PReD-Bench/PRed-Bench huggingface dataset:
Safety and Efficacy Profile of Echinacea purpurea to Prevent Common Cold Episodes: A Randomized, Double-Blind, Placebo-Controlled Trial
Authors: M Jawad
A Suter
R Eccles
R Schoop
P Klein
Journal: Evidence-based Complementary and Alternative Medicine (2012)
Discipline: CLINICAL MEDICINE
Keywords: Echinacea purpurea extract; common cold episodes; safety; efficacy; prevention
Affiliations: Common Cold Centre and Healthcare, Cardiff University, Cardiff CF10 3XQ, UK., Cardiff School of Biosciences, Common Cold Centre, The Sir Martin Evans Building, Museum Avenue, Cardiff CF10 3AX, UK, D. S. H. Statistical Services GmbH, 85296 Rohrbach, Germany, Common Cold Centre and Healthcare, Cardiff University, Cardiff CF10 3XQ, UK

Abstract:  Objective. To investigate the safety (risk) and efficacy (benefit) of Echinacea purpurea extract in the prevention of common cold episodes in a large population over a 4-month period. Methods. 755 healthy subjects were allocated to receive either an alcohol extract from freshly harvested E. purpurea (95% herba and 5% root) or placebo. Participants were required to record adverse events and to rate cold-related issues in a diary throughout the investigation period. Nasal secretions were sampled at acute colds and screened for viruses. Results. A total of 293 adverse events occurred with Echinacea and 306 with placebo treatment. Nine and 10% of participants experienced adverse events, which were at least possibly related to the study drug (adverse drug reactions). Thus, the safety of Echinacea was noninferior to placebo. Echinacea reduced the total number of cold episodes, cumulated episode days within the group, and pain-killer medicated episodes. Echinacea inhibited virally confirmed colds and especially prevented enveloped virus infections (P &lt; 0.05). Echinacea showed maximal effects on recurrent infections, and preventive effects increased with therapy compliance and adherence to the protocol. Conclusions. Compliant prophylactic intake of E. purpurea over a 4-month period appeared to provide a positive risk to benefit ratio. 

Retracted: No

PubPeer comments:
 R. Schoop and A. Suter are employees of A. Vogel Bioforce AG which is the company that produces the Echinacea preparation used in the trial. Their affiliation appears to have mistakenly been given as  Cardiff School of Biosciences . The conflict of interest statement is incomplete: **u201cProfessor R. Eccles, Dr. M. Jawad and P. Klein have no conflict of interests.u201d** But what about R. Schoop and A. Suter? Could any of the authors comment on why they didnu2019t declare the financial conflict of interest here? What (if any) was the role of A. Vogel Bioforce AG in this study (apart from supplying study materials)? Was there any other source of funding for the trial? ,
Synthesis and photocatalytic properties of visible-light-responsive, three-dimensional, flower-like La‚ÄìTiO2/g-C3N4 heterojunction composites
Authors: Shuaiqiang Jia
Yulin Zhang
Guozhe Sui
Boxin Li
Jinlong Li
Lijuan Du
Yan Zhuang
Zhiyong Xing
Journal: RSC Advances (2018)
Discipline: CHEMISTRY
Keywords: La-TiO2/g-C3N4; heterojunction; photocatalyst; solvothermal method; nanosheets
Affiliations: College of Chemistry and Chemical Engineering, Qiqihar University, Qiqihar 161006, China, College of Science, Northeast Agricultural University, Harbin

Abstract:  We prepared a new three-dimensional, flower-like La-TiO2/g-C3N4 (LaTiCN) heterojunction photocatalyst using a solvothermal method. Analysis and characterization were performed by conducting scanning electron microscopy, transmission electron microscopy, X-ray diffraction, X-ray photoelectron spectroscopy, Fourier transform-infrared spectroscopy, ultraviolet-visible spectrophotometry, and nitrogen adsorption and desorption. The prepared g-C3N4 nanosheets could reach 100 nm in size and covered the TiO2 surface. A tightly bound interface formed between the g-C3N4 and TiO2, speeding up the effective transfer of photo-induced electrons. In addition, the incorporation of La3+ reduced the electron-hole recombination efficiency. Consequently, the prepared La-TiO2/g-C3N4 composite material exhibited better visible-light catalytic activity than pure TiO2. 

Retracted: No

PubPeer comments:
 Figure 1 shows XRD patterns which are unexpectedly similar in some parts, but intensity of certain peaks is different.  ,
Novel high-affinity PPARgamma agonist alone and in combination with paclitaxel inhibits human anaplastic thyroid carcinoma tumor growth via p21WAF1/CIP1
Authors: B R Haugen
P A Kreinest
R C Smallridge
L A Marlow
J A Copland
S F Williams
J P Klopper
K Fujiwara
S Kurakata
A K C Wong
Journal: Oncogene (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: PPARgamma; agonist; antitumor activity; PAX8/PPARgamma fusion oncogene; tumor suppressor gene
Affiliations: Department of Cancer Biology, Mayo Clinic Comprehensive Cancer Center, Jacksonville, Florida 33224, USA. 

