PReD-Bench/PRed-Bench huggingface dataset:
Specific in vitro cleavage of Mason–Pfizer monkey virus capsid protein: evidence for a potential role of retroviral protease in early stages of infection
Authors: Iva Pichová
Tomás Ruml
Michaela Rumlová
Jan Pohl
Journal: Virology (2003)
Discipline: MICROBIOLOGY
Keywords: Gag polyproteins; viral protease; retroviral particles; ribonucleoprotein core; spacer peptide

Abstract:  Processing of Gag polyproteins by viral protease (PR) leads to reorganization of immature retroviral particles and formation of a ribonucleoprotein core. In some retroviruses, such as HIV and RSV, cleavage of a spacer peptide separating capsid and nucleocapsid proteins is essential for the core formation. We show here that no similar spacer peptide is present in the capsid-nucleocapsid (CA-NC) region of Mason-Pfizer monkey virus (M-PMV) and that the CA protein is cleaved in vitro by the PR within the major homology region (MHR) and the NC protein in several sites at the N-terminus. The CA cleavage product was also identified shortly after penetration of M-PMV into COS cells, suggesting that the protease-catalyzed cleavage is involved in core disintegration. 

Retracted: No

PubPeer comments:
 Concern about Figure 1A. * Red boxes: the bottom parts of lanes 2 and 4 look remarkably similar. ![file] , 
 The figure 1A shows Coomassie-stained SDS gel of MPMV CANC cleavage. As these data are 19 years old, we do not have the original ones. But, the cleavage CANC to CA and NC, shown in Fig. 1A, is specifically confirmed by immune analysis, shown in Fig. 1B and 1C. We do not know why there is a similarity in lanes 2 and 4 below the bands corresponding NC. NC is a highly basic protein and thus it might bind some nucleic acids fragment or some impurities in the SDS PAGE loading solution or in the SDS PAGE gel, or due to touching the gel by fingers during de-staining, drying and taking the picture u2026.(?). Some, although much lower similarity can be found also in the background of lanes 1 and 6. However, despite the similarity of the backgrounds, the NC bands are different. Most importantly the panels B and C in Fig. 1 support the same conclusion drawn from the panel A. We hope that this explanation fully dispelled the doubts and we strictly deny any intention to manipulate the figure ![file] ,
Insulin-like growth factor-I stimulates dephosphorylation of ikappa B through the serine phosphatase calcineurin (protein phosphatase 2B)
Authors: I Torres-Aleman
S Pons
Journal: Journal of Biological Chemistry (2000)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Astrocytes; Inflammatory cytokines; Neurotoxic free radicals; Insulin-like growth factor-I (IGF-I); NFkappaB
Affiliations: Cellular and Molecular Neuroendocrinology Laboratory, Instituto Cajal de Neurobiologia, Consejo Superior de Investigaciones Cientificas, Av. Doctor Arce 37, Madrid E28002, Spain. 

Abstract:  Astrocytes represent the most abundant cell type of the adult nervous system. Under normal conditions, astrocytes participate in neuronal feeding and detoxification. However, following brain injury, local increases in inflammatory cytokines trigger a reactive phenotype in astrocytes during which these cells produce their own inflammatory cytokines and neurotoxic free radicals. Indeed, progression of this inflammatory reaction is responsible for most neurological damage associated with brain trauma. Insulin-like growth factor-I (IGF-I) protects neurons against a variety of brain pathologies associated with glial overproduction of proinflammatory cytokines. Here, we demonstrate that in astrocyte cultures IGF-I regulates NFkappaB, a transcription factor known to play a key role in the inflammatory reaction. IGF-I induces a site-specific dephosphorylation of IkappaBalpha (phospho-Ser(32)) in astrocytes. Moreover, IGF-I-mediated dephosphorylation of IkappaBalpha protects this molecule from tumor necrosis factor alpha (TNFalpha)-stimulated degradation; therefore, IGF-I also inhibits the nuclear translocation of NFkappaB (p65) induced by TNFalpha exposure. Finally, we show that dephosphorylation of IkappaBalpha by IGF-I pathways requires activation of calcineurin. Activation of this phosphatase is independent of phosphatidylinositol 3-kinase and mitogen-activated protein kinase. Thus, these data suggest that the therapeutic benefits associated with IGF-I treatment of brain injury are derived from both its positive effects on neuronal survival and inhibition of the glial inflammatory reaction. 

Retracted: No

PubPeer comments:
 Figures 1 and 2C. Much more similar than you would expect. https: imgur.com 4Bzq165 ,
Low Temperature Synthesis of Superparamagnetic Iron Oxide (Fe3O4) Nanoparticles and Their ROS Mediated Inhibition of Biofilm Formed by Food-Associated Bacteria
Authors: Mohammad Shavez Khan
Mohammed Asif Ahmed
Mohammad Hassan Baig
Nasser A Al-Shabib
Firoz Ahmad Ansari
Javed Masood Khan
Syed Ali Shahzad
Rais Ahmad Khan
Fohad Mabood Husain
Faheem Ahmed
Iqbal Ahmad
Mohd Shahnawaz Khan
Mohammed Arshad
Mohammad Zubair Alam
Abdullah Alyousef
Journal: Frontiers in Microbiology (2018)
Discipline: MICROBIOLOGY
Keywords: ROS; bacteria; biofilm; food-borne pathogens; iron oxide nanoparticles.
Affiliations: Department of Food Science and Nutrition, College of Food and Agriculture, King Saud University, Riyadh, Saudi Arabia., College of Science and General Studies, Alfaisal University, Riyadh, Saudi Arabia., Department of Chemistry, College of Science, King Saud University, Riyadh, Saudi Arabia., Department of Agricultural Microbiology, Aligarh Muslim University, Aligarh, India., King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia., Protein Research Chair, Department of Biochemistry, College of Science, King Saud University, Riyadh, Saudi Arabia., School of Biotechnology, Yeungnam University, Gyeongsan, South Korea., Clinical Laboratory Sciences Department, College of Applied Medical Sciences, King Saud University, Riyadh, Saudi Arabia.

