PReD-Bench/PRed-Bench huggingface dataset:
β-Caryophyllene, a natural sesquiterpene, modulates carbohydrate metabolism in streptozotocin-induced diabetic rats
Authors: Rafeek Hidhayath Basha
Chandrasekaran Sankaranarayanan
Journal: Acta Histochemica (2014)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Glycogen synthase; Hexokinase; Phosphoenolpyruvate carboxykinase; Streptozotocin; β-Caryophyllene.
Affiliations: Department of Biochemistry and Biotechnology, Annamalai University, Annamalainagar 608 002, Tamil Nadu, India., Department of Biochemistry and Biotechnology, Annamalai University, Annamalainagar 608 002, Tamil Nadu, India. Electronic address: .

Abstract:  The study was designed to evaluate the antihyperglycemic effects of β-caryophyllene (BCP), a natural sesquiterpene from spices on streptozotocin (STZ) induced diabetic rats. Diabetes mellitus was induced by a single intraperitoneal injection of STZ (40 mg/kg b.w.) in adult male Wistar rats. Diabetic rats exhibited an increase in glucose and HbA1c with a significant fall in insulin and hemoglobin levels. Aberrations in carbohydrate metabolic enzymes were noticed in liver, kidney and skeletal muscle of diabetic rats. A fall in liver and skeletal muscle glycogen with alterations in glycogen synthase and phosphorylase activities was also observed. Oral administration of BCP in dose dependent manner and glibenclamide (600 μg/kg b.w.), a standard oral hypoglycemic drug to diabetic rats for 45 days significantly decreased glucose with increased plasma insulin levels and ameliorated the altered activities of carbohydrate metabolic enzymes to near normal. The insulinotropic effect of BCP was supported by immunohistochemical studies. BCP at a dose of 200mg/kg b.w. exerted significant antidiabetic effects than other two doses (100 and 400mg/kg b.w.). We conclude that administration of BCP has beneficial effects in glucose homeostasis in diabetic rats. 

Retracted: No

PubPeer comments:
 Concern about Figure 6. Each panel represents pancreatic tissue from a differently treated rat. However, all panels in this figure contain repetitive elements, which is a very unexpected finding in natural biological tissues. Let s start with the figure as it appears in the paper and then focus on the individual panels one by one. ![file] * Panel A, repetitive elements highlighted: ![file] * Panel B, repetitive elements highlighted: ![file] * Panel C, repetitive elements highlighted: ![file] * Panel D, repetitive elements highlighted: ![file] * Panel E, repetitive elements highlighted: ![file] * Panel F, repetitive elements highlighted: ![file] * Panel G, repetitive elements highlighted: ![file] Could the authors please explain what happened here? ,
Taming interfacial electronic properties of platinum nanoparticles on vacancy-abundant boron nitride nanosheets for enhanced catalysis
Authors: Katie L Browning
Mingxia Zhou
Wenshuai Zhu
Bin Liu
Huiyuan Zhu
Guo Shiou Foo
Zili Wu
Peiwen Wu
Xiang Gao
Gabriel M Veith
Huaming Li
Ho Nyung Lee
Sheng Dai
Journal: Nature Communications (2017)
Discipline: Multidisciplinary
Keywords: Pt nanoparticles; interfacial electronic effects; hexagonal boron nitride nanosheets; vacancies; CO oxidation catalysis
Affiliations: School of Chemistry and Chemical Engineering, Institute for Energy Research, Jiangsu University, Zhenjiang 212013, China., Chemical Sciences Division, Oak Ridge National Laboratory, Oak Ridge, Tennessee 37831, USA., Materials Science and Technology Division, Oak Ridge National Laboratory, Oak Ridge, Tennessee 37831, USA., Department of Chemical Engineering, Kansas State University, Manhattan, Kansas 66506, USA., Institute for Energy Research, Jiangsu University, Zhenjiang 212013, China.

Abstract:  Taming interfacial electronic effects on Pt nanoparticles modulated by their concomitants has emerged as an intriguing approach to optimize Pt catalytic performance. Here, we report Pt nanoparticles assembled on vacancy-abundant hexagonal boron nitride nanosheets and their use as a model catalyst to embrace an interfacial electronic effect on Pt induced by the nanosheets with N-vacancies and B-vacancies for superior CO oxidation catalysis. Experimental results indicate that strong interaction exists between Pt and the vacancies. Bader charge analysis shows that with Pt on B-vacancies, the nanosheets serve as a Lewis acid to accept electrons from Pt, and on the contrary, when Pt sits on N-vacancies, the nanosheets act as a Lewis base for donating electrons to Pt. The overall-electronic effect demonstrates an electron-rich feature of Pt after assembling on hexagonal boron nitride nanosheets. Such an interfacial electronic effect makes Pt favour the adsorption of O2, alleviating CO poisoning and promoting the catalysis. 

Retracted: No

PubPeer comments:
 I am curious about how the red fitting line obtained based on such noise level? From my perspective this fitting is quite subjective and unable to resolve the Pt peaks. ![file] , 
 The weak signal of Pt is due to the very low loading of Pt on SiO2. Based on analyses of the chemical environment of Pt in Pt SiO2 and the original data, the signal can be fitted into 4 peaks (two groups), being assigned to Pt0 4f5 2, Pt0 4f7 2, Pt2+ 4f5 2, and Pt2+ 4f7 2. In the raw data, the noise level was very high. The curve was smoothed for further analysis, as shown in the figure (green line). ![file] The detailed fitting process: The XPS peak fitting was realized by XPSPEAK 4.1. The original data was imported into the software, and the selected fitting range was selected from the binding energy from 68.19 eV to 77.29 eV. Afterward, a straight baseline was added. Subsequently, 4 peaks at 74.35, 71.15, 75.90, and 72.70 eV were added, and the peak type was selected as u201cfu201d. Afterward, all peaks were optimized, and the screenshot of the fitting is shown below: ![file] ,
The protective role of a small GTPase RhoE against UVB-induced DNA damage in keratinocytes
Authors: Sarah A Boswell
Paul Nghiem
Sam W Lee
Pat P Ongusaha
Journal: Journal of Biological Chemistry (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: RhoE; p53; keratinocytes; UVB; GTPases
Affiliations: Dermatology Division, University of Washington, Seattle, Washington 98109., Cutaneous Biology Research Center (CBRC), Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129 and the., Cutaneous Biology Research Center (CBRC), Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129 and the. Electronic address: .