Abstract:  Peroxisome proliferator-activated receptor gamma (PPARgamma) agonists demonstrate antitumor activity likely through transactivating genes that regulate cell proliferation, apoptosis, and differentiation. The PAX8/PPARgamma fusion oncogene, which is common in human follicular thyroid carcinomas appears to act via dominant negative suppression of wild-type PPARgamma, suggesting that it may be a tumor suppressor gene in thyroid cells. We have identified a novel high-affinity PPARgamma agonist (RS5444) that is dependent upon PPARgamma for its biological activity. This is the first report of this molecule and its antitumor activity. In vitro, the IC50 for growth inhibition is approximately 0.8 nM while anaplastic thyroid carcinoma (ATC) tumor growth was inhibited three- to fourfold in nude mice. siRNA against PPARgamma and a pharmacological antagonist demonstrated that functional PPARgamma was required for growth inhibitory activity of RS5444. RS5444 upregulated the cell cycle kinase inhibitor, p21WAF1/CIP1. Silencing p21WAF1/CIP1 rendered cells insensitive to RS5444. RS5444 plus paclitaxel demonstrated additive antiproliferative activity in cell culture and minimal ATC tumor growth in vivo. RS5444 did not induce apoptosis but combined with paclitaxel, doubled the apoptotic index compared to that of paclitaxel. Our data indicate that functional PPARgamma is a molecular target for therapy in ATC. We demonstrated that RS5444, a thiazolidinedione (Tzd) derivative, alone or in combination with paclitaxel, may provide therapeutic benefit to patients diagnosed with ATC. 

Retracted: No

PubPeer comments:
  ,
COVID-19: beta-thalassemia subjects immunised?
Authors: Philippe Pierre P√©ba√ø
Edouard Lansiaux
Joachim Son-Forget
Jean-Laurent Picard
Journal: Medical Hypotheses (2020)
Discipline: CLINICAL MEDICINE
Keywords: Beta thalassemia; Correlation; Favipiravir; Heme; Immunization
Affiliations: Henry Warembourg Medicine School, Lille University, 59000 Lille, France. Electronic address: ., NexGen Analytics, 82801 Sheridan, WY, United States., Conservatoire National des Arts et M√©tiers, 75141 Paris, France., Assembl√©e Nationale, 75355 Paris, France.

Abstract:  The novel coronavirus pneumonia (COVID-19) is a contagious acute respiratory infectious disease whose causative agent has been demonstrated to be a novel virus of the coronavirus family, SARSCoV-2. A recent PRE-print study has showed a heme attack on the 1-beta chain of hemoglobin by COVID19. Beta-thalassemia results of a default in the hemoglobin beta-chain synthesis. 1,5% global population are heterozygotes for this disease. In this study, by a multiple linear regression, we have analyzed the evolution of COVID-19 infection in three Italian regions (Puglia, Sardinia, Sicilia) with different beta-thalassemic prevalences, in order to search a link. The results have showed that betathalassemic heterozygote population prevalence is correlated to immunity against COVID-19, by a regression. This paper is only for academic discussion, the hypotheses and conclusions needs to be confirmed by further research. 

Retracted: No

PubPeer comments:
 The article contains a supplementary data file, which is in fact an XML file with no content except: _u201cData will be made available on requestu201d_  This is not an acceptable practice. , 
 A tribute to the linear regression based on 3 points, shown in Figure 6, is made in the acknowledgement of https: www.journalajmah.com index.php AJMAH article view 30232, unfortunately without citing the present article.  , 
 #1 For having personally submitted an article to Medical Hypothses, this is checked by default if the author does not upload any additional files ,
Plk3 functions as an essential component of the hypoxia regulatory pathway by direct phosphorylation of HIF-1alpha
Authors: Wei Dai
Yixin Yao
Max Costa
Luo Lu
Dazhong Xu
Journal: Journal of Biological Chemistry (2010)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Plk3; cell cycle progression; stress responses; tumor-suppressing activity; angiogenesis
Affiliations: Department of Environmental Medicine and Pharmacology, New York University School of Medicine, Tuxedo, New York 10987, USA.

Abstract:  Polo-like kinase 3 (Plk3) plays an important role in the regulation of cell cycle progression and stress responses. Plk3 also has a tumor-suppressing activity as aging PLK3-null mice develop tumors in multiple organs. The growth of highly vascularized tumors in PLK3-null mice suggests a role for Plk3 in angiogenesis and cellular responses to hypoxia. By studying primary isogenic murine embryonic fibroblasts, we tested the hypothesis that Plk3 functions as a component in the hypoxia signaling pathway. PLK3(-/-) murine embryonic fibroblasts contained an enhanced level of HIF-1Œ± under hypoxic conditions. Immunoprecipitation and pulldown analyses revealed that Plk3 physically interacted with HIF-1Œ± under hypoxia. Purified recombinant Plk3, but not a kinase-defective mutant, phosphorylated HIF-1Œ± in vitro, resulting in a major mobility shift. Mass spectrometry identified two unique serine residues that were phosphorylated by Plk3. Moreover, ectopic expression followed by cycloheximide or pulse-chase treatment demonstrated that phospho-mutants exhibited a much longer half-life than the wild-type counterpart, strongly suggesting that Plk3 directly regulates HIF-1Œ± stability in vivo. Combined, our study identifies Plk3 as a new and essential player in the regulation of the hypoxia signaling pathway. 

Retracted: No

PubPeer comments:
null, 
 Identified by another reader. Possible recycled control band. ***  ,
Long non‚Äëcoding RNA transcribed from pseudogene PPIAP43 is associated with radiation sensitivity of small cell lung cancer cells
Authors: Shilong Wang
Jinming Yu
Journal: Oncology Letters (2019)
Discipline: CLINICAL MEDICINE
Keywords: Cyclophilin A; PPAP43; potential biomarker; radiation sensitivity; small cell lung cancer cell lines.
Affiliations: Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, P.R. China., Department of Radiation Oncology, Shandong Cancer Hospital Affiliated to Shandong University, Jinan, Shandong 250117, P.R. China., Department of Radiation Oncology, Shandong Cancer Hospital and Institute, Shandong Academy of Medical Sciences, Jinan, Shandong 250117, P.R. China.