Abstract:  In the present study, a facile environmentally friendly approach was described to prepare monodisperse iron oxide (Fe3O4) nanoparticles (IONPs) by low temperature solution route. The synthesized nanoparticles were characterized using x-ray diffraction spectroscopy (XRD), Raman spectroscopy, field emission scanning electron microscopy (FESEM) measurements, Fourier-Transform Infrared Spectroscopy (FTIR), and Thermogravimetric analysis (TGA) analyses. XRD patterns revealed high crystalline quality of the nanoparticles. SEM micrographs showed the monodispersed IONPs with size ranging from 6 to 9 nm. Synthesized nanoparticles demonstrated MICs of 32, 64, and 128 μg/ml against Gram negative bacteria i.e., Serratia marcescens, Escherichia coli, and Pseudomonas aeruginosa, respectively, and 32 μg/ml against Gram positive bacteria Listeria monocytogenes. IOPNs at its respective sub-MICs demonstrated significant reduction of alginate and exopolysaccharide production and subsequently demonstrated broad-spectrum inhibition of biofilm ranging from 16 to 88% in the test bacteria. Biofilm reduction was also examined using SEM and Confocal Laser Scanning Microscopy (CLSM). Interaction of IONPs with bacterial cells generated ROS contributing to reduced biofilm formation. The present study for the first time report that these IONPs were effective in obliterating pre-formed biofilms. Thus, it is envisaged that these nanoparticles with broad-spectrum biofilm inhibitory property could be exploited in the food industry as well as in medical settings to curtail biofilm based infections and losses. 

Retracted: No

PubPeer comments:
 Some of the bands in figure 7B appear quite similar. Could the authors please post a high resolution image of the original scan? *** ![file] ,
Connexin32 plays a crucial role in ROS-mediated endoplasmic reticulum stress apoptosis signaling pathway in ischemia reperfusion-induced acute kidney injury
Authors: Yanling Wang
Shan Wu
Chaojin Chen
Shaoli Zhou
Yu Gu
Fei Huang
Dongdong Yuan
Ziqing Hei
Journal: Journal of Translational Medicine (2018)
Discipline: CLINICAL MEDICINE
Keywords: Acute kidney injury; Connexin32; Endoplasmic reticulum stress; Reactive oxygen species.
Affiliations: Department of Anesthesiology, The Third Affiliated Hospital of Sun Yat-sen University, No. 600 Tianhe Road, Guangzhou, 510630, Guangdong Province, China., Department of Anesthesiology, The Third Affiliated Hospital of Sun Yat-sen University, No. 600 Tianhe Road, Guangzhou, 510630, Guangdong Province, China. .

Abstract:  Background: Ischemia-reperfusion (I/R)-induced acute kidney injury (AKI) not only prolongs the length of hospital stay, but also seriously affects the patient's survival rate. Although our previous investigation has verified that reactive oxygen species (ROS) transferred through gap junction composed of connexin32 (Cx32) contributed to AKI, its underlying mechanisms were not fully understood and viable preventive or therapeutic regimens were still lacking. Among various mechanisms involved in organs I/R-induced injuries, endoplasmic reticulum stress (ERS)-related apoptosis is currently considered to be an important participant. Thus, in present study, we focused on the underlying mechanisms of I/R-induced AKI, and postulated that Cx32 mediated ROS/ERS/apoptosis signal pathway activation played an important part in I/R-induced AKI. Methods: We established renal I/R models with Cx32+/+ and Cx32-/- mice, which underwent double kidneys clamping and recanalization. ROS scavenger (N-acetylcysteine, NAC) and ERS inhibitors (4-phenyl butyric acid, 4-PBA, and tauroursodeoxycholic acid, TUDCA) were used to decrease the content of ROS and attenuate ERS activation, respectively. Results: Renal damage was progressively exacerbated in a time-dependent manner at the reperfusion stage, that was consistent with the alternation of ERS activation, including glucose regulated protein 78 (BiP/GRP78), X box-binding protein1, and C/EBP homologous protein expression. TUDCA or 4-PBA application attenuated I/R-induced ERS activation and protected against renal tubular epithelial cells apoptosis and renal damage. Cx32 deficiency decreased ROS generation and distribution between the neighboring cells, which attenuated I/R-induced ERS activation, and improved cell apoptosis and renal damage. Conclusion: Cx32 mediated ROS/ERS/apoptosis signal pathway activation played an important part in I/R-induced AKI. Cx32 deficiency, ROS elimination, and ERS inhibition all could protect against I/R-induced AKI. 

Retracted: No

PubPeer comments:
 Two GAPDH band in Fig. 4b was cut from Fig. 5a. Could the authors please check? ![file] ,
LGR5 interacts and cointernalizes with Wnt receptors to modulate Wnt/β-catenin signaling
Authors: Qiushi Lin
Qingyun Liu
Xing Gong
Kendra S Carmon
Anthony Thomas
Journal: Molecular and Cellular Biology (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: LGR5; R-spondin; Wnt signaling; stem cells; endocytosis
Affiliations: Brown Foundation Institute of Molecular Medicine, Texas Therapeutics Institute, University of Texas Health Science Center at Houston, Houston, Texas, USA. , Brown Foundation Institute of Molecular Medicine, Texas Therapeutics Institute, University of Texas Health Science Center at Houston, Houston, Texas, USA

Abstract:  LGR5, a seven-transmembrane domain receptor of the rhodopsin family, is a Wnt target gene and a bona fide marker of adult stem cells in the gastrointestinal tract and hair follicle bulge. Recently, we and others demonstrated that LGR5 and its homologues function as receptors of the R-spondin family of stem cell factors to potentiate Wnt/β-catenin signaling. However, the mechanism of how LGR5 enhances the signaling output remains unclear. Here we report that following costimulation with the ligands R-spondin1 and Wnt3a, LGR5 interacts and forms a supercomplex with the Wnt coreceptors LRP6 and Fzd5 which is rapidly internalized and then degraded. Internalization of LGR5 is mediated through a dynamin- and clathrin-dependent pathway. Inhibition of this endocytic process has no effect on LGR5 signaling. Deletion of the C-terminal tail of LGR5 maintains its ability to interact with LRP6, yet this LGR5 mutant exhibits increased signaling activity and a decreased rate of endocytosis in response to R-spondin1 compared to the wild-type receptor. This study provides direct evidence that LGR5 becomes part of the Wnt signaling complex at the membrane level to enhance Wnt/β-catenin signaling. However, internalization of LGR5 does not appear to be essential for potentiating the canonical Wnt signaling pathway. 

