PReD-Bench/PRed-Bench huggingface dataset:
Protective effect of RNA interference targeting Ikkβ on hepatic fibrosis in rats
Authors: Shi-Fang Wei
Yue-Rong Zhang
Jian-Jun Sun
Yao-Di Zhang
Li-Yang Wu
Yan Lin
Xiang-Lin Li
Ning Zhou
Journal: Journal of cellular biochemistry (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: IκB kinase β; RNAi; Rat liver fibrosis; lentivirus.
Affiliations: Department of Infectious DiseaseLanzhou First People's Hospital Lanzhou Gansu China, Department of Clinical LaboratoryHospital of Pulmonary Division of Lanzhou Lanzhou Gansu China

Abstract:  Nuclear factor-κB (NF-κB) is an important regulatory factor in cells. NF-κB has a wide range of biological activities. After activation, it participates in the transcription and regulation of many genes and plays a role in infection, inflammatory response, oxidative stress, cell multiplication, and apoptosis. The activation of the NF-κB signal pathway is dependent on the degradation of the IκB kinase β (IKKβ) complex. IKK β is the key kinase in the NF-κB activation pathway. After inhibition, it can block the activation of NF-κB. IKKβ is a key regulator of NF-κB activation, also an early regulator of inflammation in all stages of the immune response. This study aimed to investigate the effect of IKKβ-siRNA lentivirus vector treatment for hepatic fibrosis of rats. An IKKβ-siRNA expression plasmid was constructed and injected in the tail vein of rats. Then, IKKβ-siRNA distribution in the liver was observed by immunofluorescence, and the quantitative polymerase chain reaction was used to detect inflammation-related and fibrosis-related factors. IKKβ-siRNA lentiviruses could be delivered to the liver and significantly decrease carbon tetrachloride-induced hepatic fibrosis. Furthermore, serum transaminase levels significantly decreased, and inflammation-related and fibrosis-related factors decreased. IKKβ-siRNA can be an effective method of anti-fibrosis gene therapy for liver fibrosis. 

Retracted: No

PubPeer comments:
 The only raw data presented in this article (Figure 1) are tainted with data duplications. A micrograph has been duplicated and presented as something else. ![file] ,
Soluble epoxide hydrolase deficiency or inhibition attenuates diet-induced endoplasmic reticulum stress in liver and adipose tissue
Authors: Christophe Morisseau
Bruce D Hammock
Fawaz G Haj
Ahmed Bettaieb
Samah Chahed
Naoto Nagata
Daniel AbouBechara
Journal: Journal of Biological Chemistry (2013)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Endoplasmic Reticulum Stress; Epoxyeicosatrienoic Acids (EETs); Hydrolases; Inflammation; Insulin Resistance
Affiliations: Department of Nutrition, University of California, Davis, California 95616., Department of Entomology, University of California, Davis, California 95616; Comprehensive Cancer Center, University of California, Davis, California 95616., Department of Nutrition, University of California, Davis, California 95616; Comprehensive Cancer Center, University of California, Davis, California 95616; Department of Internal Medicine, University of California, Davis, California 95616. Electronic address: .

Abstract:  Soluble epoxide hydrolase (sEH) is a cytosolic enzyme whose inhibition has beneficial effects in cardiovascular, inflammatory, and metabolic diseases in murine models. Mice with targeted deletion or pharmacological inhibition of sEH exhibit improved insulin signaling in liver and adipose tissue. Herein, we assessed the role of sEH in regulating endoplasmic reticulum (ER) stress in liver and adipose tissue. We report that sEH expression was increased in the livers and adipose tissue of mice fed a high fat diet, the adipose tissue of overweight humans, and palmitate-treated cells. Importantly, sEH deficiency or inhibition in mice attenuated chronic high fat diet-induced ER stress in liver and adipose tissue. Similarly, pharmacological inhibition of sEH in HepG2 cells and 3T3-L1 adipocytes mitigated chemical-induced ER stress and activation of JNK, p38, and cell death. In addition, insulin signaling was enhanced in HepG2 cells treated with sEH substrates and attenuated in cells treated with sEH products. In summary, these findings demonstrate that sEH is a physiological modulator of ER stress and a potential target for mitigating complications associated with obesity. 

Retracted: No

PubPeer comments:
 Concerns about Figures 6 and 8 were shared with the journal in 2014, but nothing has happened as of today. Figure 6. * Blue boxes: The 12h and 36h panels appear to share an overlap. ![file] , 
 Perhaps Figure 8 as well (green boxes). *** ![file] , 
 Thank you, Actinopolyspora, I was planning to post that too, but you beat me to it. As I wrote above, both concerns, about Figures 6 and 8, have been shared with the journal in 2014. ,
In vivo inhibition of tryptophan catabolism reorganizes the tuberculoma and augments immune-mediated control of Mycobacterium tuberculosis
Authors: K Gus Kousoulas
Ashley V Veatch
Shabaana A Khader
Smriti Mehra
Nadia A Golden
Peter J Didier
Kaylee M Gentry
Deepak Kaushal
Kasi E Russell-Lodrigue
Uma S Gautam
Toidi Adekambi
Xavier Alvarez
James L Blanchard
Lara A Doyle-Meyers
Andrew A Lackner
Allison N Bucsan
Daniel Kalman
Taylor W Foreman
Jyothi Rengarajan
Journal: Proceedings of the National Academy of Sciences of the United States of America (2018)
Discipline: Multidisciplinary
Keywords: IDO; T cell; granuloma; macaque; tuberculosis.
Affiliations: Tulane National Primate Research Center, Tulane University School of Medicine, Covington, LA 70433., Department of Microbiology & Immunology, Tulane University School of Medicine, New Orleans, LA 70112., Emory Vaccine Center, Emory University, Atlanta, GA 30322., Department of Pathobiological Sciences, Louisiana State University School of Veterinary Medicine, Baton Rouge, LA 70803., Center for Experimental Infectious Disease Research, Louisiana State University School of Veterinary Medicine, Baton Rouge, LA 70803., Department of Molecular Microbiology, Washington University in St. Louis, St. Louis, MO 63130., Tulane National Primate Research Center, Tulane University School of Medicine, Covington, LA 70433;  .