Abstract:  Small cell lung cancer (SCLC) is a highly lethal disease. Although radiation therapy is effective for the majority of patients with SCLC, patient sensitivity to radiation varies. The lack of biomarkers impedes advances in targeting radiation-sensitive patients. In this study, the changes in transcription patterns of SCLC cell lines were evaluated with or without 2 Gy gamma radiation. The results demonstrated that peptidyl-prolyl cis-trans isomerase A pseudogene 43 (PPIAP43) transcription was increased 2-fold in cells irradiated with 2 Gy gamma radiation compared with unirradiated cells in pre-reported radio-sensitive sensitive cell lines H69, H128, H146, H209 and H187. These cells shared 259 upregulated and 96 downregulated RNA transcripts following radiation. Pre-reported less sensitive cell lines H526, D53, D114 and D153 in which PPIAP43 was not upregulated 2-fold following irradiation with 2 Gy gamma radiation compared with unirradiated cells, shared 3 upregulated and 9 downregulated RNA transcripts. The RNA transcript of PPIAP43 was aligned with the mRNA of peptidyl-prolyl cis-trans isomerase A (PPIA) at 2 sections (3,732 to 3,917 and 5,327 to 5,657 of the PPIA gene) and the sequences were shown to be 96 and 94% similar, respectively. Therefore, PPIAP43 may act as a sponge for microRNAs which bind with the RNA of PPIA. Therefore, PPIAP43 RNA transcription may serve as a potential biomarker of radio-sensitivity of SCLC. 

Retracted: No

PubPeer comments:
 Figure 6 was pointed out to me by a reader: Panels B and C look very similar.  ,
Cooperative effect of p21Cip1/WAF-1 and 14-3-3sigma on cell cycle arrest and apoptosis induction by p14ARF
Authors: P T Daniel
B D√∂rken
B Gillissen
G Normand
J Wendt
P G Hemmati
Journal: Oncogene (2008)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: p14(ARF); cell cycle regulation; apoptosis induction; p53/p21-signaling axis; G2 arrest
Affiliations: Department of Hematology, Oncology and Tumor Immunology, University Medical Center Charit√©, Campus Berlin-Buch, Germany.

Abstract:  P14(ARF) (p19(ARF) in the mouse) plays a central role in the regulation of cellular proliferation. Although the capacity of p14(ARF) to induce a cell cycle arrest in G1 phase depends on a functional p53/p21-signaling axis, the G2 arrest triggered by p14(ARF) is p53/p21-independent. Using isogeneic HCT116 cells either wild-type or homozygously deleted for p21, 14-3-3sigma or both, we further investigated the cooperative effect of p21 and 14-3-3sigma on cell cycle regulation and apoptosis induction by p14(ARF). In contrast to DNA damage, which induces mitotic catastrophe in 14-3-3sigma-deficient cells, we show here that the expression of p14(ARF) triggers apoptotic cell death, as evidenced by nuclear DNA fragmentation and induction of pan-caspase activities, irrespective of the presence or absence of 14-3-3sigma. The activation of the intrinsic mitochondrial apoptosis pathway by p14(ARF) was confirmed by cytochrome c release from mitochondria and induction of caspase-9- (LEHDase) and caspase-3/7-like (DEVDase) activities. Moreover, 14-3-3sigma/p21 double-deficient cells were exceedingly sensitive to apoptosis induction by p14(ARF) as compared to wild-type cells or cells lacking either gene alone. Notably, p14(ARF)-induced apoptosis was preceded by an arrest in the G2 phase of cell cycle, which coincided with downregulation of cdc2 (cdk1) protein expression and lack of its nuclear localization. This indicates that p14(ARF) impairs mitotic entry by targeting the distal DNA damage-signaling pathway and induces apoptotic cell death, rather than mitotic catastrophe, out of a transient G2 arrest. Furthermore, our data delineate that the disruption of G2/M cell cycle checkpoint control critically determines the sensitivity of the cell toward p14(ARF)-induced mitochondrial apoptosis. 

Retracted: No

PubPeer comments:
null, 
 #1 Figure 7d. Much more similar after horizontal and vertical re-sizing.  , 
 Publication of the cited articles dates back to the years 2006 and 2008. After a vigorous search, we were able to retrieve digital copies of the two marked Western blots. As shown in the attached plain scans (upper panel) as well as in the contrast-enhanced scans (lower panel) it is clearly visible that (1) the Western blots are fully matched with the ones shown in the two corresponding publications and (2) these are, in fact, two individual Western blots. To me, it is quite remarkable how similar blots may look like. In any event, thanks for the critical post.  ,
G3BP1 promotes DNA binding and activation of cGAS
Authors: Xinzheng Wang
Tingting Li
Sheng-Ming Wu
Zheng-Gang Liu
Tian Xia
Yi-Jiao Huang
Ming Zhao
Wen Xue
Ai-Ling Li
Jiang Dai
Wan-Jin Li
Qing Xia
Zi-Yu Zhang
Xin Liu
Shuai Chen
Tao Li
Fangting Dong
Jia-Qing Xing
Miao Wang
Xue Pang
Xue-Min Zhang
Zhao-Shan Liu
Hong Cai
Tao Zhou
Journal: Nature Immunology (2019)
Discipline: IMMUNOLOGY
Keywords: cGAS; G3BP1; DNA sensing; IFN production; EGCG
Affiliations: State Key Laboratory of Toxicology and Medical Countermeasures, Institute of Pharmacology and Toxicology, National Center of Biomedical Analysis, Beijing, China., State Key Laboratory of Proteomics, Institute of Basic Medical Sciences, National Center of Biomedical Analysis, Beijing, China., Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA., State Key Laboratory of Toxicology and Medical Countermeasures, Institute of Pharmacology and Toxicology, National Center of Biomedical Analysis, Beijing, China. ., State Key Laboratory of Proteomics, Institute of Basic Medical Sciences, National Center of Biomedical Analysis, Beijing, China. ., Cancer Research Institute of Jilin University, The First Hospital of Jilin University, Changchun, China. .