Retracted: No

PubPeer comments:
 June 2017 Correction: https: mcb.asm.org content 37 13 e00203-17 It reads:  *Page 2061, Fig. 6A legend, line 2: The following sentence should be added. u201cZero-minute images in the bottom two rows are duplicates of the 0-min images in the top two rows to make it easier to visualize the different extents of internalization in the presence and absence of ligands, especially at the 15-min time point.u201d The duplication in the figure does not affect any conclusions of the study, and we apologize for any confusion.* Here is the original Figure 6A, with orange boxes marking the panels that looked like duplicates. In a case like this, one could argue that both experiments were the t=0 timepoints before anything was added, so I thank the authors for addressing this with a clarification. ![file] This paper was part of a structured search for image duplications in Molecular and Cellular Biology paper, which was published here: https: mcb.asm.org content 38 20 e00309-18.long ,
Circular RNA circ-LDLRAD3 serves as an oncogene to promote non-small cell lung cancer progression by upregulating SLC1A5 through sponging miR-137
Authors: Weijun Hong
Fang Zhao
Xiwen Gao
Min Xue
Jun Jiang
Journal: RNA Biology (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Non-small cell lung cancer; Slc1a5; circular RNA circ-LDLRAD3; miR-137.
Affiliations: Department of Respiratory Medicine, Minhang Hospital, Fudan University , Shanghai, China., State Key Laboratory of Genetic Engineering, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Science, Fudan University , Shanghai, China., Department of Laboratory, Minhang Hospital, Fudan University , Shanghai, China.

Abstract:  Circular RNAs (circRNAs) are closely associated with the development of non-small cell lung cancer (NSCLC); however, it is still unclear whether circular RNA circ-LDLRAD3 participated in the regulation of NSCLC progression. In this study, we found that circ-LDLRAD3 was high-expressed and miR-137 was low-expressed in NSCLC tissues and cells compared to their normal counterparts, which showed negative correlations in NSCLC tissues. Further experiments validated that miR-137 could be sponged and inhibited by circ-LDLRAD3 in NSCLC cells. In addition, knock-down of circ-LDLRAD3 and miR-137 overexpression promoted NSCLC cell apoptosis, and inhibited cell proliferation and invasion. Similarly, upregulation of circ-LDLRAD3 or miR-137 ablation had opposite effects on the above cell functions. Besides, the glutamine transporter SLC1A5 was validated to be the downstream target of circ-LDLRAD3 and miR-137, and upregulated circ-LDLRAD3 increased SLC1A5 expression levels by downregulating miR-137. Furthermore, the effects of downregulated circ-LDLRAD3 on cell proliferation, apoptosis and mobility were all reversed by knocking down miR-137 and overexpressing SLC1A5. Taken together, this in vitro study found that knock-down of circ-LDLRAD3 inhibited the development of NSCLC by regulating miR-137/SLC1A5 axis. 

Retracted: No

PubPeer comments:
 Figure 8 has some image overlap (red boxes), and it also overlaps with figure 3 (orange boxes). ![file] ![file] ,
CYP enzymes, expressed within live human suspension cells, are superior to widely-used microsomal enzymes in identifying potent CYP1A1/CYP1B1 inhibitors: Identification of quinazolinones as CYP1A1/CYP1B1 inhibitors that efficiently reverse B[a]P toxicity and cisplatin resistance
Authors: Bhabatosh Chaudhuri
Ibidapo S Williams
Sandip B Bharate
Barij N Sinha
Venkatesan Jayaprakash
Vinay R Sonawane
Linda Gatchie
Mohd Usman Mohd Siddique
Journal: European Journal of Pharmaceutical Sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: CYP1A1 inhibitors; CYP1A1-mediated benzo[a]pyrene toxicity; CYP1B1 inhibitors; Cisplatin resistance; Hard to metabolize medications
Affiliations: CYP Design Ltd, The Innovation Centre, 49 Oxford Street, Leicester LE1 5XY, UK., Department of Pharmaceutical Sciences & Technology, Birla Institute of Technology, Mesra, Ranchi 835215, India., Medicinal Chemistry Division, CSIR - Indian Institute of Integrative Medicine, Canal Road, Jammu 180001, India., CYP Design Ltd, The Innovation Centre, 49 Oxford Street, Leicester LE1 5XY, UK. Electronic address: .

Abstract:  Microsomal cytochrome P450 (CYP) enzymes, isolated from recombinant bacterial/insect/yeast cells, are extensively used for drug metabolism studies. However, they may not always portray how a developmental drug would behave in human cells with intact intracellular transport mechanisms. This study emphasizes the usefulness of human HEK293 kidney cells, grown in 'suspension' for expression of CYPs, in finding potent CYP1A1/CYP1B1 inhibitors, as possible anticancer agents. With live cell-based assays, quinazolinones 9i/9b were found to be selective CYP1A1/CYP1B1 inhibitors with IC50 values of 30/21 nM, and &gt; 150-fold selectivity over CYP2/3 enzymes, whereas they were far less active using commercially-available CYP1A1/CYP1B1 microsomal enzymes (IC50, &gt;10/1.3-1.7 μM). Compound 9i prevented CYP1A1-mediated benzo[a]pyrene-toxicity in normal fibroblasts whereas 9b completely reversed cisplatin resistance in PC-3/prostate, COR-L23/lung, MIAPaCa-2/pancreatic and LS174T/colon cancer cells, underlining the human-cell-assays' potential. Our results indicate that the most potent CYP1A1/CYP1B1 inhibitors would not have been identified if one had relied merely on microsomal enzymes. 