Abstract:  Mycobacterium tuberculosis continues to cause devastating levels of mortality due to tuberculosis (TB). The failure to control TB stems from an incomplete understanding of the highly specialized strategies that M. tuberculosis utilizes to modulate host immunity and thereby persist in host lungs. Here, we show that M. tuberculosis induced the expression of indoleamine 2,3-dioxygenase (IDO), an enzyme involved in tryptophan catabolism, in macrophages and in the lungs of animals (mice and macaque) with active disease. In a macaque model of inhalation TB, suppression of IDO activity reduced bacterial burden, pathology, and clinical signs of TB disease, leading to increased host survival. This increased protection was accompanied by increased lung T cell proliferation, induction of inducible bronchus-associated lymphoid tissue and correlates of bacterial killing, reduced checkpoint signaling, and the relocation of effector T cells to the center of the granulomata. The enhanced killing of M. tuberculosis in macrophages in vivo by CD4+ T cells was also replicated in vitro, in cocultures of macaque macrophages and CD4+ T cells. Collectively, these results suggest that there exists a potential for using IDO inhibition as an effective and clinically relevant host-directed therapy for TB. 

Retracted: No

PubPeer comments:
 There are pseudoreplication problems in figure 5. Just to keep that in mind when interpreting those inflated P-values. ,
In vivo tumorigenesis was observed after injection of in vitro expanded neural crest stem cells isolated from adult bone marrow
Authors: Bernard Rogister
Virginie Neirinckx
Christophe Poulet
Sabine Wislet-Gendebien
James T Swingland
Vincent Bours
Emerence Laudet
Lukas Sommer
Olga Shakova
Benoit Hennuy
Journal: PLoS ONE (2012)
Discipline: Multidisciplinary
Keywords: Bone marrow stromal cells; mesenchymal stem cells; neural crest stem cells; tumorigenic cells; in vitro passaging
Affiliations: Groupe Interdisciplinaire de Génoprotéomique Appliquée, Unit of Neurosciences, University of Liege, Liège, Belgium. 

Abstract:  Bone marrow stromal cells are adult multipotent cells that represent an attractive tool in cellular therapy strategies. Several studies have reported that in vitro passaging of mesenchymal stem cells alters the functional and biological properties of those cells, leading to the accumulation of genetic aberrations. Recent studies described bone marrow stromal cells (BMSC) as mixed populations of cells including mesenchymal (MSC) and neural crest stem cells (NCSC). Here, we report the transformation of NCSC into tumorigenic cells, after in vitro long-term passaging. Indeed, the characterization of 6 neural crest-derived clones revealed the presence of one tumorigenic clone. Transcriptomic analyses of this clone highlighted, among others, numerous cell cycle checkpoint modifications and chromosome 11q down-regulation (suggesting a deletion of chromosome 11q) compared with the other clones. Moreover, unsupervised analysis such as a dendrogram generated after agglomerative hierarchical clustering comparing several transcriptomic data showed important similarities between the tumorigenic neural crest-derived clone and mammary tumor cell lines. Altogether, it appeared that NCSC isolated from adult bone marrow represents a potential danger for cellular therapy, and consequently, we recommend that phenotypic, functional and genetic assays should be performed on bone marrow mesenchymal and neural crest stem cells before in vivo use, to demonstrate whether their biological properties, after ex vivo expansion, remain suitable for clinical application. 

Retracted: No

PubPeer comments:
 This article features some photos of a patient s genital areas. Did the patient consent to have their photos used for this publication? I could not find any statement of consent. One would hope a patient could go to the dermatology clinic to be treated well and not worry that a photo of their nether regions would end up in a scientific paper without consent. Could the authors please comment on this lack of consent statement? ,
iEzy-drug: a web server for identifying the interaction between enzymes and drugs in cellular networking
Authors: Jian-Liang Min
Xuan Xiao
Kuo-Chen Chou
Journal: BioMed Research International (2013)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Enzymes; Drug-enzyme interactions; Computational methods; Three-dimensional structure; Sequence-based predictor
Affiliations: Computer Department, Jing-De-Zhen Ceramic Institute, Jing-De-Zhen 333046, China., Computer Department, Jing-De-Zhen Ceramic Institute, Jing-De-Zhen 333046, China ; Information School, ZheJiang Textile & Fashion College, NingBo 315211, China ; Gordon Life Science Institute, Belmont, MA 02478, USA., Gordon Life Science Institute, Belmont, MA 02478, USA ; Center of Excellence in Genomic Medicine Research (CEGMR), King Abdulaziz University, Jeddah, Saudi Arabia.