Abstract:  RhoE, a p53 target gene, was identified as a critical factor for the survival of human keratinocytes in response to UVB. The Rho family of GTPases regulates many aspects of cellular behavior through alterations to the actin cytoskeleton, acting as molecular switches cycling between the active, GTP-bound and the inactive, GDP-bound conformations. Unlike typical Rho family proteins, RhoE (also known as Rnd3) is GTPase-deficient and thus expected to be constitutively active. In this study, we investigated the response of cultured human keratinocyte cells to UVB irradiation. RhoE protein levels increase upon exposure to UVB, and ablation of RhoE induction through small interfering RNA resulted in a significant increase in apoptosis and a reduction in the levels of the pro-survival targets p21, Cox-2, and cyclin D1, as well as an increase of reactive oxygen species levels when compared with control cells. These data indicate that RhoE is a pro-survival factor acting upstream of p38, JNK, p21, and cyclin D1. HaCat cells expressing small interfering RNA to p53 indicate that RhoE functions independently of its known associates, p53 and Rho-associated kinase I (ROCK I). Targeted expression of RhoE in epidermis using skin-specific transgenic mouse model resulted in a significant reduction in the number of apoptotic cells following UVB irradiation. Thus, RhoE induction counteracts UVB-induced apoptosis and may serve as a novel target for the prevention of UVB-induced photodamage regardless of p53 status. 

Retracted: No

PubPeer comments:
null, 
null, 
null, 
null, 
null, 
 Identified by another reader. *** ![file] , 
 **[Attorney asks Retraction Watch to remove post because client has lost out on opportunities.] ** ,
Synergistic effect of gefitinib and rofecoxib in mesothelioma cells
Authors: Ada Sacchi
Claudia Canino
Alfonso Baldi
Rossella Galati
Irene Cardillo
Alessandra Verdina
Daniela Stoppoloni
Journal: Molecular Cancer (2010)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Malignant mesothelioma; EGFR; COX-2; inhibitors; cell lines
Affiliations: Department for the Development of Therapeutic Programs, Laboratory D, Centro Ricerca Sperimentale, Regina Elena Cancer Institute, Via delle Messi D'Oro 156, 00158 Rome, Italy.

Abstract:  Background: Malignant mesothelioma (MM) is an aggressive tumor that is resistant to conventional modes of treatment with chemotherapy, surgery or radiation. Research into the molecular pathways involved in the development of MM should yield information that will guide therapeutic decisions. Epidermal growth factor receptor (EGFR) and cyclooxygenase-2 (COX-2) are involved in the carcinogenesis of MM. Combination of COX-2 and EGFR inhibitors, therefore, could be an effective strategy for reducing cell growth in those lines expressing the two molecular markers. Results: In order to verify the effect of COX-2 and EGFR inhibitors, five MM cell lines NCI-2452, MPP89, Ist-Mes-1, Ist-Mes-2 and MSTO-211 were characterized for COX-2 and EGFR and then treated with respective inhibitors (rofecoxib and gefitinib) alone and in combination. Only MPP89, Ist-Mes-1 and Ist-Mes-2 were sensitive to rofecoxib and showed growth-inhibition upon gefitinib treatment. The combination of two drugs demonstrated synergistic effects on cell killing only in Ist-Mes-2, the cell line that was more sensitive to gefitinib and rofecoxib alone. Down-regulation of COX-2, EGFR, p-EGFR and up-regulation of p21 and p27 were found in Ist-Mes-2, after treatment with single agents and in combination. In contrast, association of two drugs resulted in antagonistic effect in Ist-Mes-1 and MPP89. In these cell lines after rofecoxib exposition, only an evident reduction of p-AKT was observed. No change in p-AKT in Ist-Mes-1 and MPP89 was observed after treatment with gefitinib alone and in combination with rofecoxib. Conclusions: Gefitinib and rofecoxib exert cell type-specific effects that vary between different MM cells. Total EGFR expression and downstream signalling does not correlate with gefitinib sensitivity. These data suggest that the effect of gefitinib can be potentiated by rofecoxib in MM cell lines where AKT is not activated. 

Retracted: No

PubPeer comments:
null, 
 Figure 3E * Blue boxes: The three Actin panels appear to look rather similar, albeit shown at different orientations ![file] ,
S14G-humanin alleviates insulin resistance and increases autophagy in neurons of APP/PS1 transgenic mouse
Authors: Xiuli Shang
Ning Jia
Yi Zhong
Kun Han
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: APP/PS1 transgenic mice; Alzheimer's disease; S14G-humanin; autophagy; insulin resistance.
Affiliations: Department of Neurology, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning, People's Republic of China., Department of Neurology, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning, People's Republic of China.

Abstract:  Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by Aβ plaque deposition in the brain, which is related to the disorder of autophagosome maturation, transport, and formation of autolysosome. Notably, abnormal insulin signaling is connected with cognitive dysfunction in AD. In this study, using APP/PS1 transgenic mice as AD model, we investigated the mechanism by which S14G-humanin (HNG) improved autophagy and insulin signaling in AD brain. Immunohistochemistry was used to determine the levels of mTOR and Aβ deposition, and Western blot analysis was used to determine IRS-1, IRS-1 pSEr636, ULK1, p62, LC3 I/LC3 II protein levels. Our results demonstrated that HNG could improve the learning ability and memory in APP/PS1 transgenic mice, possibly through decreasing IRS-1 Ser636 phosphorylation and mTOR protein expression in the hippocampus, thus improving insulin resistance in the brain. In addition, HNG increased ULK1 expression, decreased p62 and LC3 I/LC3 II protein levels, thus enhancing autophagy and decreasing Aβ deposition in the brain. Taken together, our results suggest that through the regulation of IRS-1/mTOR insulin signaling in the hippocampus, HNG increases the activity of autophagy and decreases Aβ deposition in the brain, and improves learning ability and memory of AD mice. 