Abstract:  Cyclic GMP-AMP synthase (cGAS) is a key sensor responsible for cytosolic DNA detection. Here we report that GTPase-activating protein SH3 domain-binding protein 1 (G3BP1) is critical for DNA sensing and efficient activation of cGAS. G3BP1 enhanced DNA binding of cGAS by promoting the formation of large cGAS complexes. G3BP1 deficiency led to inefficient DNA binding by cGAS and inhibited cGAS-dependent interferon (IFN) production. The G3BP1 inhibitor epigallocatechin gallate (EGCG) disrupted existing G3BP1-cGAS complexes and inhibited DNA-triggered cGAS activation, thereby blocking DNA-induced IFN production both in vivo and in vitro. EGCG administration blunted self DNA-induced autoinflammatory responses in an Aicardi-Gouti√®res syndrome (AGS) mouse model and reduced IFN-stimulated gene expression in cells from a patient with AGS. Thus, our study reveals that G3BP1 physically interacts with and primes cGAS for efficient activation. Furthermore, EGCG-mediated inhibition of G3BP1 provides a potential treatment for cGAS-related autoimmune diseases. 

Retracted: No

PubPeer comments:
   , 
 #1 I m not sure there s really an issue with these experiments. One is an over-expression experiment in mammalian cells (Fig 3C) whereas the other is an in vitro protein binding experiment using recombinant (E coli expressed?) protein. The issue that you re pointing out is that one of the constructs does not express as well as the others in mammalian cells (delta-RRM protein). While this isn t exactly ideal, there isn t much you can do about it, when proteins are truncated it very often changes their stability. After IP the amount captured isn t dramatically different from the full length so I think the comparison is valid. As an alternative approach the authors use recombinant protein to do the binding assay and find essentially the same result, cGAS binds only to the full length G3BP1. ,
A novel germ line-specific gene of the phosducin-like protein (PhLP) family. A meiotic function conserved from yeast to mice
Authors: Philippe Clertant
Daniel Puel
Fr√©d√©rique Vidal
Luis A Lopez-Fernandez
Ruken Yaman
Fran√ßois Cuzin
Pascal Lopez
Minoo Rassoulzadegan
Journal: Journal of Biological Chemistry (2003)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Phosducin-like protein; Germ cells; Spermatogenesis; Polyadenylation sites; Hormonal induction
Affiliations: University of Nice, INSERM U470, 06108 Nice, France.

Abstract:  We identified a new member of the phosducin-like (PhLP) protein family that is predominantly, if not exclusively, expressed in male and female germ cells. In situ analysis on testis sections and analysis of purified spermatogenic cell fractions evidenced a stage-specific expression with high levels of RNA and protein in pachytene spermatocytes and round spermatids. Three mRNA species were detected, which correspond to different polyadenylation sites and vary in abundance during germ cell maturation. Only low levels of RNA were detected in whole ovary extracts, but expression of the protein became detectable within hours after hormonal induction of superovulation. The gene (Mgcphlp) is located on mouse chromosome 5 in the immediate vicinity of the Clock locus. The predicted amino acid sequence shows extensive similarities not only with the known mammalian PhLP proteins but also with the yeast phosducin-like protein Plp2, required for the production and growth of haploid cells. Expression of the murine protein was found to complement the defect of a yeast plp2 Delta mutant. We propose that MgcPhLP/Plp2 proteins exert a function in germ cell maturation that is conserved from yeast to mammals. 

Retracted: Yes

PubPeer comments:
 Figure 6B    , 
 2019 retraction. http: www.jbc.org content 294 37 13832 This article has been withdrawn by Pascal Lopez, Luis A. Lopez-Fernandez, Franu00e7ois Cuzin, and Minoo Rassoulzadegan. Ruken Yaman, Fru00e9du00e9rique Vidal, Daniel Puel, and Philippe Clertant could not be reached. The Hss26 Northern blots from Fig. 3 (A and D) were previously published in Lopez et al. (2002) Mol. Cell. Biol. 22, 3488u20133496, with some data representing different experimental conditions. The withdrawing authors state that the same nitrocellulose filter was reused for two different probes and so the control is the same for both publications. The image in Fig. 6B was inappropriately manipulated. The withdrawing authors state that after 20 years, they cannot provide the original data. ,
Coexpression of UCA1 and ITGA2 in pancreatic cancer cells target the expression of miR‚Ä?07 through focal adhesion pathway
Authors: Wei Xiong
Jian Xu
Xiaojiong Yu
Jun Gong
Xiangyu Lu
Hao Zhang
Journal: Journal of Cellular Physiology (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: ITGA2; UCA1; lncRNAs; miR-107; pancreatic cancer cells.
Affiliations: Department of Hepatobiliary and Pancreatic Surgery, Sichuan Medical Academy & Sichuan People's Hospital, Chengdu, China.

Abstract:  Objectives: Abnormal expressions of microRNAs (miRNAs) are demonstrated in pancreatic cancer (PaC), but a major part of the mechanism remains elusive. This study mainly aimed to structure a coexpressed network of long noncoding RNA (lncRNA) and messenger RNA (mRNA) in PaC, as well as to explore their direct targets. Methods: LncRNA and mRNA microarrays were used to determine the expression profiles in PaC cells. Analysis of Kyoto Encyclopedia of Genes and Genomes pathway was performed to identify pathways associated with differentially expressed mRNAs. Coexpression profiles were identified by constructing differentially expressed lncRNA-mRNA regulatory network and further validated by quantitative real-time polymerase chain reaction assay and western blot assay. The bioinformatics computational method was applied to predict the biological target of lncRNA and mRNA, which was identified by luciferase reporter assay. Migration/invasion ability and apoptosis rate of cells were assessed by transwell assay and flow cytometry assay. Results: It was identified that the level of urothelial cancer associated 1 (UCA1) was increased in PaC cells, and the inhibition of UCA1 suppressed migration and invasion ability of the cancer cells. The luciferase reporter assay recognized that miR-107 was targeted by UCA1, and integrin subunit Œ± 2 (ITGA2) was further targeted by miR-107. This confirmed the prediction of lncRNA-miRNA-mRNA regulation mechanism. In the regulatory pathways, UCA1 and ITGA2 promoted PaC progression via focal adhesion pathway related proteins such as ITGA3, SRC protooncogene/nonreceptor tyrosine kinase, protein tyrosine kinase 2, and AKT serine/threonine kinase 1. Conclusion: The study revealed a regulatory network of UCA1-miR-107-ITGA2 and validated UCA1 and ITGA2 as potential prognostic factors for PaC. 