Abstract:  With the features of extremely high selectivity and efficiency in catalyzing almost all the chemical reactions in cells, enzymes play vitally important roles for the life of an organism and hence have become frequent targets for drug design. An essential step in developing drugs by targeting enzymes is to identify drug-enzyme interactions in cells. It is both time-consuming and costly to do this purely by means of experimental techniques alone. Although some computational methods were developed in this regard based on the knowledge of the three-dimensional structure of enzyme, unfortunately their usage is quite limited because three-dimensional structures of many enzymes are still unknown. Here, we reported a sequence-based predictor, called "iEzy-Drug," in which each drug compound was formulated by a molecular fingerprint with 258 feature components, each enzyme by the Chou's pseudo amino acid composition generated via incorporating sequential evolution information and physicochemical features derived from its sequence, and the prediction engine was operated by the fuzzy K-nearest neighbor algorithm. The overall success rate achieved by iEzy-Drug via rigorous cross-validations was about 91%. Moreover, to maximize the convenience for the majority of experimental scientists, a user-friendly web server was established, by which users can easily obtain their desired results. 

Retracted: No

PubPeer comments:
 This paper is extremely similar to the published https: doi.org 10.1371 journal.pone.0072234 ,
Insulin/IGF-1 Receptor Signaling Enhances Biosynthetic Activity and Fat Mobilization in the Initial Phase of Starvation in Adult Male C. elegans
Authors: Sheng-Ching Luo
Ying-Hue Lee
Wan-Zo Ho
Kien Thiam Tan
Journal: Cell Metabolism (2011)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: nutrient deprivation; biosynthesis; catabolic pathways; energy sources; nutrients
Affiliations: Laboratory of Molecular Pathology, Institute of Molecular Biology, Academia Sinica, Taipei 115, Taiwan.

Abstract:  Upon nutrient deprivation, cells are thought to suppress biosynthesis but activate catabolic pathways to provide alternative energy sources and nutrients. However, here we provide evidence that in adult male C. elegans, both biosynthesis and degradation activities, including ribosome biogenesis and turnover, are enhanced during early starvation and appear to depend on the availability of intestinal lipid stores. Upon depletion of the intestinal lipids, further food deprivation results in a significant reduction in metabolic activity in the starved male worms. Our data show that adult C. elegans exhibits a two-phase metabolic response to starvation stress: an initial phase with enhanced metabolic activity that rapidly exhausts the lipid stores, followed by a phase with low metabolic activity, which outlasts the life of fed control worms. DAF-2 insulin/IGF-1 receptor signaling to the RAS pathway is required for the starvation-induced ribosome biogenesis and rapid lipid depletion in the initial phase of starvation. 

Retracted: No

PubPeer comments:
 Fig.3A and 3B: More similar than expected. Could authors check please? ![file] ,
CDK4 and CDK6 Delay Senescence by Kinase-Dependent and p16 INK4a -Independent Mechanisms
Authors: Janice Rowe
Fiona Gregory
Maria Starborg
Sharon Brookes
Rebecca Jones
Robert Poolman
Gordon Peters
Margarida Ruas
Journal: Molecular and Cellular Biology (2007)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Replicative senescence; human diploid fibroblasts; cyclin-dependent kinase inhibitors; p16(INK4a); p21(CIP1)
Affiliations: Cancer Research UK, London Research Institute, 44 Lincoln's Inn Fields, London, UK.

Abstract:  Replicative senescence of human diploid fibroblasts (HDFs) is largely implemented by the cyclin-dependent kinase (CDK) inhibitors p16(INK4a) and p21(CIP1). Their accumulation results in a loss of CDK2 activity, and cells arrest with the retinoblastoma protein (pRb) in its hypophosphorylated state. It has become standard practice to bypass the effects of p16(INK4a) by overexpressing CDK4 or a variant form that is unable to bind to INK4 proteins. Although CDK4 and CDK6 and their INK4-insensitive variants can extend the life span of HDFs, they also cause a substantial increase in the levels of endogenous p16(INK4a). Here we show that CDK4 and CDK6 can extend the life span of HDFs that have inactivating mutations in both alleles of INK4a or in which INK4a levels are repressed, indicating that overexpression of CDK4/6 is not equivalent to ablation of p16(INK4a). However, catalytically inactive versions of these kinases are unable to extend the replicative life span, suggesting that the impact of ectopic CDK4/6 depends on their ability to phosphorylate as yet unidentified substrates rather than to sequester CDK inhibitors. Since p16(INK4a) deficiency, CDK4 expression, and p53 or p21(CIP1) ablation have additive effects on replicative life span, our results underscore the idea that senescence is an integrated response to diverse signals. 

Retracted: No

PubPeer comments:
 Figure 4B. Splicing in CDK4 and p16 panels, yet not apparent in CDK6, p21, or MEK panels. ![file] ,
A facile sonochemical protocol for synthesis of 3-amino- and 4-amino-1,2,4-triazole derived Schiff bases as potential antibacterial agents
Authors: Ali Irfan
Irfan Ullah
Muhammad Saleem
Aeysha Sultan
Katarzyna Kotwica-Mojzych
Mariusz Mojzych
Muhammad Khalid
Noreen Sajjad
Mian Habib Ur Rehman
Muhammad Rafiq
Muhammad Mustaqeem
Syeda Laila Rubab
Journal: PLoS ONE (2020)
Discipline: Multidisciplinary
Keywords: Schiff bases; synthesis; aminotriazoles; aromatic aldehydes; antibacterial potential
Affiliations: Division of Science and Technology, Department of Chemistry, University of Education, Lahore, Pakistan., Department of Chemistry, University of Lahore, Lahore, Pakistan., Department of Chemistry, University of Lahore Sargodha campus, Sargodha, Pakistan., Department of Chemistry, University of Sargodha Sub-campus Bhakkar, Bhakkar, Pakistan., Department of Physiology and Biochemistry, Cholistan University of Veterinary and Animal Sciences, Bahawalpur, Pakistan., Department of Chemistry, Khwaja Ghulam Fareed University of Science and Technology, Rahimyar Khan, Pakistan., Chair and Department of Histology, Embryology and Cytophisiology, Medical University of Lublin, (Collegium Medicum), Lublin, Poland., Department of Chemistry, Siedlce University of Natural Sciences and Humanities, Siedlce, Poland.