Retracted: No

PubPeer comments:
  Fig. 5 HNG treatment reduced Auf062 plaque deposition in the hippocampus. (A) Immunohistochemistry analysis of Auf062 level in hippocampus slides of HNG treated untreated APP PS1 transgenic mice and wild type C57BL 6J mice Two of the slides overlap, despite labels that identify them as coming from different mice representing the  Tg HNG-L and Tg HNG-H groups. ![file] ,
Role of the translationally controlled tumor protein in DNA damage sensing and repair
Authors: Edouard I Azzam
Debkumar Pain
Guozheng Guo
Badri N Pandey
Hong Li
Sonia M de Toledo
Jie Zhang
Journal: Proceedings of the National Academy of Sciences of the United States of America (2012)
Discipline: Multidisciplinary
Keywords: TCTP; DNA damage; ATM kinase; DNA repair; γ rays
Affiliations: Departments of Radiology, Pharmacology and Physiology, and Biochemistry and Molecular Biology, New Jersey Medical School Cancer Center, University of Medicine and Dentistry of New Jersey, Newark, NJ 07103.

Abstract:  The translationally controlled tumor protein (TCTP) is essential for survival by mechanisms that as yet are incompletely defined. Here we describe an important role of TCTP in response to DNA damage. Upon exposure of normal human cells to low-dose γ rays, the TCTP protein level was greatly increased, with a significant enrichment in nuclei. TCTP up-regulation occurred in a manner dependent on ataxia-telangiectasia mutated (ATM) kinase and the DNA-dependent protein kinase and was associated with protective effects against DNA damage. In chromatin of irradiated cells, coimmunoprecipitation experiments showed that TCTP forms a complex with ATM and γH2A.X, in agreement with its distinct localization with the foci of the DNA damage-marker proteins γH2A.X, 53BP1, and P-ATM. In cells lacking TCTP, repair of chromosomal damage induced by γ rays was compromised significantly. TCTP also was shown to interact with p53 and the DNA-binding subunits, Ku70 and Ku80, of DNA-dependent protein kinase. TCTP knockdown led to decreased levels of Ku70 and Ku80 in nuclei of irradiated cells and attenuated their DNA-binding activity. It also attenuated the radiation-induced G(1) delay but prolonged the G(2) delay. TCTP therefore may play a critical role in maintaining genomic integrity in response to DNA-damaging agents. 

Retracted: No

PubPeer comments:
 Identified by another reader. *** ![file] ,
Understanding the diversity of genetic outcomes from CRISPR-Cas generated homology-directed repair
Authors: Amanda M Hewes
Eric B Kmiec
Brett M Sansbury
Journal: Communications biology (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: CRISPR-Cas systems; CRISPR-Cas9 genome editing; DNA damage and repair.
Affiliations: 1Gene Editing Institute, Helen F. Graham Cancer Center & Research Institute, Christiana Care Health System, Newark, DE USA., 2Department of Medical and Molecular Sciences, University of Delaware, Newark, DE USA.

Abstract:  As CRISPR-Cas systems advance toward clinical application, it is essential to identify all the outcomes of gene-editing activity in human cells. Reports highlighting the remarkable success of homology-directed repair (HDR) in the treatment of inherited diseases may inadvertently underreport the collateral activity of this remarkable technology. We are utilizing an in vitro gene-editing system in which a CRISPR-Cas complex provides the double-stranded cleavage and a mammalian cell-free extract provides the enzymatic activity to promote non-homologous end joining, micro-homology mediated end joining, and homology-directed repair. Here, we detail the broad spectrum of gene-editing reaction outcomes utilizing Cas9 and Cas12a in combination with single-stranded donor templates of the sense and nonsense polarity. This system offers the opportunity to see the range of outcomes of gene-editing reactions in an unbiased fashion, detailing the distribution of DNA repair outcomes as a function of a set of genetic tools. 

Retracted: No

PubPeer comments:
 Another paper that warns of the significant off-targets in CRISPR - one has to read deep to get that, it is not mentioned explicitly in the abstract. A better place is this [interview] :  it shows there may be many more unintended changes to DNA around the site of a CRISPR repair than previously thought,u201d said Eric Kmiec, PhD, director of Christiana Careu2019s Gene Editing Institute My analysis shows [off-targets away from the edit site] are much higher. And that because there are [100ks possible targets] for any gRNA. ,
Peripherally administrated prions reach the brain at sub-infectious quantities in experimental hamsters
Authors: Claudio Soto
Baian Chen
Rodrigo Morales
Journal: FEBS Letters (2014)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: 263K; Prion; Protein Misfolding Cyclic Amplification (PMCA); Syrian hamster.
Affiliations: Protein Misfolding Disorders Laboratory, Mitchell Center for Alzheimer's Disease and Related Brain Disorders, University of Texas Medical School at Houston, Houston, TX 77030, USA; Department of Laboratory Animal Science, School of Basic Medical Science, Capital Medical University, Beijing 100069, China., Protein Misfolding Disorders Laboratory, Mitchell Center for Alzheimer's Disease and Related Brain Disorders, University of Texas Medical School at Houston, Houston, TX 77030, USA., Protein Misfolding Disorders Laboratory, Mitchell Center for Alzheimer's Disease and Related Brain Disorders, University of Texas Medical School at Houston, Houston, TX 77030, USA. Electronic address: .