Retracted: No

PubPeer comments:
 In figures 1A, 2A, 7C and 7D the same actin controls are used for cultured cells (HEK and EC) and tissues (aorta and kidney). ![file] ![file] ![file] ![file] ,
Intracellular delivery of doxorubicin encapsulated in novel pH-responsive chitosan/heparin nanocapsules
Authors: Dipshikha Chakravortty
Krishna Radhakrishnan
Divya P Gnanadhas
Ashok M Raichur
Midhun B Thomas
Journal: International Journal of Nanomedicine (2013)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: biocompatible; drug delivery; electrostatic interaction; layer-by-layer.
Affiliations: Department of Materials Engineering, Indian Institute of Science, Bangalore, India.

Abstract:  A novel polyelectrolyte nanocapsule system composed of biopolymers, chitosan and heparin has been fabricated by the layer-by-layer technique on silica nanoparticles followed by dissolution of the silica core. The nanocapsules were of the size range 200 ± 20 nm and loaded with the positively charged anticancer drug doxorubicin with an efficiency of 89%. The loading of the drug into the capsule happens by virtue of the pH-responsive property of the capsule wall, which is determined by the pKa of the polyelectrolytes. As the pH is varied, about 64% of the drug is released in acidic pH while 77% is released in neutral pH. The biocompatibility, efficiency of drug loading, and enhanced bioavailability of the capsule system was confirmed by MTT assay and in vivo biodistribution studies. 

Retracted: No

PubPeer comments:
 Much more similar than expected ![file] ,
Dexmedetomidine attenuates ischemia and reperfusion-induced cardiomyocyte injury through p53 and forkhead box O3a (FOXO3a)/p53-upregulated modulator of apoptosis (PUMA) signaling signaling
Authors: Feng Yun Yang
He Dong
Yan Zheng
Lu Zhang
Journal: Bioengineered (2022)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Dexmedetomidine; apoptosis; forkhead box o3a; ischemia and reperfusion; p53
Affiliations: Departments of Anesthesiology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China, Emergency, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China, Operating Room, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China

Abstract:  Dexmedetomidine (DEX) has been reported to attenuate the ischemia and reperfusion (I/R) induced cardiomyocyte apoptosis. However, mechanisms underlying these protective effect remain to be fully elucidated. Cardiomyocyte apoptosis is associated with ischemic heart disease. Here we investigated the role of DEX in I/R -induced cardiomyocyte apoptosis. Mice and H9c2 cardiomyocyte cells were subjected to cardiomyocyte I/R injury and hypoxia/reoxygenation (H/R) injury, respectively. The roles and mechanisms of DEX on H9c2 cardiomyocyte cells and mice cardiomyocyte cells exposured to H/R or I/R injury were explored. The results showed that DEX attenuates H/R injury-induced H9c2 cell apoptosis and alleviated mitochondrial oxidative stress; it also reduced myocardial infarct size and protected the cardiac function following cardiomyocyte I/R injury. In addition, H/R and I/R injury increased p53 expression and forkhead box O3a (FOXO3a)/p53-upregulated modulator of apoptosis (PUMA) signaling in H9c2 cardiomyocyte cells and cardiomyocytes. Targeting p53 expression or FOXO3a/PUMA signaling inhibited cell apoptosis and protected against H/R injury in H9c2 cardiomyocyte cells and cardiomyocytes. Pretreatment with DEX reduced the H/R or I/R injury-induced activation of p53 expression and FOXO3a/PUMA signaling, and alleviated H/R or I/R injury-induced apoptosis and mitochondrial oxidative stress. Therefore, DEX could alleviate H/R- or I/R-induced cardiomyocytes injury by reducing cell apoptosis and blocking p53 expression and FOXO3a/PUMA signaling. Targeting p53 or/and FOXO3a/PUMA signaling could alleviate cardiomyocyte I/R injury. 

Retracted: No

PubPeer comments:
 Fig 3A:  P-JAK2 and p-STAT protein content in myocardial cells stimulated by Ang II at 5 min, 30 min, 2 h, and 24 h detected via Western blotting. At right, Fig 4A C:  Bax [Bcl-2] protein content in myocardial cells stimulated by Ang II for 24 h in Cont group, Ang II group, Losartan group and Losartan + Ang II group detected via Western blotting . Loading control appears to be the same in both figures, despite different lanes. Background details emphasised in high-contrast version below. ![file] ,
An activated mTOR/p70S6K signaling pathway in esophageal squamous cell carcinoma cell lines and inhibition of the pathway by rapamycin and siRNA against mTOR
Authors: Lexun Xue
Tianli Fan
Yanli Xue
Zhaoming Lu
Guiqin Hou
Fang Tian
Journal: Cancer letters (2007)
Discipline: CLINICAL MEDICINE
Keywords: mTOR; p70S6K; pathway; esophageal squamous cell carcinoma; ESCC
Affiliations: Laboratory for Cell Biology, The First Affiliated Hospital, Zhengzhou University, 40 Daxue Road, Zhengzhou, Henan 450052, PR China.

Abstract:  mTOR/p70S6K pathway is considered a central regulator in various malignant tumors, but its roles in esophageal squamous cell carcinoma (ESCC), which is a common cause of mortality in China, remain unknown. Here, we identify that the mTOR/p70S6K pathway is activated in ESCC; rapamycin and siRNA against mTOR rapidly inhibited expression of mTOR and the phosphorylation of its major downstream effectors, p70S6K and 4E-BP1, arrested cells in the G(0)/G(1) phase and induced apoptosis of ESCC cells. The findings may lay a foundation for making further investigations on the mTOR/p70S6K pathway as a potential target for ESCC therapy. 