Abstract:  A facile method has been developed for the synthesis of Schiff bases derived from substituted and unsubstituted 3-amino- and 4-amino-1,2,4-triazoles. Condensation of the aminotrizoles with a variety of aromatic aldehydes afforded desired Schiff bases in excellent yields in 3-5 minutes of exposure to ultra-sound. The synthesized compounds were characterized by means of IR, 1HNMR and Mass spectrometry. The synthesized compounds were also screened for their antibacterial potential against Gram-negative (Escherichia coli, Shigella sonnei, Pseudomonas aeruginosa and Salmonella typhi) and two Gram-positive (Staphylococcus aureus and Bacillus subtilis) strains. 

Retracted: Yes

PubPeer comments:
 Figure 1B https: imgur.com a pfoobCT ,
TPEN induces apoptosis independently of zinc chelator activity in a model of acute lymphoblastic leukemia and ex vivo acute leukemia cells through oxidative stress and mitochondria caspase-3- and AIF-dependent pathways
Authors: Miguel Mendivil-Perez
Marlene Jimenez-Del-Rio
Carlos Velez-Pardo
Journal: Oxidative Medicine and Cellular Longevity (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Acute lymphoblastic leukemia; TPEN; apoptosis; oxidative stress; chemotherapy resistance
Affiliations: Medical Research Institute School of Medicine, University of Antioquia (UdeA), Medellin, Colombia., Neuroscience Research Group, Medical Research Institute School of Medicine, University of Antioquia (UdeA), Calle 62 No. 52-59, Building 1, Laboratory 411/412, SIU, Medellin, Colombia

Abstract:  Acute lymphoblastic leukemia is still an incurable disease with resistance to therapy developing in the majority of patients. We investigated the effect of TPEN, an intracellular zinc chelator, in Jurkat and in ex vivo acute lymphoblastic leukemia (ALL) cells resistant to chemotherapy. Changes of nuclei morphology, reactive oxygen species generation, presence of hypodiploid cells, phosphatidylserine translocation, mitochondrial membrane depolarization, immunohistochemical identification of cell death signalling molecules, and pharmacological inhibition were assayed to detect the apoptotic cell death pathways. We found that TPEN induces apoptosis in both types of cells by a molecular oxidative stress pathway involving O(2)(•-) &gt; H(2)O(2) &gt;&gt; NF-κB (JNK/c-Jun) &gt;p53&gt; loss ΔΨ(m)&gt; caspase-3, AIF &gt; chromatin condensation/DNA fragmentation. Interestingly, TPEN induced apoptosis independently of glucose; leukemic cells are therefore devoid of survival capacity by metabolic resistance to treatment. Most importantly, TPEN cytotoxic effect can eventually be regulated by the antioxidant N-acetyl-cysteine and zinc ions. Our data suggest that TPEN can be used as a potential therapeutic prooxidant agent against refractory leukemia. These data contribute to understanding the importance of oxidative stress in the treatment of ALL. 

Retracted: No

PubPeer comments:
 image duplication ![file] 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. , 
 #1 I agree with the finding above in Figure 7 and have indicated a couple of additional probable overlaps in Figure 4. *** ![file] ,
Intra-generational protein malnutrition impairs temporal astrogenesis in rat brain
Authors: Nisha Patro
Aijaz Ahmad Naik
Ishan K Patro
Pankaj Seth
Journal: Biology open (2017)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Astrocyte; BLBP; GFAP; Hippocampus; Protein malnutrition
Affiliations: School of Studies in Neuroscience, Jiwaji University, Gwalior 474011, India., School of Studies in Zoology, Jiwaji University, Gwalior 474011, India., National Brain Research Centre, Manesar, Haryana 122051, India., School of Studies in Neuroscience, Jiwaji University, Gwalior 474011, India .

Abstract:  The lack of information on astrogenesis following stressor effect, notwithstanding the imperative roles of astroglia in normal physiology and pathophysiology, incited us to assess temporal astrogenesis and astrocyte density in an intra-generational protein malnutrition (PMN) rat model. Standard immunohistochemical procedures for glial lineage markers and their intensity measurements, and qRT-PCR studies, were performed to reveal the spatio-temporal origin and density of astrocytes. Reduced A2B5+ glia restricted precursor population in ventricles and caused poor dissemination to cortex at embryonic days (E)11-14, and low BLBP+ secondary radial glia in the subventricular zone (SVZ) of E16 low protein (LP) brains reflect compromised progenitor pooling. Contrary to large-sized BLBP+ gliospheres in high protein (HP) brains at E16, small gliospheres and discrete BLBP+ cells in LP brains evidence loss of colonization and low proliferative potential. Delayed emergence of GFAP expression, precocious astrocyte maturation and significantly reduced astrocyte number suggest impaired temporal and compromised astrogenesis within LP-F1 brains. Our findings of protein deprivation induced impairments in temporal astrogenesis, compromised density and astrocytic dysfunction, strengthen the hypothesis of astrocytes as possible drivers of neurodevelopmental disorders. This study may increase our understanding of stressor-associated brain development, opening up windows for effective therapeutic interventions against debilitating neurodevelopmental disorders. 