Abstract:  The mechanisms implicated in prion infection and tissue distribution are not completely understood. In this study we investigated the levels of 263K prions in brain and spleen of Syrian hamsters few days after intra-peritoneal challenge. For this purpose we utilized the PMCA technology which permits to detect as little as few PrP(Sc) molecules. Our results show that peripherally administered prions directly reach the brain, although at levels below the minimum necessary to produce disease. PrP(Sc) remains in the brain several days after administration suggesting inefficient clearance or early replication. Understanding the fate of the infectious agent after administration and its uptake in different organs and fluids may provide useful information to develop strategies to minimize further spreading of prion diseases. 

Retracted: No

PubPeer comments:
 Correction https: febs.onlinelibrary.wiley.com doi epdf 10.1016 j.febslet.2014.06.039 ,
Fusion proteins comprising a Fusarium-specific antibody linked to antifungal peptides protect plants against a fungal pathogen
Authors: Yu-Cai Liao
Rainer Fischer
Dieter Peschen
He-Ping Li
Fritz Kreuzaler
Journal: Nature Biotechnology (2004)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: recombinant antibodies; pathogen-specific antigens; crop protection; fusion proteins; antifungal peptides
Affiliations: Institut für Biologie VII (Molekulare Biotechnologie), RWTH Aachen, D-52074 Aachen, Germany.

Abstract:  In planta expression of recombinant antibodies recognizing pathogen-specific antigens has been proposed as a strategy for crop protection. We report the expression of fusion proteins comprising a Fusarium-specific recombinant antibody linked to one of three antifungal peptides (AFPs) as a method for protecting plants against fungal diseases. A chicken-derived single-chain antibody specific to antigens displayed on the Fusarium cell surface was isolated from a pooled immunocompetent phage display library. This recombinant antibody inhibited fungal growth in vitro when fused to any of the three AFPs. Expression of the fusion proteins in transgenic Arabidopsis thaliana plants conferred high levels of protection against Fusarium oxysporum f.sp. matthiolae, whereas plants expressing either the fungus-specific antibody or AFPs alone exhibited only moderate resistance. Our results demonstrate that antibody fusion proteins may be used as effective and versatile tools for the protection of crop plants against fungal infection. 

Retracted: No

PubPeer comments:
 Figure 1: when contrast is enhanced signs of manipulation seem to appear. Could the authors please comment and post the uncropped scan of the blot? ![file] ,
Immunoglobulin immobilized liposomal constructs for transmucosal vaccination through nasal route
Authors: Gauravkant Saraogi
Himanshu Agrawal
Narendra Lariya
Abhinav Agarwal
Govind P Agrawal
Anil K Kharya
Brajesh Tiwari
Journal: Journal of liposome research (2011)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: surface-engineered vesicular carriers; mucosal immunization; nasal route; IgG antibody; hepatitis B surface antigen (HBsAg)
Affiliations: Department of Pharmaceutical Sciences, Pharmaceutics Research Laboratory, Dr. H.S. Gour University, Sagar, India.

Abstract:  The aim of the present investigation was to evaluate the prospective of surface-engineered vesicular carriers for mucosal immunization via the nasal route. IgG antibody was immobilized on the surface of hepatitis B surface antigen (HBsAg) antigen-loaded liposomes. The developed formulations were characterized on the basis of physicochemical parameters, such as morphology, particle size, polydispersity index, entrapment efficiency, and zeta potential. Liposomal formulations were then evaluated for in-process antigen stability and storage stability. In vivo studies were conducted to visualize targeting potential, localization pattern, and immunogenicity. In addition, immune response was compared with alum-HBsAg vaccine injected intramuscularly. The serum anti-HBsAg titer, obtained from the postnasal administration of IgG-coupled liposomes, was significantly higher than plain liposomes. Moreover, IgG-coupled liposomes generated both humoral (i.e., systemic and mucosal) and cellular immune responses upon nasal administration, while the alum-adsorbed antigen displayed neither cellular (cytokine level) nor mucosal (IgA) response. The formulation also displayed enhanced transmucosal transport, improved in vitro stability, and effective immunoadjuvant property. To conclude, IgG antibody-coupled liposomes may serve as novel carriers to augment the secretory immune response of antigen encapsulated in the liposomes, apparently by escalating liposome uptake via M cells, thereby rationalizing their use as a carrier adjuvant for nasal subunit vaccines. 

Retracted: No

PubPeer comments:
 Figure 1. Photomicrograph of (A) plain liposomes (B) antibody coupled liposomes. ![file] Two surprisingly similar liposomes in 1(B). , 
  Figure 4. SDS-PAGE of protein antigen from different liposomal formulations. Lane A, molecular weight marker; lane B, pure antigen HBsAg; lane C, antigen HBsAg from plain liposomal formulation; lane D, protein HBsAg and antibody IgG from antibody conjugated liposomal formulation. At right: Fig 3 from [Tiwari et al (2011)] ,  Molecular characterization of antigen-(A) SDS-PAGE analysis-Lane A: pure HBsAg; Lane B: encapsulated HBsAg in liposome; Lane C: pure HA; Lane D: HA complexed liposomes formulation. ![file] Blots are the same in the same three right-hand lanes. Has one or other been edited? , 
 #2 I guess you meant  same three left-hand lanes ? , 
 #3 Whoops, you re right. ![file] , 
 #1 ![] ![file] ,
Retracted: Long non‐coding RNA TP73‐AS1 facilitates progression and radioresistance in lung cancer cells by the miR‐216a‐5p / CUL4B axis with exosome involvement
Authors: Conghua Xie
Tienan Yi
Kai Yang
Huibing Qiu
Yan Gong
Lingyun Zhang
Journal: Thoracic Cancer (2021)
Discipline: CLINICAL MEDICINE
Keywords: Retraction; Long non-coding RNA; TP73-AS1; Progression; Radioresistance
Affiliations: Department of Radiation and Medical Oncology Zhongnan Hospital of Wuhan University  Wuhan China, Xiangyang Central Hospital Affiliated Hospital of Hubei University of Arts and Science  Xiangyang China, Department of Biological Repositories Zhongnan Hospital of Wuhan University  Wuhan China, Hubei Key Laboratory of Tumor Biological Behaviors Zhongnan Hospital of Wuhan University  Wuhan China, Hubei Cancer Clinical Study Center Zhongnan Hospital of Wuhan University  Wuhan China

