PReD-Bench/PRed-Bench huggingface dataset:
Myc downregulation by transforming growth factor beta required for activation of the p15(Ink4b) G(1) arrest pathway
Authors: J Seoane
S W Blain
B J Warner
J Massagué
Journal: Molecular and Cellular Biology (1999)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Transforming growth factor beta; TGF-beta; c-Myc; cyclin-dependent kinase; cdk
Affiliations: Cell Biology Program and Howard Hughes Medical Institute, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA.

Abstract:  The antimitogenic action of transforming growth factor beta (TGF-beta) in epithelial cells involves cyclin-dependent kinase (cdk) inhibitory gene responses and downregulation of c-Myc expression. Although the cdk inhibitory responses are sufficient for G(1) arrest, enforced expression of c-Myc prevents G(1) arrest by TGF-beta. We investigated the basis of this antagonism by using Mv1Lu lung epithelial cell lines that conditionally express levels of human c-Myc. We show that c-Myc prevents induction of the cdk4 inhibitor p15(Ink4b) and the subsequent inhibition of G(1) cdks by TGF-beta. We assessed the significance of this effect by analyzing the oligomeric state of cdk4 in these cells. In proliferating cells, endogenous cdk4 is distributed among three populations: an abundant high-molecular-mass (&gt;400-kDa) pool of latent cdk4 that serves as a source of cdk4 for cyclin D, a low-abundance pool containing active cyclin D-cdk4 complexes, and an inactive population of monomeric cdk4. Cell stimulation with TGF-beta converts the latent and active cdk4 pools into inactive cdk4, an effect that is specifically mimicked by overexpression of p15 but not by other forms of G(1) arrest. This process of TGF-beta-induced cdk4 inactivation is completely blocked by expression of c-Myc, even though the latent and active cdk4 complexes from c-Myc-expressing cells remain sensitive to dissociation by p15 in vitro. c-Myc causes a small increase in cyclin D levels, but this effect contributes little to the loss of TGF-beta responses in these cells. The evidence suggests that c-Myc interferes with TGF-beta activation of the p15 G(1) arrest pathway. TGF-beta must therefore downregulate c-Myc in order to activate this pathway. 

Retracted: No

PubPeer comments:
 Figure 2C. Much more similar than you would expect. https: imgur.com ATA2ex1 , 
 https: retractionwatch.com 2022 08 25 exclusive-cancer-researcher-sues-med-school-for-retaliation-after-research-misconduct-finding ,
EOFAZ inhibits endothelial‑to‑mesenchymal transition through downregulation of KLF4
Authors: Yongpan Huang
Chen Li
Ling Tao
Yan Chen
Xiangchun Shen
Yanyan Zhang
Yini Xu
Feng Jiang
Shuang Zhao
Journal: International Journal of Molecular Medicine (2020)
Discipline: CLINICAL MEDICINE
Keywords: Essential oil; Alpinia zerumbet rhizome; Yan shanjiang; cardiovascular injury; endothelial-to-mesenchymal transition
Affiliations: The State Key Laboratory of Functions and Applications of Medicinal Plants, School of Basic Medical Sciences, Guizhou Medical University, Guiyang, Guizhou 550025, P.R. China., Department of Clinical Pharmacy, School of Pharmaceutical Sciences, Guizhou Medical University, Guiyang, Guizhou 550025, P.R. China.

Abstract:  Essential oil from Alpinia zerumbet rhizome (EOFAZ), which is termed Yan shanjiang in China, is extensively used as an herbal medicine in the Guizhou area and has been shown to protect against the damaging effects of cardiovascular injury in vitro and in vivo. In the present study, it was hypothesized that the protective effects of EOFAZ on transforming growth factor (TGF)‑β1‑induced endothelial‑to‑mesenchymal transition (EndMT) in human umbilical vein endothelial cells (HUVECs) were mediated by inhibition of Krüppel‑like factor 4 (KLF4). Cell motility was assessed using wound healing and Transwell assays. The expression of endothelial markers and mesenchymal markers were determined by reverse transcription‑quantitative PCR, immunoﬂuorescence staining and western blotting, and additionally, phosphorylated NF‑κB p65 expression was determined by western blotting. Furthermore, the involvement of KLF4 in EndMT was determined using RNA interference to knockdown the expression of KLF4. TGF‑β1 treatment significantly promoted EndMT, as evidenced by downregulation of vascular endothelial‑cadherin and upregulation of α‑smooth muscle actin in HUVECs, and by enhancing cell migration. Small interfering RNA‑mediated knockdown of KLF4 reversed TGF‑β1‑induced EndMT. Additionally, treatment with EOFAZ inhibited TGF‑β1‑induced EndMT in a dose‑dependent manner. These results suggest that TGF‑β1 may induce EndMT through upregulation of KLF4, and this may be reversed by EOFAZ. Therefore, EOFAZ was shown to inhibit TGF‑β1‑induced EndMT through regulation of KLF4. 