Retracted: No

PubPeer comments:
 Image recycled from a previous paper although treatments are different. ![file] , 
 ![file] , 
 Unfortunately, i am not able to make an account here and post the comment as author of the study, i am commenting here with my information in case anybody has more queries. I will be happy to take any questions and present the raw data on request. Aijaz A. Naik (Ist Author) Personal Email- Neuroaijaz@gmail.com Institutional email- aijaznaik@jiwaji.edu ,
Metastatic Heterogeneity of Breast Cancer Cells Is Associated with Expression of a Heterogeneous TGFβ-Activating miR424–503 Gene Cluster
Authors: Yun Li
Xun Zhu
Zhe Ying
Jun Li
Mengfeng Li
Wei Li
Han Tian
Journal: Cancer Research (2014)
Discipline: CLINICAL MEDICINE
Keywords: TGFβ signaling; metastasis; miR424-503 cluster; breast cancer; Smad7
Affiliations: Department of Microbiology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, Guangdong, China. Key Laboratory of Tropical Disease Control (Sun Yat-Sen University), Chinese Ministry of Education, Guangzhou, Guangdong, China., Key Laboratory of Tropical Disease Control (Sun Yat-Sen University), Chinese Ministry of Education, Guangzhou, Guangdong, China. Department of Biochemistry, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, Guangdong, China., Department of Microbiology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, Guangdong, China. Key Laboratory of Tropical Disease Control (Sun Yat-Sen University), Chinese Ministry of Education, Guangzhou, Guangdong, China. .

Abstract:  TGFβ signaling is known to drive metastasis in human cancer. Under physiologic conditions, the level of TGFβ activity is tightly controlled by a regulatory network involving multiple negative regulators. At metastasis, however, these inhibitory mechanisms are usually overridden so that oncogenic TGFβ signaling can be overactivated and sustained. To better understand how the TGFβ inhibitors are suppressed in metastatic breast cancer cells, we compared miRNA expression profiles between breast cancers with or without metastasis and found that the miR424-503 cluster was markedly overexpressed in metastatic breast cancer. Mechanistic studies revealed that miR424 and miR503 simultaneously suppressed Smad7 and Smurf2, two key inhibitory factors of TGFβ signaling, leading to enhanced TGFβ signaling and metastatic capability of breast cancer cells. Moreover, antagonizing miR424-503 in breast cancer cells suppressed metastasis in vivo and increased overall host survival. Interestingly, our study also found that heterogeneous expression of the miR424-503 cluster contributed to the heterogeneity of TGFβ activity levels in, and metastatic potential of, breast cancer cell subsets. Overall, our findings demonstrate a novel mechanism, mediated by elevated expression of the miR424-503 cluster, underlying TGFβ activation and metastasis of human breast cancer. 

Retracted: No

PubPeer comments:
 Fig. 2A. Image overlap and regional repetition. ![file] ,
Effect of SOCS3 on lung injury in rats with severe acute pancreatitis through regulating JAK2/STAT3 signaling pathway
Authors: Z-H Liang
M-B Qin
G-D Tang
M-Z Qin
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Suppressor of cytokine signaling 3 (SOCS3); lung injury; severe acute pancreatitis (SAP); Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway; rats
Affiliations: Department of Gastroenterology, The First Affiliated Hospital of Guangxi Medical University, Nanning, China. .

Abstract:  Objective: To explore the effect of suppressor of cytokine signaling 3 (SOCS3) on the lung injury in rats with severe acute pancreatitis (SAP) by regulating the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway. Materials and methods: Sprague-Dawley rats were divided into control group (n=20) and SAP model group (established via injection of 5% sodium taurocholate, n=40). Then, SOCS3 was overexpressed using the adenovirus in 20 rats in SAP model group. The serum amylase (AMY) was detected, whether the transfection was successful was verified via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR), the hepatic function indexes were detected, the pathological changes were observed using hematoxylin-eosin (HE) staining, and the wet/dry weight ratio (W/D) was calculated. Moreover, the content of serum inflammatory factors was detected via enzyme-linked immunosorbent assay (ELISA) and the expression levels of JAK2/STAT3 signaling pathway genes and proteins were detected through RT-PCR and Western blotting. Results: The content of AMY in SAP model group was significantly increased, indicating the successful modeling. SOCS3 was significantly increased in transfection group, suggesting that the transfection efficiency was significant. The content of alanine aminotransferase (ALT), and aspartate aminotransferase (AST) in SOCS3 transfection group was significantly lower than in model group. According to the histopathological observation, there were lung injury, pulmonary edema, hemorrhage, severe inflammatory response, and alveolar congestion in SAP model group. There were almost no pathological changes in SOCS3 transfection group. In SOCS3 transfection group, the content of serum interleukin-6 (IL-6), IL-18 and tumor necrosis factor-α (TNF-α), the mRNA and protein expressions of IL-6, JAK2, and STAT3 were all remarkably declined. Conclusions: SOCS3 inhibits the activation of the JAK2/STAT3 pathway and the increase of inflammatory factors, promoting the repair of lung injury in SAP rats. 

Retracted: No

PubPeer comments:
 ![file] Three identical patterns for different samples. ,
High Prevalence of Mansonella perstans Filariasis in Rural Senegal
Authors: Hubert Bassene
Oleg Mediannikov
Florence Fenollar
Masse Sambou
Didier Raoult
Alioune Badara L Y
Sawdiatou Djiba
Gaël Mourembou
Siân Clarke
Journal: American Journal of Tropical Medicine and Hygiene (2015)
Discipline: CLINICAL MEDICINE
Keywords: Mansonella; Culicoides; Senegal; real-time quantitative polymerase chain reaction (qPCR); microfilaria
Affiliations: Unité de Recherche sur les Maladies Infectieuses et Tropicales Emergentes (URMITE), Aix Marseille Université, Marseille, France, and Campus Universitaire UCAD-IRD de Hann, Dakar, Senegal; London School of Hygiene and Tropical Medicine, London, United Kingdom; Ministry of Health, Fann Résidence, Rue Aimé Césaire, Dakar, Senegal., Unité de Recherche sur les Maladies Infectieuses et Tropicales Emergentes (URMITE), Aix Marseille Université, Marseille, France, and Campus Universitaire UCAD-IRD de Hann, Dakar, Senegal; London School of Hygiene and Tropical Medicine, London, United Kingdom; Ministry of Health, Fann Résidence, Rue Aimé Césaire, Dakar, Senegal .