Abstract:  Retraction: Qiu, H., Zhang, L., Yi, T., Yang, K., Gong, Y. and Xie, C. (2020), Long non-coding RNA TP73-AS1 facilitates progression and radioresistance in lung cancer cells by the miR-216a-5p/CUL4B axis with exosome involvement. Thorac Cancer. https://doi.org/10.1111/1759-7714.13602 The above article, published online on 25 August 2020 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement among the authors, the journal Editor in Chief Qinghua Zhou, and John Wiley &amp; Sons Ltd. The retraction has been agreed after the results reported in Figures 3B, 3C, 3I, and 3J were found to be not repeatable in authors' further study. 

Retracted: No

PubPeer comments:
 Retracted (no separate retraction note).  The above article, published online on 25 August 2020 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement among the authors, the journal Editor in Chief Qinghua Zhou, and John Wiley Sons Ltd. The retraction has been agreed after the results reported in Figures 3B, 3C, 3I, and 3J were found to be not repeatable in authors further study. Figs 2G H,  The apoptotic rate was determined by flow cytometry . ![file] For comparison: Fig 2G of [Jiang et al (2020)] **[retracted on authors request]** ![] Fig 2C of [Gong Zhu (2020)] **[retracted for papermill origins]**. ![] ,
Chimeric STAR receptors using TCR machinery mediate robust responses against solid tumors
Authors: Jiasheng Wang
Yue Liu
Song Lin
Xin Lin
Guangna Liu
Xueqiang Zhao
Zhe-Yu Zheng
Xin Wu
Zhi-Xiao Zhou
Wei Rui
Daosheng Huang
Lemei Jia
Liqun Zhou
Journal: Science Translational Medicine (2021)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: CAR-T cell therapies; B cell malignancies; solid tumors; chimeric receptor; synthetic T cell receptor
Affiliations: Institute for Immunology and School of Medicine, Tsinghua University, Beijing 100084, China., China Immunotech (Beijing) Biotechnology Co., Ltd, Beijing 102206, China., Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China.

Abstract:  Chimeric antigen receptor T (CAR-T) cell therapies have demonstrated high response rate and durable disease control for the treatment of B cell malignancies. However, in the case of solid tumors, CAR-T cells have shown limited efficacy, which is partially attributed to intrinsic defects in CAR signaling. Here, we construct a double-chain chimeric receptor, termed as synthetic T cell receptor (TCR) and antigen receptor (STAR), which incorporates antigen-recognition domain of antibody and constant regions of TCR that engage endogenous CD3 signaling machinery. Under antigen-free conditions, STAR does not trigger tonic signaling, which has been reported to cause exhaustion of traditional CAR-T cells. Upon antigen stimulation, STAR mediates strong and sensitive TCR-like signaling, and STAR-T cells exhibit less susceptibility to dysfunction and better proliferation than traditional 28zCAR-T cells. In addition, STAR-T cells show higher antigen sensitivity than CAR-T cells, which holds potential to reduce the risk of antigen loss-induced tumor relapse in clinical use. In multiple solid tumor models, STAR-T cells prominently outperformed BBzCAR-T cells and generated better or equipotent antitumor effects to 28zCAR-T cells without causing notable toxicity. With these favorable features endowed by native TCR-like signaling, STAR-T cells may provide clinical benefit in treating refractory solid tumors. 

Retracted: No

PubPeer comments:
  Phosphorylation of ITAMs by the Src family kinase Lck initiates downstream T cell signaling , how could this MHC independent construct induce Phosphorylation of ITAM in TCR complex? ,
REV-ERBα integrates colon clock with experimental colitis through regulation of NF-κB/NLRP3 axis
Authors: Yanke Lin
Xue Yuan
Shuai Wang
Lianxia Guo
Baojian Wu
Feng Li
Journal: Nature Communications (2018)
Discipline: Multidisciplinary
Keywords: Rev-erbα; circadian clock; colonic inflammation; DSS-induced colitis; clock genes
Affiliations: Reserach Center for Biopharmaceutics and Pharmacokinetics, College of Pharmacy, Jinan University, Guangzhou, 510632, China., Guangdong Province Key Laboratory of Pharmacodynamic Constituents of TCM and New Drugs Research, Jinan University, Guangzhou, 510632, China., Guangzhou Jinan Biomedicine Research and Development Center, Jinan University, Guangzhou, 510632, China., Reserach Center for Biopharmaceutics and Pharmacokinetics, College of Pharmacy, Jinan University, Guangzhou, 510632, China. ., Guangdong Province Key Laboratory of Pharmacodynamic Constituents of TCM and New Drugs Research, Jinan University, Guangzhou, 510632, China. .

Abstract:  The roles of Rev-erbα and circadian clock in colonic inflammation remain unclarified. Here we show colon clock genes (including Rev-erbα) are dysregulated in mice with DSS-induced colitis. In turn, disruption of the circadian clock exacerbates experimental colitis. Rev-erbα-deficient mice are more sensitive to DSS-induced colitis, supporting a critical role of Rev-erbα in disease development. Further, Rev-erbα ablation causes activation of Nlrp3 inflammasome in mice. Cell-based experiments reveal Rev-erbα inactivates Nlrp3 inflammasome mainly at the priming stage. Rev-erbα directly represses Nlrp3 transcription through specific binding to the promoter region. Additionally, Rev-erbα represses p65 transcription and indirectly repressed Nlrp3 via the NF-κB pathway. Interestingly, Rev-erbα activation in wild-type mice by SR9009 attenuates DSS-induced colitis, whereas the protective effects are lost in Nlrp3-/- and Rev-erbα-/- mice. Taken together, Rev-erbα regulates experimental colitis through its repressive action on the NF-κB/Nlrp3 axis. Targeting Rev-erbα may represent a promising approach for prevention and management of colitis. 