Retracted: No

PubPeer comments:
null, 
 This is great news! ,
miR-124 functions as a tumor suppressor in the endometrial carcinoma cell line HEC-1B partly by suppressing STAT3
Authors: Xin Liu
Kui Hong
Yang Shen
Tingting Huang
Zhongzu Zhang
Wenfeng He
Qing Cao
Xiuxia Liu
Yunyun Li
Journal: Molecular and Cellular Biochemistry (2014)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: MicroRNAs; miR-124; endometrial carcinoma; cell proliferation; migration
Affiliations: Department of Gynecology and Obstetrics, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, People's Republic of China.

Abstract:  MicroRNAs (miRNAs) play an important role in the development and progression of endometrial carcinoma (EC). Recently, several studies have shown that microRNA-124 (miR-124) is downregulated in various cancers, which can affect tumor initiation and maintenance. However, the effects of miR-124 on EC are largely unknown. In this study, we identified the under-expression of miR-124 in 35 paired EC tissues and adjacent normal tissues. Further, functional experiments found that ectopic expression of miR-124 markedly suppressed cell proliferation, migration, and invasion of EC cells. It also induced cell apoptosis and G1-phase cell cycle arrest. Moreover, we identified signal transducer and activator of transcription 3 (STAT3) as a direct target of miR-124, and over expression of miR-124 not only induced changes in STAT3 expression but also altered expression of its target genes, cyclin D2 and matrix metalloproteinase 2, in the human endometrial carcinoma cell line HEC-1B. In addition to targeting STAT3 directly, we found that miR-124 suppresses phosphorylation of STAT3 through targeting IL-6R indirectly. Restored STAT3 expression through treatment with IL-6 cytokine partly abolished miR-124-mediated cell cycle arrest and apoptosis induction. These results combined with the tumorigenetic role of STAT3 in HEC-1B cells suggest that the antitumor effects of miR-124 are achieved, at least partly, through down regulation of STAT3 mRNA and its downstream target genes. Therefore, inhibition of constitutively activated STAT3 by ectopic expression of miR-124 in EC may provide a novel therapeutic strategy for the treatment of EC. 

Retracted: No

PubPeer comments:
 Figure 5 appears to have some image overlap ![file] , 
 #1 Fig 5 again: ![file] Possible overlap with a panel of Fig 3. ![file] ,
Microalgae immobilization: current techniques and uses
Authors: Ignacio Moreno-Garrido
Journal: Bioresource Technology (2008)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: immobilization techniques; biotechnology; microalgae; growth; metabolism
Affiliations: Institute of Marine Sciences of Andalucía (CSIC), Campus Río San Pedro, s/n 11510, Puerto Real, Cádiz, Spain. 

Abstract:  Information about advances in immobilization techniques and biotechnology use of freshwater and marine microalgae is scattered. This work aims to bring together the main recent research about the topic. Passive and active immobilization techniques used on microalgae are listed and described in the text. Effect of immobilization on growth and metabolism of the cells is also reviewed. Current uses of immobilized microalgae include metabolite production, culture collection handling, obtaining of energy and removing of undesired or valuable substances from media (nutrients, metals and different pollutant agents). Applications of immobilized microalgae in environmental aquatic research have been recently increased: novel immobilization techniques as well as the use of living microalgae as biosensors in electronic devices designed to measure toxicity of substances and effluents demonstrated to be a very promising topic in biotechnology research. Recent research pointed out the advantages of mixed bacterial-algal co-immobilized systems in water treatment plants. Application of immobilized systems to the production of non-contaminant energy (as H(2) obtained from algal cultures) is also an important topic to be explored in the next years. 

Retracted: No

PubPeer comments:
 This review article has described immobilization methods in algae very broadly. The article is published in 2008. However while going through the literature I found another article I can say maybe copy and paste some parts of 2008 article by Ignacio Moreno-Garrido. I attached the link of other article too. Maybe the author would like to check. From text to section titles and conclusion I found some similarities in the flow. J. Algal Biomass Utln. 2016, 7 (2): 122- 128 Applications of immobilized algae ,
Tumor necrosis factor-like weak inducer of apoptosis attenuates the action of insulin in hepatocytes
Authors: Feng Feng
Lijun Wang
Nathaniel Albanese
Andrew Holmes
Pu Xia
Journal: Endocrinology (2008)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: TWEAK; insulin resistance; hepatocytes; Akt phosphorylation; Fn14
Affiliations: Signal Transduction Laboratory, Centenary Institute, Locked Bag 6, Newtown, New South Wales 2042, Australia.

Abstract:  TNF-like weak inducer of apoptosis (TWEAK), a relatively new member of the TNF superfamily, is an important immune/inflammatory regulator that has different functional properties from that of other members of this superfamily. We report herein that TWEAK induces cellular insulin resistance in both human hepatocellular carcinoma cell lines (Huh7 and HepG2) and primary rat hepatocytes by inhibiting both early insulin receptor (IR) signaling events and the downstream actions of insulin. TWEAK profoundly inhibited insulin-induced Akt phosphorylation in both a concentration- and time-dependent manner. This inhibitory effect occurred via mechanisms that involved the TWEAK receptor Fn14 and the activation of the canonical and noncanonical nuclear factor-kappaB signaling pathways. Furthermore, TWEAK significantly inhibited IRbeta autophosphorylation and IR substrate-1 activation, with concomitant increases in serine phosphorylation of IR substrate-1. Moreover, insulin-induced reduction of gluconeogenic enzyme gene expression and increases in glycogen synthesis in hepatocytes were significantly attenuated by TWEAK treatment. Therefore, these findings not only reveal a novel pathophysiological function of TWEAK/Fn14 but also uncover a new player that may contribute to the development of cellular insulin resistance in hepatocytes. 