Abstract:  Large parts of African and American countries are colonized by Mansonella, a very common but poorly described filarial nematode. Bloodsucking flies of the genus Culicoides are suspected to be the vector of Mansonella perstans, but no study in Senegal has confirmed that Culicoides can transmit the parasite. Designed specific real-time quantitative polymerase chain reaction (qPCR) can be used to identify microfilaria in stained blood smears. This study was performed in July and December 2010 in the southeastern Senegal, which is known to be endemic for M. perstans. We analyzed 297 blood smears from febrile and afebrile resident people by qPCR. The global prevalence of M. perstans was approximately 14.5% in both febrile and afebrile individuals. The age group of &gt; 30 years had the highest prevalence (22.0%). No Culicoides among 1,159 studied specimens was positive for M. perstans and its vector in Senegal still requires identification. 

Retracted: No

PubPeer comments:
 Concerns about Figure 5A, reported to the journal in 2015: * Red boxes: The PY and Abl panels in the K562 column look very similar to each other. ![file] ,
Epigenetic activation of AP1 promotes squamous cell carcinoma metastasis
Authors: Jiong Li
Qi Zhong
Cun-Yu Wang
Xiangming Ding
Xiaohong Chen
Hongya Pan
Sarah M Dry
Journal: Science signaling (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: transcription factor; AP1; histone demethylase; KDM4A; invasive growth
Affiliations: Laboratory of Molecular Signaling, Division of Oral Biology and Medicine, School of Dentistry, University of California, Los Angeles, Los Angeles, CA 90095, USA.

Abstract:  The transcription factor AP1 (activating protein 1), a heterodimer of the JUN and FOS proteins, promotes the invasive growth and metastasis of various tumors such as squamous cell carcinoma (SCC), breast cancer, and melanoma. AP1 activity is transcriptionally induced through a positive feedback loop. We identified the histone demethylase KDM4A (lysine-specific demethylase 4A) as a key epigenetic priming factor in this positive feedback loop. KDM4A contributed to the induction of genes encoding the AP1 transcription factors and the invasive growth and metastasis of SCC. KDM4A knockdown decreased the growth factor-induced messenger RNA expression and protein abundance of AP1 family members, including JUN and FOSL1. Mechanistically, histone demethylation by KDM4A facilitated the binding of the AP1 complex to the promoters of JUN and FOSL1, thereby promoting the positive feedback loop that maintains activation of AP1. In a mouse model of SCC, KDM4A knockdown inhibited lymph node metastasis. Moreover, the abundance of KDM4A correlated with the abundance of JUN and FOSL1 in human SCC tissues, and KDM4A expression was increased in human lymph node metastases. Our studies provide insights into the epigenetic control of AP1 and tumor invasion and suggest that KDM4A could be an important therapeutic target for inhibiting invasive SCC growth and metastasis. 

Retracted: No

PubPeer comments:
 Figure 1H shows *Representative images (n = 3) from (G) in cells treated with scrambled siRNA (Scrsi) or siRNA targeting either KDM4A (KDM4Asi) or KDM4B (KDM4Bsi).* Could the authors check why the top and bottom panel, which represent different experiments, appear to show an overlap, please? Shown with red boxes. ![file] ,
Lack of galectin-3 disturbs mesenteric lymph node homeostasis and B cell niches in the course of Schistosoma mansoni infection
Authors: Radovan Borojevic
Fu-Tong Liu
Felipe L Oliveira
Kátia D Arcanjo
Roger Chammas
Adelzon A Paula
Márcia C El-Cheikh
Daniel K Hsu
Christina M Takiya
Camila Brand
Journal: PLoS ONE (2011)
Discipline: Multidisciplinary
Keywords: Galectin-3; B cell differentiation; lymphoid organization; mesenteric lymph nodes; chronic schistosomiasis
Affiliations: Laboratório de Proliferação e Diferenciação Celular, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil. 

Abstract:  Galectin-3 is a β-galactoside-binding protein that has been shown to regulate pathophysiological processes, including cellular activation, differentiation and apoptosis. Recently, we showed that galectin-3 acts as a potent inhibitor of B cell differentiation into plasma cells. Here, we have investigated whether galectin-3 interferes with the lymphoid organization of B cell compartments in mesenteric lymph nodes (MLNs) during chronic schistosomiasis, using WT and galectin-3(-/-) mice. Schistosoma mansoni synthesizes GalNAcβ1-4(Fucα1-3)GlcNAc(Lac-DiNAc) structures (N-acetylgalactosamine β1-4 N-acetylglucosamine), which are known to interact with galectin-3 and elicit an intense humoral response. Antigens derived from the eggs and adult worms are continuously drained to MLNs and induce a polyclonal B cell activation. In the present work, we observed that chronically-infected galectin-3(-/-) mice exhibited a significant reduced amount of macrophages and B lymphocytes followed by drastic histological changes in B lymphocyte and plasma cell niches in the MLNs. The lack of galectin-3 favored an increase in the lymphoid follicle number, but made follicular cells more susceptible to apoptotic stimuli. There were an excessive quantity of apoptotic bodies, higher number of annexin V(+)/PI(-) cells, and reduced clearance of follicular apoptotic cells in the course of schistosomiasis. Here, we observed that galectin-3 was expressed in non-lymphoid follicular cells and its absence was associated with severe damage to tissue architecture. Thus, we convey new information on the role of galectin-3 in regulation of histological events associated with B lymphocyte and plasma cell niches, apoptosis, phagocytosis and cell cycle properties in the MLNs of mice challenged with S.mansoni. 