Retracted: No

PubPeer comments:
 I have a question with this articleuff1a I m going on a study about UCA1, and i used to contact the authors for some help and had no reponse. When checking the the email address: yfylmh@126.com, i found that this address was also used in another paper published in 2018 (pubmed: 30565858), however, the author Zhenfeng Ye was from Nanchang, Jiangxi, China, not from Chengdu, China. It makes me confused, and could the authors explain it? pubmed: 30569514:  pubmed: 30565858:  ,
Regulation of mitochondrial iron import through differential turnover of mitoferrin 1 and mitoferrin 2
Authors: Barry H Paw
Jerry Kaplan
Diane M Ward
Kimberley B Zumbrennen
Prasad N Paradkar
Journal: Molecular and cellular biology (2009)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Mitoferrin 1; Mitoferrin 2; mitochondrial iron delivery; heme synthesis; iron-sulfur cluster synthesis
Affiliations: Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah 84132, USA., Eccles Program in Human Molecular Biology and Genetics, University of Utah, Salt Lake City, Utah 84132, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, Department of Pathology, University of Utah School of Medicine

Abstract:  Mitoferrin 1 and mitoferrin 2 are homologous members of the mitochondrial solute carrier family. Mitoferrin 1 is required for mitochondrial iron delivery in developing erythrocytes. Here we show that mitoferrin 1 and mitoferrin 2 contribute to mitochondrial iron delivery in a variety of cells. Reductions in mitoferrin 1 and/or mitoferrin 2 levels by RNA interference result in decreased mitochondrial iron accumulation, heme synthesis, and iron-sulfur cluster synthesis. The ectopic expression of mitoferrin 1 in nonerythroid cells silenced for mitoferrin 2 or the expression of mitoferrin 2 in cells silenced for mitoferrin 1 restored heme synthesis to "baseline" levels. The ectopic expression of mitoferrin 2, however, did not support hemoglobinization in erythroid cells deficient in mitoferrin 1. Mitoferrin 2 could not restore heme synthesis in developing erythroid cells because of an inability of the protein to accumulate in mitochondria. The half-life of mitoferrin 1 was increased in developing erythroid cells, while the half-life of mitoferrin 2 did not change. These results suggest that mitochondrial iron accumulation is tightly regulated and that controlling mitoferrin levels within the mitochondrial membrane provides a mechanism to regulate mitochondrial iron levels. 

Retracted: No

PubPeer comments:
 Figure 4. * Red boxes: two lanes in the Tubulin panel in Figure 4A look very similar to lanes in the left Tubulin panel of Figure 4C, where they appear to represent different experiments.  Reported to the journal in 2016, and 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 ,
DICER-dependent biogenesis of let-7 miRNAs affects human cell response to DNA damage via targeting p21/p27
Authors: Ping Wang
Ya Wang
Jian Wang
Min Liu
Wei Li
Bailong Liu
Xiang Wang
Hongyan Wang
Xiangming Zhang
Journal: Nucleic acids research (2015)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: DICER; DNA damage response; homologous recombination repair; small RNAs; ATM
Affiliations: Department of Radiation Oncology, The First Hospital of Jilin University, Changchun 130021,¬†China Department of Radiation Oncology, Emory University School of Medicine and Winship Cancer Institute, Atlanta, GA 30322, USA., Department of Radiation Oncology, Emory University School of Medicine and Winship Cancer Institute, Atlanta, GA 30322, USA., Department of Cancer Center, The First Hospital of Jilin University, Changchun 130021, China ., Department of Radiation Oncology, Emory University School of Medicine and Winship Cancer Institute, Atlanta, GA 30322, USA .

Abstract:  Recently, it was reported that knockdown of DICER reduced the ATM-dependent DNA damage response and homologous recombination repair (HRR) via decreasing DICER-generated small RNAs at the damage sites. However, we found that knockdown of DICER dramatically increased cell resistance to camptothecin that induced damage required ATM to facilitate HRR. This phenotype is due to a prolonged G1/S transition via decreasing DICER-dependent biogenesis of miRNA let-7, which increased the p21(Waf1/Cip1)/p27(Kip1) levels and resulted in decreasing the HRR efficiency. These results uncover a novel function of DICER in regulating the cell cycle through miRNA biogenesis, thus affecting cell response to DNA damage. 

Retracted: No

PubPeer comments:
 It appears that- Fig. 1-a Fig. 1-c are same (with a slight tilt) Fig. 1-e Fig. 1-f (reverse with tilt)  ,
Celastrol Attenuates Angiotensin II‚ÄìInduced Cardiac Remodeling by Targeting STAT3
Authors: Xiang Hu
Lina Xuan
Gaojun Wu
Zia A Khan
Shengjie Wang
Jingying Wang
Shiju Ye
Peiren Shan
Taiwei Chen
Wu Luo
Guang Liang
Weijian Huang
Ke Lin
Journal: Circulation Research (2020)
Discipline: CLINICAL MEDICINE
Keywords: angiotensin II; heart failure; hypertension; molecular targeted therapy; signal transducer and activator of transcription 3.
Affiliations: From the Department of Cardiology in the First Affiliated Hospital (S.Y., G.W., P.S., K.L., T.C., W.H., G.L.), Wenzhou Medical University, Zhejiang, China., Chemical Biology Research Center in School of Pharmaceutical Sciences (S.Y., W.L., Z.A.K., K.L., T.C., J.W., G.L.), Wenzhou Medical University, Zhejiang, China., Department of Pharmacology at College of Pharmacy (the Key Laboratory of Cardiovascular Medicine Research, Ministry of Education), Harbin Medical University, Heilongjiang, China (L.X., S.W.)., Department of Endocrinology in the First Affiliated Hospital (X.H.), Wenzhou Medical University, Zhejiang, China.

