). In Figure 3A, two of the beta-actin blots look very similar, but they represent two different samples (A549 vs H1299).  ,
Effects of IL-1Œ≤ on hippocampus cell apoptosis and learning ability of vascular dementia rats
Authors: L-L Guo
K-G Cui
D-S Wang
Y-Y Xu
Journal: European review for medical and pharmacological sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Vascular dementia; Interleukin-1Œ≤; Inflammation; Stroke; Memory
Affiliations: Department of Neurology, The Fifth Affiliated Hospital of Harbin Medical University, Daqing People's Hospital, Daqing, Heilongjiang, China. .

Abstract:  Objective: Vascular dementia (VD) is a type of memory, cognition, and behavior disorder caused by ischemic stroke or hemorrhagic stroke. It is a common pathogenesis of dementia that is only second to Alzheimer's disease. Inflammation plays a key role in VD. Interleukin-1Œ≤ (IL-1Œ≤) is a kind of pro-inflammatory cytokine, while its mechanism in VD occurrence and development is still unclear. Materials and methods: The healthy male rats were randomly divided into three groups, including sham group, VD model group (established by bilateral common carotid artery ligation), and IL-1Œ≤ group (treated by IL-1Œ≤ monoclonal antibody intracerebroventricular injection on based on model group). Rat learning ability was evaluated by Morris water maze assay. IL-1Œ≤ expression in brain tissue and peripheral blood was examined by using Real Time-PCR and enzyme-linked immunosorbent assay (ELISA), respectively. Hippocampus apoptosis was detected by caspase 3 activity detection kit. B-cell lymphoma-2 (Bcl-2) and p38 mitogen-activated protein kinase (MAPK) protein levels were assessed by Western blot assay. Results: IL-1Œ≤ expression was increased, caspase 3 activity was enhanced, Bcl-2 level was declined, and p-P38 phosphorylation was elevated in brain tissue and peripheral blood from VD model group compared to sham group (p&lt;0.05). IL-1Œ≤ monoclonal antibody significantly reduced IL-1Œ≤ expression, improved learning ability, attenuated caspase 3 activity, increased Bcl-2 level, and declined p-P38 expression in VD rats compared to model group (p&lt;0.05). Conclusions: IL-1Œ≤ can delay VD occurrence and development through the P38-MAPK signaling pathway to regulate cell apoptosis and improve learning ability. 

Retracted: Yes

PubPeer comments:
 Retracted [January 2021] . The article u201cEffects of IL-1u03b2 on hippocampus cell apoptosis and learning ability of vascular dementia rats, by L.-L. Guo, D.-S. Wang, Y.-Y. Xu, K.-G. Cui, published in Eur Rev Med Pharmacol Sci 2018; 22 (18): 6042-6048u2013DOI: 10.26355 eurrev_201809_15941u2013PMID: 30280789u201d has been withdrawn from the authors due to substantial deficiency in the experimental design. The Publisher apologizes for any inconvenience this may cause. The rationale for the paper s disappearance is not generous with details, but I think we can agree that the similarity of Figs 2 and 7 is unfortunate.  ,
Identification of an Arabidopsis mitochondrial succinate-fumarate translocator
Authors: Wolf B Frommer
Rebecca Schwab
Melanie Hilpert
Marcelo Desimone
Elisabetta Catoni
Karin Schumacher
Ulf Ingo Fl√ºgge
Rainer Schwacke
Journal: FEBS letters (2003)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Yeast; Arabidopsis thaliana; Mitochondrial succinate translocator; Organellar transporters; Fumarate
Affiliations: Plant Physiology, ZMBP, Auf der Morgenstelle 1, 72076 T√ºbingen, Germany.

Abstract:  Complementation of a yeast acr1 mutant carrying a deletion of the succinate/fumarate carrier gene enabled functional identification of a mitochondrial succinate translocator from Arabidopsis thaliana (AtmSFC1). Thus complementation of yeast mutants is applicable also for identification and characterization of organellar transporters. Reverse transcription polymerase chain reaction and promoter-GUS fusion showed expression of AtmSFC1 in 2 day old dark grown seedlings, which declined in cotyledons during further development, consistent with a role in export of fumarate for gluconeogenesis during lipid mobilization at early germination of Arabidopsis seeds. In mature plants, expression was found in developing and germinating pollen, suggesting a role in ethanolic fermentation. 