Retracted: No

PubPeer comments:
null, 
 Fig.2 pairs of actin bands look more similar than expected. ![file] ,
Intestinal trefoil factor activates the PI3K/Akt signaling pathway to protect gastric mucosal epithelium from damage
Authors: Yi Ren
Hongmei Liu
Wei Zhang
Zhizhou Yang
Zhaorui Sun
Baodi Sun
Jinfeng Lin
Danbing Shao
Shinan Nie
Min Xu
Journal: International journal of oncology (2014)
Discipline: CLINICAL MEDICINE
Keywords: Intestinal trefoil factor; TFF3; cell survival; cell migration; mucosal epithelial integrity
Affiliations: Department of Emergency, Jinling Hospital, Medical School of Nanjing University, Nanjing 210002, P.R. China.

Abstract:  Intestinal trefoil factor (ITF, also named as trefoil factor 3, TFF3) is a member of the TFF-domain peptide family, which plays an essential role in the regulation of cell survival, cell migration and maintains mucosal epithelial integrity in the gastrointestinal tract. However, the underlying mechanisms and associated molecules remain unclear. The aim of this study was to explore the protective effects of ITF on gastric mucosal epithelium injury and its possible molecular mechanisms of action. In the present study, we show that ITF was able to promote the proliferation and migration of GES-1 cells via a mechanism that involves the PI3K/Akt signaling pathway. Western blot results indicated that ITF induced a dose- and time-dependent increase in the Akt signaling pathway. ITF also plays an essential role in the restitution of GES-1 cell damage induced by lipopolysaccharide (LPS). LPS induced the apoptosis of GES-1 cells, decreased cell viability significantly (P&lt;0.01) and led to epithelial tight junction damage, which is attenuated via ITF treatment. The protective effect of ITF on the integrity of GES-1 was abrogated by inhibition of the PI3K/Akt pathway. Taken together, our results demonstrate that ITF promotes the proliferation and migration of gastric mucosal epithelial cells and preserves gastric mucosal epithelial integrity after damage is mediated by activation of the PI3K/Akt signaling pathway. This study suggested that the PI3K/Akt pathway could act as a key intracellular pathway in the gastric mucosal epithelium that may serve as a therapeutic target to preserve epithelial integrity during injury. 

Retracted: No

PubPeer comments:
 Figure 1C and 3C. * Green boxes: Unexpected overlapping panels. * Red and blue boxes might represent the same experiments. ![file] , 
 Figure 5. * Yellow boxes: Two panels representing different experiments appear to show an overlap ![file] ,
A surveillance pathway monitors the fitness of the endoplasmic reticulum to control its inheritance
Authors: Joel Tourtellotte
Alicia A Bicknell
Maho Niwa
Anna Babour
Journal: Cell (2010)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Endoplasmic reticulum; ER stress; MAP kinase Slt2; ERSU pathway; unfolded protein response
Affiliations: Division of Biological Sciences, Section of Molecular Biology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0377, USA.

Abstract:  The endoplasmic reticulum (ER) plays an essential role in the production of lipids and secretory proteins. Because the ER cannot be generated de novo, it must be faithfully transmitted or divided at each cell division. Little is known of how cells monitor the functionality of the ER during the cell cycle or how this regulates inheritance. We report here that ER stress in S. cerevisiae activates the MAP kinase Slt2 in a new ER stress surveillance (ERSU) pathway, independent of the unfolded protein response. Upon ER stress, ERSU alters the septin complex to delay ER inheritance and cytokinesis. In the absence of Slt2 kinase, the stressed ER is transmitted to the daughter cell, causing the death of both mother and daughter cells. Furthermore, Slt2 is activated via the cell surface receptor Wsc1 by a previously undescribed mechanism. We conclude that the ERSU pathway ensures inheritance of a functional ER. 

Retracted: No

PubPeer comments:
 Comparison between Fig. 3C and Fig. 6A u2013 more similar than expected. Could authors check and or provide the raw data please? ![file] ,
Porcine reproductive and respiratory syndrome virus nonstructural protein 4 induces apoptosis dependent on its 3C-like serine protease activity
Authors: Zhitao Ma
Haiyan Zhao
Jun Tang
Ao-Tian Xu
Wen-hai Feng
Yalan Wang
Yongqiang Wang
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: Porcine reproductive and respiratory syndrome; PRRS virus; nsp4; apoptosis; caspase-3
Affiliations: State Key Laboratory of Agrobiotechnology, China Agricultural University, Beijing, China.

Abstract:  Porcine reproductive and respiratory syndrome (PRRS) is a highly contagious disease in pigs caused by PRRS virus (PRRSV). Although PRRSV infection-induced cell apoptosis has been established, the related viral protein is still unknown. Here, we reported that PRRSV nonstructural protein 4 (nsp4) was a critical apoptosis inducer. Nsp4 could activate caspase-3, -8, and -9. Using truncated constructs without different domains in nsp4, we demonstrated that the full-length of nsp4 structure was required for its apoptosis-inducing activity. Furthermore, using site-directed mutagenesis to inactivate the 3C-like serine protease activity of nsp4, we showed that nsp4-induced apoptosis was dependent on its serine protease activity. The ability of nsp4 to induce apoptosis was significantly impaired by His39, Asp64, and Ser118 mutations, suggesting that His39, Asp64, and Ser118 were essential for nsp4 to trigger apoptosis. In conclusion, our present work showed that PRRSV nsp4 could induce apoptosis in host cells and might be partially responsible for the apoptosis induced by PRRSV infection. PRRSV 3C-like protease-mediated apoptosis represents the first report in the genus Arterivirus, family Arteriviridae. 