Retracted: No

PubPeer comments:
 It is unreasonable of which described in Methods that  Reads were aligned to the hg38 genome using Maximal Mappable Prefix method by STAR (v2.5.1b) . Of note, all the samples subjected to RNA-sequencing are isolated from mice, why their sequencing data can be aligned to the hg38. Such error needs to be present clearly! ,
ABCG2-overexpressing H460/MX20 cell xenografts in athymic nude mice maintained original biochemical and cytological characteristics
Authors: Fang Wang
Likun Chen
Furong Li
Zhen Chen
Xiaokun Wang
Wei Zhang
Liwu Fu
Journal: Scientific Reports (2017)
Discipline: Multidisciplinary
Keywords: H460/MX20; multidrug resistance; ABCG2; xenografts; cell proliferation
Affiliations: Experimental Animal Center, Sun Yat-sen University, Guangzhou, 510080, China., Collaborative Innovation Center for Cancer Medicine, State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou 510060, China., Guangdong Esophageal Cancer Institute, Guangzhou, 510060, China.

Abstract:  H460/MX20 are derived from large cell lung cancer H460 cell line and then transformed into ABCG2-overexpressing cells by mitoxantrone's induction, which are widely used in study of multidrug resistance (MDR) in vitro. To establish and spread the model of H460/MX20 cell xenografts, we investigated whether cell biological characteristics and the MDR phenotype were maintained in vivo model. Our results demonstrated that the cell proliferation, cell cycle, and ABCG2 expression level in xH460/MX20 cells isolated from H460/MX20 cell xenografts were similar to H460/MX20 cells in vitro. Importantly, xH460/MX20 cells exhibited high levels of resistance to ABCG2 substrates such as mitoxantrone and topotecan as H460/MX20 cells did. Furthermore, lapatinib, the inhibitor of ABCG2, potently reversed mitoxantrone- and topotecan-resistance of xH460/MX20 cells. Taken together, these results suggest that H460/MX20 cell xenografts in athymic nude mice still retain their original cytological characteristics and MDR phenotype. Thus, the H460/MX20 cell xenografts model could serve as a sound model in vivo for study on reversal MDR. 

Retracted: No

PubPeer comments:
 On the Figure 1D, H460 cell xenograft and H460 MX20 were shown as same group of mice. Even all the posture of animals (eg. tails) are same.![] , 
 #1 ![file] ,
Exosome secretion, including the DNA damage-induced p53-dependent secretory pathway, is severely compromised in TSAP6/Steap3-null mice
Authors: L Blanc
A Lespagnol
C Beekman
D Duflaut
A Telerman
M Vidal
G Fiucci
J-C Marine
R Amson
Journal: Cell death and differentiation (2008)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: TSAP6; p53; protein secretion; TCTP; glycosylated protein
Affiliations: Laboratoire de Biotechnologie et Pharmacologie génétique Appliquée (LBPA), Ecole Normale Supérieure, Cachan, France.

Abstract:  TSAP6 (tumor suppressor-activated pathway 6), also known as Steap3, is a direct p53 transcriptional target gene. It regulates protein secretion, for example translationally controlled tumor protein (TCTP), which is implicated in tumor reversion. In keeping with the latter, we show herein that TSAP6 is a glycosylated protein present in the trans-Golgi network, endosomal-vesicular compartment and cytoplasmic membrane. To further investigate the physiological function of TSAP6, we have generated TSAP6-deficient mice. These mice exhibit microcytic anemia with abnormal reticulocyte maturation and deficient transferrin receptor downregulation, a process known to be dependent on exosomal secretion. Moreover, we provide direct evidence that exosome production is severely compromised in TSAP6-null cells. Finally, we show that the DNA damage-induced p53-dependent nonclassical exosomal secretory pathway is abrogated in TSAP6-null cells. Given the fact that exosomes are used as cell-free vaccines against cancer and that they could be involved in the biogenesis and spread of human immunodeficiency virus, it is important to understand their regulation. The results presented here provide the first genetic demonstration that exosome formation is a tightly controlled biological process dependent of TSAP6. 

Retracted: No

PubPeer comments:
 Figure 3d. Much more similar than expected. https: imgur.com ZU8rODh ,
Neutrophil Adhesion and Transmigration through Bovine Endothelial Cells in vitro by Protein H and LPS of Pasteurella Multocida
Authors: M Galdiero
A Folgore
I Nuzzo
E Galdiero
Journal: Immunobiology (2000)
Discipline: IMMUNOLOGY
Keywords: Pasteurella multocida; neutrophil adhesion; migration; protein H; LPS

Abstract:  This study describes an in vitro investigation on the role of Pasteurella multocida cells and its isolated protein H and LPS on neutrophil adhesion and migration through bovine endothelial cell monolayers. P. multicoda cells, protein H and LPS increased the adhesion and transmigration of neutrophils through BAEC. The bacteria/cell ratio of 100 for P. multocida, protein H concentration 0.05-0.2 microM and LPS concentration 0.5-1.0 microM respectively, induced the maximum adhesion and transmigration of neutrophils through BAEC. The optimal time of incubation with bacteria or bacterial products was 4-6 h. Our results confirm the role of Gram-negative bacteria and of components of the outer membrane such as protein H or LPS in activating the neutrophils and in promoting the adhesion and cells transmigration from the vessels to the site of inflammation. 

Retracted: No

PubPeer comments:
 Two sets of plots in Figure I appear to be repeated. While there should be some overlap, these appear identical. *** ![file] ,
A novel CXCR3-B chemokine receptor-induced growth-inhibitory signal in cancer cells is mediated through the regulation of Bach-1 protein and Nrf2 protein nuclear translocation
Authors: Murugabaskar Balan
Soumitro Pal
Journal: Journal of Biological Chemistry (2014)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Apoptosis; Chemokines; Heme Oxygenase; Nrf2; Nuclear Transport
Affiliations: From the Division of Nephrology, Boston Children's Hospital, Boston, Massachusetts 02115 and.