Retracted: No

PubPeer comments:
 Figure 2B and C have the **exact** same pattern, although they should represent different conditions. Could the authors check if this is by chance a mistake? ![file] , 
 #1 Dear Daemonorops Rarispinosa, Many thanks for contact us. Probably, a problem of  copy paste . The same representative dot plot was inappropriately  pasted . I will check and contact the journal to correct this serious mistake. Best regards Felipe Oliveira ,
The role of properdin in murine zymosan-induced arthritis
Authors: Cordula Stover
Petya Dimitrova
Valeriya Gyurkovska
Wilhelm Schwaeble
Nina Ivanovska
Journal: Molecular Immunology (2010)
Discipline: IMMUNOLOGY
Keywords: properdin; zymosan-induced arthritis; inflammation; bone erosion; proteoglycan loss
Affiliations: Department of Immunology, Institute of Microbiology, Bulgarian Academy of Sciences, 1113 Sofia, Bulgaria.

Abstract:  Using properdin-deficient and wild-type mice, we have investigated the role of properdin in development and progression of zymosan-induced arthritis. At the initial phase of local, zymosan-induced inflammation, properdin-deficient and wild-type mice showed bone erosion, proteoglycan loss and cell infiltration. Compared to wild-type, properdin-deficient mice had reduced C5a and IL-6 but similar synovial TNF-alpha and sRANKL levels. Both groups showed a systemic immune response. Elevated IFN-gamma production and STAT1 signaling in splenocytes and a shift to Th1 response in popliteal lymph nodes were observed in properdin-deficient mice. Properdin-deficient mice had significantly less circulating zymosan-specific IgG antibodies than wild-type. In the chronic phase, the lack of properdin resulted in significant proteoglycan loss in the joints and lower cartilageneous STAT1 expression. The level of synovial C5a on day 30 was comparable in both groups, but C5aR staining was more apparent in the joints of properdin-deficient mice. Our data show that properdin is an important player in processes involved in inflammatory joint degradation. 

Retracted: No

PubPeer comments:
 Figure 2D appears to have some bands that have been reused, in one case flipped horizontally. There may be an additional issue in this figure, but I ll leave it to the authors to provide the uncropped original scans to reassure readers. *** ![file] ,
Normalization of RNA-seq data using factor analysis of control genes or samples
Authors: John Ngai
Sandrine Dudoit
Davide Risso
Terence P Speed
Journal: Nature Biotechnology (2014)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: RNA-sequencing; normalization; ERCC spike-ins; library preparation; technical effects
Affiliations: Department of Statistics, University of California, Berkeley, Berkeley, California, USA., 1] Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, USA. [2] Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, California, USA. [3] Functional Genomics Laboratory, University of California, Berkeley, Berkeley, California, USA., 1] Department of Statistics, University of California, Berkeley, Berkeley, California, USA. [2] Bioinformatics Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia. [3] Department of Mathematics and Statistics, The University of Melbourne, Victoria, Australia., 1] Department of Statistics, University of California, Berkeley, Berkeley, California, USA. [2] Division of Biostatistics, University of California, Berkeley, Berkeley, California, USA.

Abstract:  Normalization of RNA-sequencing (RNA-seq) data has proven essential to ensure accurate inference of expression levels. Here, we show that usual normalization approaches mostly account for sequencing depth and fail to correct for library preparation and other more complex unwanted technical effects. We evaluate the performance of the External RNA Control Consortium (ERCC) spike-in controls and investigate the possibility of using them directly for normalization. We show that the spike-ins are not reliable enough to be used in standard global-scaling or regression-based normalization procedures. We propose a normalization strategy, called remove unwanted variation (RUV), that adjusts for nuisance technical effects by performing factor analysis on suitable sets of control genes (e.g., ERCC spike-ins) or samples (e.g., replicate libraries). Our approach leads to more accurate estimates of expression fold-changes and tests of differential expression compared to state-of-the-art normalization methods. In particular, RUV promises to be valuable for large collaborative projects involving multiple laboratories, technicians, and/or sequencing platforms. 

Retracted: No

PubPeer comments:
null, 
 Concerns are explained in detail at the blog post above. Have the authors addressed these with Dr. Pachter or elsewhere? *** ![file] ,
The role of Hot13p and redox chemistry in the mitochondrial TIM22 import pathway
Authors: Carla M Koehler
Edward P Leverich
Kristen N Beverly
Danielle Leuenberger
David K Hwang
Sean P Curran
Journal: Journal of Biological Chemistry (2004)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: small Tim proteins; mitochondrial intermembrane space; TIM22 import pathway; inner membrane assembly; twin CX3C motif
Affiliations: Department of Chemistry and Biochemistry, University of California, Los Angeles 90095-1569, USA.