Abstract:  Rationale: Excessive Ang II (angiotensin II) levels lead to a profibrotic and hypertrophic milieu that produces deleterious remodeling and dysfunction in hypertension-associated heart failure. Agents that disrupt Ang II-induced cardiac dysfunction may have clinical utility in the treatment of hypertension-associated heart failure. Objective: We have examined the potential effect of celastrol-a bioactive compound derived from the Celastraceae family-on Ang II-induced cardiac dysfunction. Methods and results: In rat primary cardiomyocytes and H9C2 (rat cardiomyocyte-like H9C2) cells, celastrol attenuates Ang II-induced cellular hypertrophy and fibrotic responses. Proteome microarrays, surface plasmon resonance, competitive binding assays, and molecular simulation were used to identify the molecular target of celastrol. Our data showed that celastrol directly binds to and inhibits STAT (signal transducer and activator of transcription)-3 phosphorylation and nuclear translocation. Functional tests demonstrated that the protection of celastrol is afforded through targeting STAT3. Overexpression of STAT3 dampens the effect of celastrol by partially rescuing STAT3 activity. Finally, we investigated the in vivo effect of celastrol treatment in mice challenged with Ang II and in the transverse aortic constriction model. We show that celastrol administration protected heart function in Ang II-challenged and transverse aortic constriction-challenged mice by inhibiting cardiac fibrosis and hypertrophy. Conclusions: Our studies show that celastrol inhibits Ang II-induced cardiac dysfunction by inhibiting STAT3 activity. 

Retracted: No

PubPeer comments:
 Figure 6A. The two pictures in group Cel(1mg kg) seem to be composed of the left and right parts because there are discontinuities.  , 
 #1 Thanks for your comment. The indicated discontinuity may be caused by splits when we made tissue sections. The attached file is the original staining image.   ,
Aflatoxin B1 induced multiple epigenetic modulators in human epithelial cell lines
Authors: Md Sajid Ghufran
Santosh R Kanade
Priyanka Soni
Journal: Toxicon (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Aflatoxin B(1); DNMTs; HAT; HDACs; Polycomb repressor complex.
Affiliations: Department of Biochemistry and Molecular Biology, School of Biological Sciences, Central University of Kerala, Kasargod 671314, Kerala, India., Department of Biochemistry and Molecular Biology, School of Biological Sciences, Central University of Kerala, Kasargod 671314, Kerala, India. Electronic address: .

Abstract:  The compulsive and insidious secondary metabolite aflatoxin B1, produced by the opportunistic fungi Aspergillus flavus, upholds a distinguished place in midst of the toxicants causing fatal hazards to humans. Aflatoxins alter the function of host cells by inducing multiple effects through genetic and non-genetic pathways. Epigenetic mechanisms drag major attention towards finding novel and new mechanisms involved in this process. Our present work intends to study the functional expression profile of multiple epigenetic regulators. AFB1 modulates multiple epigenetic regulators like DNA methyltransferases (DMNTs), histones modifying enzymes and polycomb proteins. AFB1 upregulates the expression of DNMTs at gene and protein level in a dose dependent manner. It reduced the histone acetyl transferase (HAT) activity significantly with a remarkable increase in histone deacetylase (HDAC) activity along with an induction in expression of HDACs gene and protein in a dose dependent manner. The gene and protein expression of polycomb repressor proteins B cell specific moloney murine leukemia virus integration site 1 (BMI-1) and enhancer of zeste homolog 2 (EZH2) was significantly over expressed with enhanced trimethylation of H3K27 and ubiquitination of H2AK119. In summary, our results show impact of aflatoxin B1 on multiple epigenetic modulations known to be pivotal in oncogenic processes. 

Retracted: No

PubPeer comments:
 In Figure 2D,E, a part of a Western blot has been duplicated, modified and presented as something else. This is seen by increasing the contrast and compare the background. In Figure 4A,C, a part of a Western bot has been duplicated, modified and presented as something else. This is seen by increasing the contrast and compare the background.   ,
The mitochondrial genome encodes abundant small noncoding RNAs
Authors: Huili Zheng
Seungil Ro
Loredana Moro
Wei Yan
Chanjae Park
Nicole Ortogero
Hsiu-Yen Ma
Grant W Hennig
Jer-Tsong Hsieh
Yung-Ming Lin
Rui Song
Journal: Cell research (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: small noncoding RNAs; mitochondrial genomes; mitosRNAs; DICER; mitochondrial ribonucleases
Affiliations: Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, NV 89557, USA.

Abstract:  Small noncoding RNAs identified thus far are all encoded by the nuclear genome. Here, we report that the murine and human mitochondrial genomes encode thousands of small noncoding RNAs, which are predominantly derived from the sense transcripts of the mitochondrial genes (host genes), and we termed these small RNAs mitochondrial genome-encoded small RNAs (mitosRNAs). DICER inactivation affected, but did not completely abolish mitosRNA production. MitosRNAs appear to be products of currently unidentified mitochondrial ribonucleases. Overexpression of mitosRNAs enhanced expression levels of their host genes in vitro, and dysregulated mitosRNA expression was generally associated with aberrant mitochondrial gene expression in vivo. Our data demonstrate that in addition to 37 known mitochondrial genes, the mammalian mitochondrial genome also encodes abundant mitosRNAs, which may play an important regulatory role in the control of mitochondrial gene expression in the cell. 