Retracted: No

PubPeer comments:
null, 
 February 2020 correction at https: journals.plos.org plosone article?id=10.1371 journal.pone.0230086.  After this article [1] was published, concerns were raised about similarities between flow cytometry results reported in the following figure panels: * pCDNA3.1 and NSP4 panels in Fig 3A * MID and C157 panels in Fig 5C The authors noted that due to figure preparation errors the pCDNA3.1 and MID dot plots were mistakenly duplicated in the NSP4 and C157 panels, respectively. These errors are addressed in the revised Figs 3 and 5 provided here, in which the NSP4 (Fig 3A) and C157 (Fig 5C) panels have been replaced with the correct plots from the original experiments. The underlying data for Figs 3A and 5C are no longer available. A member of PLOS ONEu2019s Editorial Board advised that the updated figures support the results as reported in the original article. The original data are available upon request from the corresponding author for Figs 1B, 3B, 3C, 4A, 4E, 5E, 6B, 6E. The original underlying data to support the other results in the article are not available, although the authors can provide supporting data for Figs 1A, 2A and 3D that were obtained in replication experiments. The authors apologize for the errors in the published figures. ,
Cellular and humoral immune responses in the early stages of diabetic nephropathy in NOD mice
Authors: Bin Ma
Ningwen Tai
Li Wen
Li Chen
Peng Zhao
F Susan Wong
Xiaoyan Xiao
Baojun Dong
Journal: Journal of Autoimmunity (2009)
Discipline: IMMUNOLOGY
Keywords: immunopathology; diabetic nephropathy; NOD mice; cellular immunity; humoral immunity
Affiliations: Section of Endocrinology, Department of Internal Medicine, Yale School of Medicine, New Haven, CT 06520, USA.

Abstract:  This study was designed to examine immunopathology of diabetic nephropathy in non-obese diabetic (NOD) mice and to investigate the involvement of cellular and humoral immunity at various time points after diabetes onset. We found that the glomeruli of diabetic NOD mice were infiltrated with T and B cells, as well as CD11c+ dendritic cells, which had close contact with CD4+ and CD8+ T cells in the infiltrates. We also found that IgG deposits in the glomeruli of diabetic NOD mice were accompanied by the presence of complement C3. Moreover, the serum from diabetic mice contained autoantibodies directed towards components of the glomeruli and these antibodies were not present in non-diabetic NOD mice. The immune changes in the kidney occurred together with increasing kidney weight and urinary albumin excretion along with duration of diabetes. We provide evidence that infiltrating lymphocytes and anti-kidney autoantibodies may be involved in diabetic nephropathy in autoimmune diabetes in the NOD mouse. Understanding the role that the immune system plays in the pathogenesis of diabetic nephropathy could lead to identification of new strategies and/or additional therapeutic targets for prevention and treatment of diabetic nephropathy. 

Retracted: No

PubPeer comments:
 Figure 7A. * Red boxes: Two panels appear to show an overlap. Reported to the journal in October 2015, with a reminder in November 2016, but the journal has not taken any action. ![file] ,
Quercetin sensitizes glioblastoma to t-AUCB by dual inhibition of Hsp27 and COX-2 in vitro and in vivo
Authors: Chao Tang
Youwu Fan
Liwen Li
Rujun Li
Junyang Li
Journal: Journal of Experimental & Clinical Cancer Research (2016)
Discipline: CLINICAL MEDICINE
Keywords: Cyclooxygenase 2; Glioma; Heat shock protein 27; Inhibitor; Soluble epoxide hydrolase.
Affiliations: Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, 305 East Zhongshan Road, Nanjing City, 210002, Jiangsu Province, China. ., Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, 305 East Zhongshan Road, Nanjing City, 210002, Jiangsu Province, China., Department of Neurosurgery, Second Affiliated Hospital of Soochow University, 1055 Sanxiang Road, Suzhou, 215004, China.

Abstract:  Background: Evidences indicate that inflammatory process plays pivotal role in tumor disease. Soluble epoxide hydrolase inhibitors (sEHIs) have been shown to participate in anti-inflammation and tumorigenesis by protecting epoxyeicosatrienoic acids (EETs). Although we have previously revealed some effects of t-AUCB on glioma in vitro, further investigations are needed to demonstrate its effects on glioblastoma growth in vivo and how to strengthen its antitumor effect. Methods: CCK-8 kit was used to test cell growth. Cell migration capacity was performed by wound healing assays. Transwell assay was used to test cell invasion potency. Cell-cycle analysis and cell apoptosis was performed by flow cytometry. The activity of caspase-3 in cells was measured using caspase-3 activity assay kits. Total RNA was extracted from cells lysated by TRIzol reagent. qRT-PCR was performed by ABI 7500 fast RT- PCR system. Lipofectamine RNAiMAX Transfection Reagent (Invitrogen) was used for siRNA transfection. Western blootting was used to test protein expression. Tumor cell xenograft mouse models were used for in vivo study. The SPSS version 17.0 software was applied for statistical analysis. Results: Our data shown that t-AUCB inhibits cell proliferation, migration and invasion and induces cell cycle G1 phase arrest in vitro but induces no cell apoptosis; increased Hsp27 activation and following COX-2 overexpression confer resistance to t-AUCB treatment in glioblastoma both in vitro and in vivo; quercetin sensitizes glioblastoma to t-AUCB by dual inhibition of Hsp27 and COX-2 in vitro and in vivo. Conclusions: These results indicate that combination of t-AUCB and quercetin may be a potential approach to treating glioblastoma. 

Retracted: No

PubPeer comments:
 Can someone review the Forest plots for accuracy, itu2019s possible they are reversed ,
Orphan nuclear receptor Nur77 induces zinc finger protein GIOT-1 gene expression, and GIOT-1 acts as a novel corepressor of orphan nuclear receptor SF-1 via recruitment of HDAC2
Authors: Kwang-Hoon Song
Hye-Jin Kim
Yong-Soo Lee
Yun-Yong Park
Hyun Kook
Hueng-Sik Choi
Keesook Lee
Hae Jin Kee
Cheol Yi Hong
In-Kyu Lee
Seung-Won Ahn
Journal: Journal of Biological Chemistry (2006)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Kruppel-associated box (KRAB); GIOT-1; orphan nuclear receptor; Nur77; SF-1
Affiliations: Hormone Research Center, School of Biological Sciences and Technology, Chonnam National University, Gwangju 500-757, Republic of Korea.