Retracted: No

PubPeer comments:
 Fig 7B.  Representative images of xenograft tumours .  Some of the tumors have shadows and some do not. Some are surrounded by grey featureless areas of erasure. It appears that they have been assembled digitally rather than physically, so the presence of an image of a ruler as part of the composition does not really provide any assurance about their absolute or relative scale. The same image of the same ruler is also part of the composition of another digital composite, Fig 6B of [Wen et al (2020)] .  Tumor images was captured at the end of the experiments .   UPDATE: Another sighting of the same ruler! Fig 7B from [Fei et al (2020)] .  Representative images of formed tumors that were subcutaneously injected with U2OS cells stable transfected with sh-AFAP1-AS1 and sh-NC plasmid.  ,
Coformulation of doxorubicin and curcumin in poly(D,L-lactide-co-glycolide) nanoparticles suppresses the development of multidrug resistance in K562 cells
Authors: Sanjeeb K Sahoo
Ranjita Misra
Journal: Molecular Pharmaceutics (2011)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Doxorubicin; Chronic myeloid leukemia; Drug resistance; Curcumin; Nanoparticle formulation
Affiliations: Institute of Life Sciences, Nalco Square, Chandrasekharpur, Bhubaneswar, Orissa, India., Institute of Life Sciences, Nalco Square, Chandrasekharpur, Bhubaneswar, Orissa, India

Abstract:  Doxorubicin (DOX) is a broad-spectrum anthracycline antibiotic used to treat a variety of cancers including leukemia. Chronic myeloid leukemia (CML) blasts like K562 cells are resistant to apoptosis induced by DOX due to several reasons, the primary being the sequestration of drug into cytoplasmic vesicles and induction of multidrug resistance (MDR) gene expression with DOX treatment resulting in intracellular resistance to this drug. Moreover, expression of antiapoptotic protein BCL-2 and the hybrid gene bcr/abl in K562 cells contributes resistance to DOX. Studies have shown that curcumin (CUR) has a pleiotropic therapeutic effect in cancer treatment, as it is an inhibitor of nuclear factor kappa B (NFŒ∫B) as well as a potent downregulator of MDR transporters. In this study, we investigated the potential benefit of using DOX and CUR in a single nanoparticle (NP) formulation to inhibit the development of drug resistance for the enhancement of antiproliferative activity of DOX in K562 cells. Results illustrate that the dual (DOX+CUR) drug loaded NPs were effectively delivered into K562 cells. CUR not only facilitates the retention of DOX in nucleus for a longer period of time but also inhibits the gradual expression of MDR1 and BCL-2 at the mRNA level in K562 cells. Moreover, Western blot results confirm that in combination both of the drugs were capable of inducing apoptosis even if in a lower concentration compared to either single drug in both solution or in formulation. Combinational therapy by using DOX and CUR, especially when administered in the NP formulation, has enhanced the cytotoxicity in K562 cells by promoting the apoptotic response. Overall, this combinational strategy has significant promise in the clinical management of intractable diseases, especially leukemia. 

Retracted: No

PubPeer comments:
 Corrected [November 2013] . Old news, almost pre-dating PubPeer and not previously flagged here. ----------------------------------------- In the original version of the published article, the authors have noticed that, in Figure 1d, the TEM image of PLGA NPs was erroneously represented. A new figure has been provided.  ------------------------------------------------ Before the authors discovery, an [anonymous blogpost](http: sk-sahoo.blogspot.com 2013 05 mol-pharm-2011-jun-683852-66.html) had called attention to the original Fig 1d and its  erroneous representation , i.e. its similarity to a rotated, enlarged detail of Fig 1b of [Acharya, Dilnawaz Sahoo (2009)] .  ,
Wnt/Frizzled activation of Rho regulates vertebrate gastrulation and requires a novel Formin homology protein Daam1
Authors: X He
R Habas
Y Kato
Journal: Cell (2001)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Wnt signaling; Frizzled receptor; cell polarity; movement; development
Affiliations: Division of Neuroscience, Children's Hospital, Department of Neurology, Harvard Medical School, Boston, MA 02115, USA.

Abstract:  Wnt signaling via the Frizzled (Fz) receptor controls cell polarity and movement during development, but the molecular nature of Wnt/Fz polarity signal transduction remains poorly defined. Here we report that in human cells and during Xenopus embryogenesis, Wnt/Fz signaling activates the small GTPase Rho, a key regulator of cytoskeleton architecture. Wnt/Fz activation of Rho requires the cytoplasmic protein Dishevelled (Dvl) and a novel Formin homology protein Daam1. Daam1 binds to both Dvl and Rho, and mediates Wnt-induced Dvl-Rho complex formation. Inhibition or depletion of Daam1 prevents Wnt/Fz activation of Rho and of Xenopus gastrulation, but not of beta-catenin signaling. Our study illustrates a molecular pathway from Wnt/Fz signaling to Rho activation in cell polarity signal transduction. 