Abstract:  Chemokines and their receptors play diverse roles in regulating cancer growth and progression. The receptor CXCR3 can have two splice variants with opposite functions. CXCR3-A promotes cell growth, whereas CXCR3-B mediates growth-inhibitory signals. However, the negative signals through CXCR3-B in cancer cells are not well characterized. In this study, we found that CXCR3-B-mediated signaling in MCF-7 and T47D breast cancer cells induced apoptotic cell death. Signals through CXCR3-B decreased the levels of the antiapoptotic proteins Bcl-2 and Bcl-xL and increased the expression of apoptotic cleaved poly(ADP-ribose) polymerase. Along with up-regulation in apoptosis, CXCR3-B signals were associated with a decrease in cellular autophagy with reduced levels of the autophagic markers Beclin-1 and LC3B. Notably, CXCR3-B down-regulated the expression of the cytoprotective and antiapoptotic molecule heme oxygenase-1 (HO-1) at the transcriptional level. There was an increased nuclear localization of Bach-1 and nuclear export of Nrf2, which are important negative and positive transcription factors, respectively, for HO-1 expression. We also observed that CXCR3-B promoted the activation of p38 MAPK and the inhibition of ERK-1/2. CXCR3-B could not induce cancer cell apoptosis at the optimal level when we either inhibited p38 activity or knocked down Bach-1. Further, CXCR3-B-induced apoptosis was down-regulated when we overexpressed HO-1. Together, our data suggest that CXCR3-B mediates a growth-inhibitory signal in breast cancer cells through the modulations of nuclear translocation of Bach-1 and Nrf2 and down-regulation of HO-1. We suggest that the induction of CXCR3-B-mediated signaling can serve as a novel therapeutic approach where the goal is to promote tumor cell apoptosis. 

Retracted: No

PubPeer comments:
 Green boxes: The FACS dot plots are unexpected similar in different groups of Fig.6C. ![file] , 
 2020 correction. https: www.jbc.org content 295 30 10509.short There was an error in Fig 6C. The dot plot in panel 1 (Control siRNA + Vector) was mistakenly duplicated with the dot plot in panel 4 (Bach-1 siRNA + CXCR3-B). However, the numbers of the % apoptotic cells were correct. This error happened inadvertently during the preparation of the figure panels. This error has now been corrected and does not affect the results or conclusions of the work reported in this study. The authors apologize for this error. ,
Immune-mediated myelitis following hepatitis B vaccination
Authors: Joerg-Patrick Stübgen
Journal: Autoimmunity Reviews (2012)
Discipline: IMMUNOLOGY
Keywords: Hepatitis B virus; HBV vaccines; immune-mediated myelitis; autoimmune events; causal relationship
Affiliations: Department of Neurology and Neuroscience, Weill Cornell Medical College/New York Presbyterian Hospital, NY 10065-4885, USA. 

Abstract:  The hepatitis B virus (HBV) is an important international cause of infectious acute and chronic liver diseases. HBV vaccines were developed to combat the potential life-threatening effects of HBV infection. Published case histories, retrospective reviews and analyses of epidemiological data report on the onset of immune-mediated myelitis after recombinant HBV vaccination, mostly in adults with a presumed genetic/immunologic predisposition. However, HBV vaccination has not borne out to be a significant trigger of serious autoimmune events, including acute myelitis, in populations at large over prolonged observation periods after immunization. Published study methods lack the sensitivity to categorically establish a causal relationship between exposure to HBV vaccine components and immune mediated myelitis, but in practice the faint possibility of such a link should not be totally rejected. 

Retracted: No

PubPeer comments:
  [R]ecombinant hepatitis B virus (HBV) vaccines ... have been associated with diverse adverse events, and **are the second most common vaccines reported to the US Vaccine Adverse Events Reporting System** [VAERS] (www.hrsa.gov vaccinecompensation index.html). In a recent multi-analysis review of literature case reports of acute myelitis following immunization, HBV vaccines were the most common vaccines associated with acute myelitis [14]. I can t find any breakdown of reports by vaccine types at the provided link. Is there any other source for this claim? Citation 14 is  Transverse myelitis and vaccines: a multi-analysis [(Agmon-Levin et al 2009)] , which states that * HBV vaccine... has been associated with many adverse events, and is the second most common vaccine reported to the USA Vaccine Adverse Events Report System.29 * No effective source was provided, and I haven t been able to find one. ,
The Breast Cancer Tumor Suppressor TRIM29 Is Expressed via ATM-dependent Signaling in Response to Hypoxia
Authors: W Stratford May
Kevin D Brown
W Scott Streitfeld
Lingbao Ai
Tsz Ching Chloe Tang
Muzaffer Dükel
Lindsey R F Backman
Journal: Journal of Biological Chemistry (2016)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: breast cancer; cell signaling; hypoxia; hypoxia-inducible factor (HIF); tumor suppressor gene.
Affiliations: From the Departments of Biochemistry and Molecular Biology and., Medicine, University of Florida College of Medicine, Gainesville, Florida 32610., From the Departments of Biochemistry and Molecular Biology and .

Abstract:  Reduced ATM function has been linked to breast cancer risk, and the TRIM29 protein is an emerging breast cancer tumor suppressor. Here we show that, in cultured breast tumor and non-tumorigenic mammary epithelial cells, TRIM29 is up-regulated in response to hypoxic stress but not DNA damage. Hypoxia-induced up-regulation of TRIM29 is dependent upon ATM and HIF1α and occurs through increased transcription of the TRIM29 gene. Basal expression of TRIM29 is also down-regulated in cells expressing diminished levels of ATM, and findings suggest that this occurs through basal NF-κB activity as knockdown of the NF-κB subunit RelA suppresses TRIM29 abundance. We have previously shown that the activity of the TWIST1 oncogene is antagonized by TRIM29 and now show that TRIM29 is necessary to block the up-regulation of TWIST1 that occurs in response to hypoxic stress. This study establishes TRIM29 as a hypoxia-induced tumor suppressor gene and provides a novel molecular mechanism for ATM-dependent breast cancer suppression. 