Abstract:  Kruppel-associated box (KRAB) domain-containing proteins consist of potential transcriptional repression modules. Previously, gonadotropin-inducible ovarian transcription factor-1 (GIOT-1) was identified as a novel KRAB-containing zinc finger protein and shown to have transcriptional repression activity. Here, we demonstrate that orphan nuclear receptor Nur77 regulates GIOT-1 gene expression in testicular Leydig cell lines and that GIOT-1 acts as a novel corepressor of the orphan nuclear receptor steroidogenic factor 1 (SF-1). Mutation analysis of the GIOT-1 promoter and overexpression analysis of dominant-negative Nur77 revealed that luteinizing hormone activates GIOT-1 gene expression through Nur77. Electrophoretic mobility shift and chromatin immunoprecipitation assays showed that Nur77 directly binds to the GIOT-1 promoter. GIOT-1 represses the SF-1 transactivation, and specific interaction between GIOT-1 and SF-1 was observed. We also demonstrate an interaction between GIOT-1 and histone deacetylase 2 (HDAC2). GIOT-1-mediated transrepression was recovered by down-regulation of HDAC2 expression with small interfering RNA of HDAC2. Knock down of the endogenous GIOT-1 results in significant enhancement of CYP17 expression in Leydig cells. In conclusion, this study of cross-talk between GIOT-1 and orphan nuclear receptors will provide new insights into the role of KRAB-containing zinc finger proteins in nuclear receptor action. 

Retracted: Yes

PubPeer comments:
 ![file] , 
 ![file] , 
 2019 retraction. http: www.jbc.org content 294 50 19448 This article has been withdrawn by the authors. The actin panels for siHDAC2-I and siHDAC2-IV in Fig. 7E were duplicated. Additionally, in Fig. 7E, a portion of the HDAC2 gel from siHDAC2-II was duplicated in siHDAC2-III and siHDAC2-IV. ,
NADH oxidase activity of mitochondrial apoptosis-inducing factor
Authors: L Ravagnan
D Haouzi
M L Peleato
P Costantini
G Brothers
J M Penninger
S A Susin
M D Miramar
L M Saraiva
G Kroemer
Journal: Journal of Biological Chemistry (2001)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Apoptosis-inducing factor; AIF; redox activity; NADH oxidase; FAD
Affiliations: Departamento de Bioquimica y Biologia Molecular y Celular. Universidad de Zaragoza, Plaza San Francisco s/n 50009 Zaragoza, Spain.

Abstract:  Apoptosis-inducing factor (AIF) is a mitochondrial flavoprotein, which translocates to the nucleus during apoptosis and causes chromatin condensation and large scale DNA fragmentation. Here we report the biochemical characterization of AIF's redox activity. Natural AIF purified from mitochondria and recombinant AIF purified from bacteria (AIFDelta1-120) exhibit NADH oxidase activity, whereas superoxide anion (O(2)(-)) is formed. AIFDelta1-120 is a monomer of 57 kDa containing 1 mol of noncovalently bound FAD/mol of protein. ApoAIFDelta1-120, which lacks FAD, has no NADH oxidase activity. However, native AIFDelta1-120, apoAIFDelta1-120, and the reconstituted (FAD-containing) holoAIFDelta1-120 protein exhibit a similar apoptosis-inducing potential when microinjected into the cytoplasm of intact cells. Inhibition of the redox function, by external addition of superoxide dismutase or covalent derivatization of FAD with diphenyleneiodonium, failed to affect the apoptogenic function of AIFDelta1-120 assessed on purified nuclei in a cell-free system. Conversely, blockade of the apoptogenic function of AIFDelta1-120 with the thiol reagent para- chloromercuriphenylsulfonic acid did not affect its NADH oxidase activity. Altogether, these data indicate that AIF has a marked oxidoreductase activity which can be dissociated from its apoptosis-inducing function. 

Retracted: No

PubPeer comments:
 Figure 8A. Much more similar than expected. https: imgur.com gRP0Ez7 , 
 Bands in Fig 8B also appear unexpectedly like mirror images ![file] ,
Varicella-zoster virus IE63 protein represses the basal transcription machinery by disorganizing the pre-initiation complex
Authors: Lionel Habran
Catherine Sadzot-Delvaux
Jacques Piette
Emmanuel Di Valentin
Alain Vanderplasschen
Nicolas Markine-Goriaynoff
Olivier Jolois
Sébastien Bontems
Journal: Biological chemistry (2005)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: transient transfection assays; varicella-zoster virus (VZV); IE63 protein; promoters; repression
Affiliations: Laboratory of Virology and Immunology, University of Liège, B-4000 Liège, Belgium.

Abstract:  Using transient transfection assays, regulation properties of varicella-zoster virus (VZV)-encoded IE63 protein were analyzed on several VZV immediate early (ORF4), early (ORF28) and late (ORF67) promoters. IE63 was shown to repress the basal activity of most of the promoters tested in epithelial (Vero) and neuronal (ND7) cells to various extents. Trans-repressing activities were also observed on heterologous viral and cellular promoters. Since a construct carrying only a TATA box sequence and a series of wild-type or mutated interleukin (IL)-8 promoters was also repressed by IE63, the role of upstream regulatory elements was ruled out. Importantly, the basal activity of a TATA-less promoter was not affected by IE63. Using a series of IE63 deletion constructs, amino acids 151-213 were shown to be essential to the trans-repressing activity in Vero cells, while in ND7 cells the essential region extended to a much larger carboxy-terminal part of the protein. We also demonstrate that IE63 is capable of disrupting the transcriptional pre-initiation complex and of interacting with several general transcription factors. The central and carboxy-terminal domains of IE63 are important for these effects. Altogether, these results demonstrate that IE63 protein is a transcriptional repressor whose activity is directed towards general transcription factors. 

Retracted: No

PubPeer comments:
 Figure 6B. https: imgur.com lk0iKrj ,