Retracted: No

PubPeer comments:
 Figure 1B: Possible splicing in GST-PBD band, but not in other bands.  Similar issue with Figure 1F:  Figure 2D u2013 possible differential splicing:  Figure 5D: Similarities between the panels. Could the authors comment?  ,
Triggering senescence programs suppresses Chk1 kinase and sensitizes cells to genotoxic stresses
Authors: Julia Yaglom
Le Meng
Vladimir L Gabai
Cornelia O&#x27;Callaghan-Sunol
Michael Y Sherman
Journal: Cancer Research (2008)
Discipline: CLINICAL MEDICINE
Keywords: Hsp72; senescence program; p53; Chk1; genotoxic stresses
Affiliations: Department of Biochemistry, Boston University Medical School, Boston, MA 02118, USA.

Abstract:  Depletion of the major heat shock protein Hsp72 leads to activation of the senescence program in a variety of tumor cell lines via both p53-dependent and p53-independent pathways. Here, we found that the Hsp72-depleted cells show defect in phosphorylation and activation of the protein kinase Chk1 by genotoxic stresses, such as UVC irradiation or camptothecin. Under these conditions, phosphorylation of Rad17 was also suppressed, whereas phosphorylation of p53 at Ser(15) was not affected, indicating a specific defect in phosphorylation of a subset of the ATR kinase substrates. Similarly, suppression of Chk1 activation was seen when senescence signaling was triggered by direct stimulation of p53, depletion of Cdc2, or overexpression of the cell cycle inhibitors p21 or p16. Thus, defect in Chk1 activation was not a consequence of the chaperone imbalance, but rather a downstream effect of activation of the senescence signaling. Inhibition of Chk1 was associated with inefficient inter-S phase checkpoint, as Hsp72 depleted cells failed to halt cell cycle progression upon UVC irradiation. Accordingly, sensitivity of cells to genotoxic stimuli after Hsp72 depletion was significantly enhanced. Thus, activation of the senescence signaling causes a defect in the DNA damage response manifested in increased sensitivity to genotoxic stresses. 

Retracted: No

PubPeer comments:
 Figures 4B and 5B. * Red boxes: four lanes in the actin panels look very similar.  ,
The ubiquitin ligase Mul1 induces mitophagy in skeletal muscle in response to muscle-wasting stimuli
Authors: Ravi Kambadur
Isuru W Wijesoma
Peter D Gluckman
Sudarsanareddy Lokireddy
Sabeera Bonala
Mridula Sharma
Craig McFarlane
Serena Teng
Journal: Cell Metabolism (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Mitochondria; Mitophagy; Muscle wasting; Mul1; FoxO1/3
Affiliations: School of Biological Sciences, Nanyang Technological University, Singapore 637551, Singapore.

Abstract:  Recent research reveals that dysfunction and subsequent loss of mitochondria (mitophagy) is a potent inducer of skeletal muscle wasting. However, the molecular mechanisms that govern the deregulation of mitochondrial function during muscle wasting are unclear. In this report, we show that different muscle-wasting stimuli upregulated mitochondrial E3 ubiquitin protein ligase 1 (Mul1), through a mechanism involving FoxO1/3 transcription factors. Overexpression of Mul1 in skeletal muscles and myoblast cultures was sufficient for the induction of mitophagy. Consistently, Mul1 suppression not only protected against mitophagy but also partially rescued the muscle wasting observed in response to muscle-wasting stimuli. In addition, upregulation of Mul1, while increasing mitochondrial fission, resulted in ubiquitination and degradation of the mitochondrial fusion protein Mfn2. Collectively, these data explain the molecular basis for the loss of mitochondrial number during muscle wasting. 