Retracted: No

PubPeer comments:
 Nice work, but I have a question as to why the Mm2 and Mm4 constituents are missing from the source code. These are nodal satellites to the primary Mm3 = Mm(27.55d) constituent, at least in the top 10 in terms of strength. Mm2 = Mm+D - F + M Mm4 = Mm- D + F - M see Ray Erofeeva https: agupubs.onlinelibrary.wiley.com doi 10.1002 2013JB010830 These factors are also missing from the NASA JPL Horizons ephemeris output. ,
Influence of nanoparticles size, per cent mass ratio, and temperature on the thermal properties of water-based MgO–ZnO nanofluid: an experimental approach
Authors: Giwa, S. O.
Momin, M.
Nwaokocha, C. N.
Sharifpur, M.
Meyer, J. P.
Journal: Journal of Thermal Analysis and Calorimetry (2021)
Discipline: CHEMISTRY
Keywords: nanoparticles size; per cent mass ratio; temperature; thermal properties; MgO-ZnO/deionised water nanofluids

Abstract: This paper experiments the trio influence of nanoparticles size (NS), per cent mass ratio (PWR), and temperature (T) on the thermal properties of MgO–ZnO/deionised water (DIW) nanofluids. MgO nanoparticles (20&nbsp;nm and 100&nbsp;nm) were hybridised with ZnO nanoparticles (20&nbsp;nm) and suspended in DIW to formulate 0.1&nbsp;vol% hybrid nanofluids at PWRs of 20:80, 40:60, 60:40, and 80:20 (MgO/ZnO). The pH, electrical conductivity (σ), viscosity (μ), and thermal conductivity (κ) of the hybrid nanofluids were experimentally determined at temperatures of 20–50&nbsp;°C. The stability was monitored, while the morphology was examined using standard instruments. Findings showed that the suspension of the hybrid nanoparticles enhanced the pH and thermal properties of DIW. The hybrid nanofluids with 100&nbsp;nm-MgO nanoparticles were observed to possess slightly higher values of pH, σ, and μ than those with 20&nbsp;nm-MgO nanoparticles except for κ. An increase in temperature augmented κ and σ of MgO–ZnO/DIW nanofluids, while it detracted pH and μ. Maximum enhancements of 453.70–550.62% (40:60), 14.95–22.33% (40:60), and 8.29–17.46% (60:40) were evaluated for σ, κ, and μ, respectively. The influence of PWR, NS, and temperature on the σ, κ, μ, and pH of the hybrid nanofluids was in the order of PWR\u2009&gt;\u2009NS\u2009&gt;\u2009T, NS\u2009&gt;\u2009PWR\u2009&gt;\u2009T, T\u2009&gt;\u2009NS\u2009&gt;\u2009PWR, and T\u2009&gt;\u2009NS\u2009&gt;\u2009PWR, respectively. Subject to the experimental data obtained, correlations were developed for each hybrid nanofluid and thermal property as a function of temperature. The MgO–ZnO/DIW nanofluids with a 40:60 PWR appeared to be the best in terms of heat transfer capability.

Retracted: No

PubPeer comments:
 No references and or legends for the TEM images in Figure 5! Marker bars are damaged and not visible! ![file] ,
CitE Enzymes Are Essential for Mycobacterium tuberculosis to Establish Infection in Macrophages and Guinea Pigs
Authors: Ramandeep Singh
Deepika Chaudhary
Saqib Kidwai
Garima Arora
Deepak Sharma
Journal: Frontiers in Cellular and Infection Microbiology (2018)
Discipline: MICROBIOLOGY
Keywords: Mycobacterium tuberculosis; oxidative stress; reverse TCA; virulence; β-subunit of citrate lyase.
Affiliations: Tuberculosis Research Laboratory, Vaccine and Infectious Disease Research Centre, Translational Health Science and Technology Institute, Faridabad, India., Symbiosis School of Biological Sciences, Symbiosis International University, Lavale, India., Manipal Academy of Higher Education, Manipal, India., Department of Biotechnology, Indian Institute of Technology Roorkee, Roorkee, India.

Abstract:  Bacterial citrate lyase activity has been demonstrated in various eukaryotes, bacteria and archaea, underscoring their importance in energy metabolism of the cell. While the bacterial citrate lyase comprises of three different subunits, M. tuberculosis genome lacks CitD and CitF subunits of citrate lyase complex but encodes for 2 homologs of CitE subunits, Rv2498c and Rv3075c. Using temperature sensitive mycobacteriophages, we were able to generate both single and double citE mutant strains of M. tuberculosis. The survival experiments revealed increased susceptibility of the double mutant strain to oxidative stress in comparison to the parental strain. Also, simultaneous deletion of both citE1 and citE2 in M. tuberculosis genome resulted in impairment of intracellular replication in macrophages. The double mutant strain displayed reduced growth in lungs and spleens of guinea pigs. This is the first study demonstrating that M. tuberculosis critically requires CitE subunits of citrate lyase for pathogenesis. Taken together, these findings position these enzymes as potential targets for development of anti-tubercular small molecules. 

Retracted: No

PubPeer comments:
 In Tiwari et al., 2015, the wild type well is rigorously identical to the wt well from Arora et al., 2018 while the mazF396 well is rigorously identical to the ppx1 well from Tiwari et al., 2019. ![file] , 
 The wild type histology slides from Arora et al., 2018 look identical to the ones from Tiwari et al., 2019. Were controls using wild type materials actually performed for both of these experiments ? ![file] , 
 Thank you for bringing this to our attention. We have discussed and resolved this matter with the Editorial Office of the Journal. , 
 The corrigendum for this article is available at: https: doi.org 10.3389 fcimb.2020.587907 ,