Retracted: No

PubPeer comments:
 Figure 3A u2013 more similar than expected. Could the authors check please?  , 
 Thanks for bringing this issue to our attention. By examining the lab records, we found that the gel image of H-X1_30-51 appeared to be used as a place holder for mmu-let-7d (a loading control) when the original figure was first assembled. Unfortunately, it was never replaced by the real mmu-let-7d gel image. We repeated the PCR assays and added the correct mmu-let-7d gel image to the revised Fig. 3A. We have submitted our request for correction to the journal. We apologize for this oversight. The corrected Fig. 3A can be found here: https: figshare.com articles figure Fig_3A_new_tif 16435332 , 
 The correction has been published: https: www.nature.com articles s41422-021-00571-0 ,
<p>Long Noncoding RNA <em>RGMB-AS1</em> Acts as a microRNA-574 Sponge Thereby Enhancing the Aggressiveness of Gastric Cancer via HDAC4 Upregulation</p>
Authors: Dongqiang Jiang
Ying Song
Yueli Tian
Xiaodong Wang
Xin Chen
Journal: OncoTargets and Therapy (2020)
Discipline: CLINICAL MEDICINE
Keywords: RGMB-AS1; gastric cancer; histone deacetylase 4; miR-574; tumor therapy.
Affiliations: Department of Gastroenterology and Digestive Endoscopy Center, The Second Hospital of Jilin University, Changchun, Jilin 130041, People's Republic of China.

Abstract:  Purpose: The long noncoding RNA RGMB-AS1 plays an important part in the genesis and progression of multiple human cancers. Nonetheless, little is known regarding its expression, roles, and mechanisms of action in gastric cancer (GC). This study was aimed at investigating the relationship between RGMB-AS1 and GC and illustrating the mechanisms of action of RGMB-AS1 therein. Methods: RGMB-AS1 expression in GC was measured via reverse-transcription quantitative PCR. A series of experiments including Cell Counting Kit-8 assay, flow-cytometric analysis of apoptosis, Transwell migration and invasion assays, and in vivo tumorigenesis experiment were conducted to test the effects of RGMB-AS1 on the malignant phenotype of GC cells. The molecular events behind the oncogenic actions of RGMB-AS1 in GC were elucidated through subcellular fractionation, RNA immunoprecipitation assay, bioinformatics analysis and luciferase reporter assay. Results: RGMB-AS1 upregulation was confirmed in GC tissues and cell lines. Higher RGMB-AS1 expression was associated with adverse clinical parameters and negatively correlated with patient overall survival. RGMB-AS1 knockdown inhibited GC cell proliferation, facilitated apoptosis, and reduced migration and invasion in vitro. Further experiments revealed that RGMB-AS1 knockdown decreased the tumor growth of GC cells in vivo. Mechanistically, RGMB-AS1 functioned as a competing endogenous RNA upregulating histone deacetylase 4 (HDAC4) by sponging microRNA-574 (miR-574). Rescue experiments indicated that miR-574 inhibition and HDAC4 reintroduction reversed the effects of the RGMB-AS1 knockdown on GC cells. Conclusion: The RGMB-AS1-miR-574-HDAC4 regulatory network contributes to the malignancy of GC, thereby offering a novel target for the diagnosis, prognosis, and/or treatment of GC. 

Retracted: Yes

PubPeer comments:
 Some parts of RED and BLUE curves in Fig. 3, which are indicated by PURPLE boxes, are highly similar to each other. Could the authors give a reason for this unexpected similarity ?  , 
  #1 Thanks for your concerns. You should see the difference at the C=O bands ,
Interaction of Tumor Necrosis Factor Receptor-associated Factor 6 (TRAF6) and Vav3 in the Receptor Activator of Nuclear Factor Œ∫B (RANK) Signaling Complex Enhances Osteoclastogenesis
Authors: Yongjin Kim
Masamichi Takami
Sumi Kim
Jungeun Yu
Matthew C Walsh
Jaerang Rho
Dulshara Sachini Amarasekara
Hyeongseok Yun
Seunga Choi
Eui-Soon Park
Yongwon Choi
Bongjin Shin
Jun-Ichiro Inoue
Jiyeon Yu
Journal: Journal of Biological Chemistry (2016)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: NFAT transcription factor; mitogen-activated protein kinase (MAPK); osteoclast; osteoporosis; signal transduction.
Affiliations: From the Department of Microbiology and Molecular Biology, Chungnam National University, Daejeon 305-764, Korea., the Division of Cellular and Molecular Biology, Department of Cancer Biology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan., the Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, and., the Department of Biochemistry, School of Dentistry, Showa University, Shinagawaku, 142-8555, Japan., From the Department of Microbiology and Molecular Biology, Chungnam National University, Daejeon 305-764, Korea, .

Abstract:  The signaling pathway downstream of stimulation of receptor activator of nuclear factor Œ∫B (RANK) by RANK ligand is crucial for osteoclastogenesis. RANK recruits TNF receptor-associated factor 6 (TRAF6) to TRAF6-binding sites (T6BSs) in the RANK cytoplasmic tail (RANKcyto) to trigger downstream osteoclastogenic signaling cascades. RANKcyto harbors an additional highly conserved domain (HCR) that also activates crucial signaling during RANK-mediated osteoclastogenesis. However, the functional cross-talk between T6BSs and the HCR in the RANK signaling complex remains unclear. To characterize the cross-talk between T6BSs and the HCR, we screened TRAF6-interacting proteins using a proteomics approach. We identified Vav3 as a novel TRAF6 binding partner and evaluated the functional importance of the TRAF6-Vav3 interaction in the RANK signaling complex. We demonstrated that the coiled-coil domain of TRAF6 interacts directly with the Dbl homology domain of Vav3 to form the RANK signaling complex independent of the TRAF6 ubiquitination pathway. TRAF6 is recruited to the RANKcyto mutant, which lacks T6BSs, via the Vav3 interaction; conversely, Vav3 is recruited to the RANKcyto mutant, which lacks the IVVY motif, via the TRAF6 interaction. Finally, we determined that the TRAF6-Vav3 interaction resulting from cross-talk between T6BSs and the IVVY motif in RANKcyto enhances downstream NF-Œ∫B, MAPK, and NFATc1 activation by further strengthening TRAF6 signaling, thereby inducing RANK-mediated osteoclastogenesis. Thus, Vav3 is a novel TRAF6 interaction partner that functions in the activation of cooperative signaling between T6BSs and the IVVY motif in the RANK signaling complex. 