Retracted: No

PubPeer comments:
 An unusual citation pattern appears in this paper which is associated with **Dey A**.. Besides, the most cited author in this paper is G.W. Wei (12 50). ![file] ![file] , 
 A decision making theory, whether it makes sense or not, is presented based on evaluation pairs of form $(mu,  u)$ with $0le mu+ u le 1$. However, the illustrated numerical example uses pairs of form $(mu,  u)$ with $mu+ u = 1$. ![file] ,
Monoclonal Antibodies for the Diagnosis of Borrelia crocidurae
Authors: Didier Raoult
Michel Drancourt
Aurélien Fotso Fotso
Saïd Azza
Oleg Mediannikov
Claude Nappez
Journal: American Journal of Tropical Medicine and Hygiene (2016)
Discipline: CLINICAL MEDICINE
Keywords: Relapsing fever; Borreliae; Monoclonal antibodies; Flagellin B; Variable-like protein

Abstract:  Relapsing fever borreliae, produced by ectoparasite-borne Borrelia species, cause mild to deadly bacteremia and miscarriage. In the perspective of developing inexpensive assays for the rapid detection of relapsing fever borreliae, we produced 12 monoclonal antibodies (MAbs) against Borrelia crocidurae and characterized the two exhibiting the highest titers. P3A10 MAb reacts with the 35.6-kDa flagellin B (flaB) of B. crocidurae while P6D9 MAb recognizes a 35.1-kDa variable-like protein (Vlp) in B. crocidurae and a 35.2-kDa Vlp in Borrelia duttonii. Indirect immunofluorescence assay incorporating relapsing fever and Lyme group borreliae and 11 blood-borne organisms responsible for fever in West Africa confirmed the reactivity of these two MAbs. Combining these two MAbs in indirect immunofluorescence assays detected relapsing fever borreliae including B. crocidurae in ticks and the blood of febrile Senegalese patients. Both antibodies could be incorporated into inexpensive and stable formats suited for the rapid point-of-care diagnosis of relapsing fever. These first-ever MAbs directed against African relapsing fever borreliae are available for the scientific community to promote research in this neglected field. 

Retracted: No

PubPeer comments:
 This is a strange paper. The title of the paper includes  Fractional differential equations but there are no fractional differential equations in the whole paper. The majority of the references seem do not related with the topic of the paper. Figure 4 and 5 are the same (just in lower resolution) of Figure 1.1 in https: publications.lib.chalmers.se records fulltext 218339 218339.pdf which is a Master s Thesis on  Industrialisation of a Finite Element Active Human Body Model for Vehicle Crash Simulations , a not related topic. , 
 You get better at football if you have a mechanical knee joint and wear a shoe? ![file] ,
Murine protein serine/threonine kinase 38 stimulates TGF-beta signaling in a kinase-dependent manner via direct phosphorylation of Smad proteins
Authors: Hyunjung Ha
Haiyoung Jung
Hyun-A Seong
Journal: Journal of Biological Chemistry (2010)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: MPK38; Smad proteins; TGF-β; ASK1 signals; kinase domain
Affiliations: Department of Biochemistry, School of Life Sciences, Chungbuk National University, Cheongju 361-763, Republic of Korea.

Abstract:  The present study demonstrated that murine protein serine/threonine kinase 38 (MPK38) coimmunoprecipitates with Smad proteins (Smad2, -3, -4, and -7) and that this association is mediated by the catalytic kinase domain of MPK38. The association between MPK38 and Smad2, -3, and -4 was significantly increased by TGF-β or ASK1 signals, whereas these signals decreased association of MPK38 with Smad7. MPK38 stimulated TGF-β-induced transcription required for TGF-β-mediated biological functions, such as apoptosis and cell growth arrest, in a kinase-dependent manner. Knockdown of endogenous MPK38 showed an opposite effect, inhibiting TGF-β signaling. MPK38-mediated phosphorylation of Smad proteins (Ser(245) of Smad2, Ser(204) of Smad3, Ser(343) of Smad4, and Thr(96) of Smad7) was also found to be crucial to the positive regulation of TGF-β signaling induced by MPK38. In addition, MPK38 enhanced nuclear translocation of Smad3, as well as redistribution of Smad7 from the nucleus to the cytoplasm, in response to TGF-β. Together, these results indicate that MPK38 functions as a stimulator of TGF-β signaling through direct interaction with and phosphorylation of Smad proteins. 

Retracted: No

PubPeer comments:
 There are many signs of smudging in Fig 2B (red arrows), lysate panel. ![file] ,
The lncRNA ROR/miR-124-3p/TRAF6 axis regulated the ischaemia reperfusion injury-induced inflammatory response in human cardiac myocytes
Authors: Chang-Qing Deng
Yan-Hui Hu
Yong Chen
Guo-Hai Xu
Jing Zhang
Ying-Ping Liang
Fu-Zhou Hua
Qin Liu
Journal: Journal of Bioenergetics and Biomembranes (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: HCM; LncRNA ROR; MIRI; TRAF6; miR-124-3p.
Affiliations: Department of Anesthesiology, Second Affiliated Hospital of Nanchang University, No.1, Minde Road, Nanchang, 330006, Jiangxi Province, People's Republic of China., Department of Gastroenterology, The Affiliated Hospital of Jiangxi University of Traditional Chinese Medicine, Nanchang, 330006, Jiangxi Province, People's Republic of China., Department of Anesthesiology, Second Affiliated Hospital of Nanchang University, No.1, Minde Road, Nanchang, 330006, Jiangxi Province, People's Republic of China. .