Retracted: Yes

PubPeer comments:
 Figure 5B. * Pink boxes: the WT and mutant larvae photos appear to show the same larva.  , 
 Figure 6B. * Cyan boxes: the WT LP and IB LP photos appear to look very similar.  , 
 Figure 9C D. * Boxes of the same color focus attention to lanes that look more similar than expected.  ,
3-Formylchromone interacts with cysteine 38 in p65 protein and with cysteine 179 in IŒ∫BŒ± kinase, leading to down-regulation of nuclear factor-Œ∫B (NF-Œ∫B)-regulated gene products and sensitization of tumor cells
Authors: Bokyung Sung
Sharangdhar S Phatak
Shuxing Zhang
Bharat B Aggarwal
Sahdeo Prasad
Vivek R Yadav
Subash C Gupta
Journal: Journal of Biological Chemistry (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: 3-Formylchromone; NF-Œ∫B activation pathway; IKK activation; IŒ∫BŒ± degradation; p65 phosphorylation
Affiliations: Cytokine Research Laboratory, Department of Experimental Therapeutics., Integrated Molecular Discovery Laboratory, Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030., Cytokine Research Laboratory, Department of Experimental Therapeutics. Electronic address: .

Abstract:  3-Formylchromone (3-FC) has been associated with anticancer potential through a mechanism yet to be elucidated. Because of the critical role of NF-Œ∫B in tumorigenesis, we investigated the effect of this agent on the NF-Œ∫B activation pathway. Whether activated by inflammatory agents (such as TNF-Œ± and endotoxin) or tumor promoters (such as phorbol ester and okadaic acid), 3-FC suppressed NF-Œ∫B activation. It also inhibited constitutive NF-Œ∫B expressed by most tumor cells. This activity correlated with sequential inhibition of IŒ∫BŒ± kinase (IKK) activation, IŒ∫BŒ± phosphorylation, IŒ∫BŒ± degradation, p65 phosphorylation, p65 nuclear translocation, and reporter gene expression. We found that 3-FC inhibited the direct binding of p65 to DNA, and this binding was reversed by a reducing agent, thus suggesting a role for the cysteine residue. Furthermore, mutation of Cys38 to Ser in p65 abolished this effect of the chromone. This result was confirmed by a docking study. 3-FC also inhibited IKK activation directly, and the reducing agent reversed this inhibition. Furthermore, mutation of Cys179 to Ala in IKK abolished the effect of the chromone. Suppression of NF-Œ∫B activation led to inhibition of anti-apoptotic (Bcl-2, Bcl-xL, survivin, and cIAP-1), proliferative (cyclin D1 and COX-2), invasive (MMP-9 and ICAM-1), and angiogenic (VEGF) gene products and sensitization of tumor cells to cytokines. Thus, this study shows that modification of cysteine residues in IKK and p65 by 3-FC leads to inhibition of the NF-Œ∫B activation pathway, suppression of anti-apoptotic gene products, and potentiation of apoptosis in tumor cells. 

Retracted: Yes

PubPeer comments:
null, 
  ,
Interferon-omega: Current status in clinical applications
Authors: Yin-Li Xie
Fu-Rong Zhao
Jun-Jun Shao
Shi-Fang Li
Yong-Guang Zhang
Hui-Yun Chang
Journal: International Immunopharmacology (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Application; Biological activity; Interferon omega; Type I IFN.
Affiliations: State Key Laboratory of Veterinary Etiological Biology, OIE/National Foot-and-Mouth Disease Reference Laboratory, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou 730046, Gansu, China.; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, Jiangsu Province 225009, China., State Key Laboratory of Veterinary Etiological Biology, OIE/National Foot-and-Mouth Disease Reference Laboratory, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou 730046, Gansu, China.; Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, Jiangsu Province 225009, China.. Electronic address: .

Abstract:  Since 1985, interferon (IFN)-œâ, a type I IFN, has been identified in many animals, but not canines and mice. It has been demonstrated to have antiviral, anti-proliferation, and antitumor activities that are similar to those of IFN-Œ±. To date, IFN-œâ has been explored as a treatment option for some diseases or viral infections in humans and other animals. Studies have revealed that human IFN-œâ displays antitumor activities in some models of human cancer cells and that it can be used to diagnose some diseases. While recombinant feline IFN-œâ has been licensed in several countries for treating canine parvovirus, feline leukemia virus, and feline immunodeficiency virus infections, it also exhibits a certain efficacy when used to treat other viral infections or diseases. This review examines the known biological activity of IFN-œâ and its clinical applications. We expect that the information provided in this review will stimulate further studies of IFN-œâ as a therapeutic agent. 

Retracted: No

PubPeer comments:
 The one currently in-use  interferon omega cited here, recombinant feline interferon omega, is in fact an alpha interferon. The study showing such by L.M. Yang (PMID 17316139) is cited by this very article, so I have no idea how the authors made this mistake. Readers are strongly advised to ignore all passages with reference to RFeIFN-u03c9. ,