Retracted: No

PubPeer comments:
 The cell morphology of different groups in red boxes appear to look similar in Fig 2B.  ,
Long non-coding RNA CCAT1 promotes metastasis and poor prognosis in epithelial ovarian cancer
Authors: Ruitao Zhang
Yuan Cao
Fang Ren
Yanyan Jia
Huirong Shi
Journal: Experimental Cell Research (2017)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Epithelial ovarian cancer; LncRNA CCAT1; Metastasis; miR-130b; miR-152.
Affiliations: Department of Gynaecology, the First Affiliated Hospital of Zhengzhou University, China., Department of Gynaecology, the First Affiliated Hospital of Zhengzhou University, China. Electronic address: .

Abstract:  In this study, we reported that long non-coding RNA (lncRNA) CCAT1 was upregulated in epithelial ovarian cancer (EOC) tissues, and was associated with FIGO stage, histological grade, lymph node metastasis and poor survival of EOC patients. Multivariate Cox regression analysis showed that CCAT1 was an independent prognostic indicator. While CCAT1 downregulation inhibited EOC cell epithelial-mesenchymal transition (EMT), migration and invasion, CCAT1 upregulation promoted EOC cell EMT, migration and invasion. We further identified and confirmed that miR-152 and miR-130b were the targets of CCAT1, and CCAT1 functioned by targeting miR-152 and miR-130b. Subsequently, ADAM17 and WNT1, and STAT3 and ZEB1 were confirmed to be the targets of miR-152 and miR-130b, respectively, and could be regulated by CCAT1 in EOC cells. Knockdown of anyone of these four proteins inhibited EOC cell EMT, migration and invasion. Taken together, our study first revealed a critical role of CCAT1-miR-152/miR-130b-ADAM17/WNT1/STAT3/ZEB1 regulatory network in EOC cell metastasis. These findings provide great insights into EOC initiation and progression, and novel potential therapeutic targets and biomarkers for diagnosis and prognosis for EOC. 

Retracted: No

PubPeer comments:
 Figure 2E and Figure 4F and G are tainted with serious problems, where most of the presented micrographs are falsification.  ,
The synergistic effects of cinnamon essential oil and nano TiO on antimicrobial and functional properties of sago starch films
Authors: Mohammadi Nafchi Abdorreza
Ehsani Mohammadreza
Esfahani Arezoo
Mizani Maryam
Journal: International Journal of Biological Macromolecules (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Bionanocomposite film; Cinnamon essential oil; Nano titanium dioxide.
Affiliations: Department of Food Science and Technology, Science and Research Branch, Islamic Azad University, Tehran, Iran., Department of Food Science and Technology, Science and Research Branch, Islamic Azad University, Tehran, Iran. Electronic address: ., Food Technology Division, School of Industrial Technology, Universiti Sains Malaysia, 11800 USM, Penang, Malaysia.

Abstract:  This study describes a sago starch-based film by incorporation of cinnamon essential oil (CEO) and nano titanium dioxide (TiO2-N). Different concentrations (i.e., 0%, 1%, 3%, and 5%, w/w) of TiO2-N and CEO (i.e., 0%, 1%, 2%, and 3%, v/w) were incorporated into sago starch film, and the physicochemical, barrier, mechanical, and antimicrobial properties of the bionanocomposite films were estimated. Incorporation of CEO into the sago starch matrix increased oxygen and water vapor permeability of starch films while increasing TiO2-N concentration decreased barrier properties. Moisture content also decreased from 12.96% to 8.04%, solubility in water decreased from 25% to 13.7%, and the mechanical properties of sago starch films improved. Sago starch bionanocomposite films showed excellent antimicrobial activity against Escherichia coli, Salmonella typhimurium, and Staphylococcus aureus. Results also showed that incorporation of TiO2-N and CEO had synergistic effects on functional properties of sago starch films. In summary, sago starch films incorporated with both TiO2-N and CEO shows potential application for active packaging in food industries such as fresh pistachio packaging. 

Retracted: No

PubPeer comments:
 Please clarify if it is misunderstood! Authors say that: **3.6. Effects of TiO2-N and CEO on UVu2013vis-NIR spectra of sago starch films** Fig. 7(I) shows the UVu2013vis-NIR spectra of the sago starch incorporated with TiO2-N. Sago starch films in the UV range **(200 nm to 400 nm)** of spectra showed **very low absorbance**. Addition of **5% TiO2-N increased UV absorbance to 100%.** * Q(1): Very low absorbance in the range (200 -400 nm) compared to what, or what other range? Because much lower measures of absorbance still could be seen for the other ranges up to 1100 nm! * Q(2): In order to complete an  Uncertainty Analysis , wouldn t it be better to show the measures for 4% and 6% of TiO2-N increase in advance to? It is only to see if there will be a jump from 100% to a higher or lower absorbance rate! * C (1): Following the authors claim, there is also a 100% absorbance seen in the figure for 3% addition of TiO2-N exactly at UVW of 200 nm! Is that right?  ,