Abstract:  The small Tim proteins in the mitochondrial intermembrane space participate in the TIM22 import pathway for assembly of the inner membrane. Assembly of the small TIM complexes requires the conserved "twin CX3C" motif that forms juxtapositional intramolecular disulfide bonds. Here we identify a new intermembrane space protein, Hot13p, as the first component of a pathway that mediates assembly of the small TIM complexes. The small Tim proteins require Hot13p for assembly into a 70-kDa complex in the intermembrane space. Once assembled the small TIM complexes escort hydrophobic inner membrane proteins en route to the TIM22 complex. The mechanism by which the small Tim proteins bind and release substrate is not understood, and we investigated the affect of oxidant/reductant treatment on the TIM22 import pathway. With in organello import studies, oxidizing agents arrest the ADP/ATP carrier (AAC) bound to the Tim9p-Tim10p complex in the intermembrane space; this productive intermediate can be chased into the inner membrane upon subsequent treatment with reductant. Moreover, AAC import is markedly decreased by oxidant treatment in Deltahot13 mitochondria and improved when Hot13p is overexpressed, suggesting Hot13p may function to remodel the small TIM complexes during import. Together these results suggest that the small TIM complexes have a specialized assembly pathway in the intermembrane space and that the local redox state of the TIM complexes may mediate translocation of inner membrane proteins. 

Retracted: No

PubPeer comments:
 Figure 3A - possible image duplication ![file] ,
Regulation of AIF expression by p53
Authors: M Oren
I Shats
V Rotter
L Weisz
P Stambolsky
Y Klein
N Goldfinger
Journal: Cell death and differentiation (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: p53; AIF; apoptosis; transcriptional regulation; genotoxic stress
Affiliations: Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel.

Abstract:  The tumor suppressor p53 plays a pivotal role in suppressing tumorigenesis by inducing genomic stability, cell cycle arrest or apoptosis. AIF is a mitochondrial protein, which, upon translocation to the nucleus, can participate in apoptosis, primarily in a caspase-independent contexts. We now report that AIF gene expression is subject to positive transcriptional regulation by p53. Interestingly, unlike most known p53 target genes, the AIF gene is regulated by basal levels of p53, and activation of p53 by genotoxic stress does not result in a substantial further increase in AIF expression. The AIF gene harbors a p53 responsive element, which is bound by p53 within cells. p53 drives efficient induction of large-scale DNA fragmentation, a hallmark of AIF activity. Importantly, caspase-independent death is compromised in cells lacking functional p53, in line with the known role of AIF in this process. Thus, in addition to its documented effects on caspase-dependent apoptosis, p53 may also sensitize cells to caspase-independent death through positive regulation of AIF expression. Moreover, in the absence of overt apoptotic signals, the constitutive induction of AIF by p53 may underpin a cytoprotective maintenance role, based on the role of AIF in ensuring proper mitochondrial function. 

Retracted: No

PubPeer comments:
 While waiting for the Biochemical Journal to eventually decide the fate of the 3rd worst-ever paper published from the Weizmann, https: pubpeer.com publications 86E709835E96908738330ED4B849CC I couldnu2019t help but notice that a 2006 CDDif paper shares a control Weizmann ImmunoBlot (WIB) with a Cancer Cell paper published some four years later. Although the WIB is the same source image, the labelling is entirely unrelated. Will Nature Publishing Group be sending Cancer Cell a DRM takedown notice for this violation of their precious copyright? ![image] ,
Effects of microRNA‐494 on proliferation, migration, invasion, and apoptosis of medulloblastoma cells by mediating c‐myc through the p38 MAPK signaling pathway
Authors: Xiao-Heng Xu
Qi-Bo Hu
Wei Pan
Xing-Yu Song
Si-Jin Zhang
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: apoptosis; c-myc; invasion; medulloblastoma; microRNA-494
Affiliations: Department of Pediatrics, The Second Hospital of Jilin University, Changchun, China.

Abstract:  Medulloblastoma (MB) is the most prevalent brain tumor that occurs during childhood and originates from cerebellar granule cell precursors. Based on recent studies, the differential expression of several microRNAs is involved in MB, while the role of microRNA-494 (miR-494) in MB remains unclear. Therefore, we conducted this study to investigate the regulative role of miR-494 in MB cells via the p38 mitogen-activated protein kinase (MAPK) signaling pathway by mediating c-myc. In the current study, MB cells were collected and transfected with miR-494 mimic, miR-494 inhibitor, siRNA- c-myc, and miR-494 inhibitor + siRNA-c-myc. The expressions of miR-494, c-myc, p38 MAPK, B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), interleukin-6 (IL-6), metadherin (MTDH), phosphatase and tensin homolog (PTEN) and survivin were determined. Cell proliferation, cell-cycle distribution, apoptosis, migration, and invasion were evaluated. The results revealed that there was a poor expression of miR-494 and high expression of c-myc in MB tissues. C-myc was determined as the target gene of miR-494. In response to miR-494 mimic, MB cells were found to have increased Bax and PTEN expressions, as well as cell number in G1 phase and cell apoptosis and decreased c-myc, p38 MAPK, Bcl-2, MTDH, IL-6, and survivin expression and cell number count in the S phase, cell proliferation, migration, and invasion. In conclusion, the results demonstrated that the upregulation of miR-494 results in the suppression of cell proliferation, migration, and invasion, while it promotes apoptosis of MB cells through the negative mediation of c-myc, which in turn inactivates the p38 MAPK pathway. 

Retracted: Yes

PubPeer comments:
 Figure 8 appears to have partially duplicated images for different treatments ![file] There could be more , 
 Retracted [19 July 2021] . ---------------------------------------------- The above article, published online on 10 October 2018 in Wiley Online Library , has been retracted by agreement between the journal s Editor in Chief, Prof. Dr. Christian Behl, and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. Several flaws and inconsistencies between results presented and experimental methods described were found. Thus, the editors consider the conclusions of this article to be invalid. ,