Abstract:  Myocardial ischaemia reperfusion injury (MIRI) is considered the primary cause of death in patients with cardiovascular diseases. Recently, long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have been found to be involved in the pathogenesis of MIRI. However, whether lncRNA ROR and miR-124-3p play roles in MIRI and the underlying mechanism remain undetermined. HCMs were exposed to hypoxic conditions for 2 h followed by re-oxygenation (H/R) treatment. Expression of miR-124-3p and lncRNA ROR in HCMs was measured by qRT-PCR. TRAF6 expression was evaluated by qRT-PCR and western blotting. ELISA and qRT-PCR were conducted to assess the production of TNF-α, IL-6, and IL-1β. The interaction between miR-124-3p and TRAF6, as well as between miR-124-3p and lncRNA ROR, was verified by dual-luciferase reporter assay. Cell apoptosis was detected by flow cytometry analysis. Our data revealed that miR-124-3p was significantly downregulated, while TRAF6 and lncRNA ROR were upregulated in both MIRI rat model and H/R treated HCMs. Overexpression of miR-124-3p reversed the H/R-induced cell apoptosis and upregulation of TNF-α, IL-6, and IL-1β. Mechanistically, miR-124-3p bound and negatively regulated TRAF6 expression in HCMs. Moreover, TRAF6 overexpression significantly blocked the effects of miR-124-3p mimics on cell apoptosis and inflammatory response of HCMs, which involved the NF-κB pathway. Further analysis showed that lncRNA ROR sponged and negatively regulated miR-124-3p in HCMs. Overexpression of IL-1β was demonstrated to promote H/R induced cell apoptosis in HCMs. In addition, overexpression of ROR further enhanced the H/R-induced inflammation and cell apoptosis through its action on miR-124-3p. The lncRNA ROR/miR-124-3p/TRAF6 axis regulated the H/R-induced cell apoptosis and inflammatory response of HCMs. 

Retracted: No

PubPeer comments:
 Readers should become aware that a paper published in Angewandte Chemie in 2019 entitled NMR Analysis of Apo Glutamine-Binding Protein Exposes Challenges in the Study of Interdomain Dynamics could not reproduce the findings of Feng et al. https: onlinelibrary.wiley.com doi 10.1002 anie.201911015 https: www.ncbi.nlm.nih.gov pmc articles PMC6848765 ,
Long non-coding RNA GAS5 aggravates myocardial depression in mice with sepsis via the microRNA-449b/HMGB1 axis and the NF-κB signaling pathway
Authors: Aichun Chen
Jixi Yan
Huijing Ma
Hongfeng Gao
Shujuan Zha
Min Gao
Journal: Bioscience Reports (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: HMGB1; Long-noncoding RNA GAS5; Myocardial depression; Myocardial injury; Sepsis
Affiliations: Department of Emergency Medicine, Wuhan Wuchang Hospital, Wuchang Hospital Affiliated to Wuhan University of Science and Technology, Wuhan 430000, Hubei, P.R. China, Department of Image, Wuhan Children’s Hospital (Wuhan Maternal and Child Healthcare Hospital), Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430000, Hubei, P.R. China, Department of Anesthesia, Hanyang Hospital Affiliated to Wuhan University of Science and Technology, Wuhan 430000, Hubei, P.R. China

Abstract:  Sepsis is a common cause of deaths of patients in intensive care unit. The study aims to figure out the role of long non-coding RNA (lncRNA) GAS5 in the myocardial depression in mice with sepsis. Cecal ligation and puncture (CLP) was applied to induce sepsis in mice, and then the heart function, myocardium structure, and the inflammatory response were evaluated. Differentially expressed lncRNAs in mice with sepsis were identified. Then gain- and loss-of-functions of GAS5 were performed in mice to evaluate its role in mouse myocardial depression. The lncRNA-associated microRNA (miRNA)-mRNA network was figured out via an integrative prediction and detection. Myocardial injury was observed by overexpression of high-mobility group box 1 (HMGB1) in septic mice with knockdown of GAS5 expression. Activity of NF-κB signaling was evaluated, and NF-κB inhibition was induced in mice with sepsis and overexpression of GAS5. Collectively, CLP resulted in myocardial depression and injury, and increased inflammation in mice. GAS5 was highly expressed in septic mice. GAS5 inhibition reduced myocardial depression, myocardial injury and inflammation responses in septic mice. GAS5 was identified to bind with miR-449b and to elevate HMGB1 expression, thus activating the NF-κB signaling. HMGB1 overexpression or NF-κB inactivation reduced the GAS5-induced myocardial depression and inflammation in septic mice. Our study suggested that GAS5 might promote sepsis-induced myocardial depression via the miR-449b/HMGB1 axis and the following NF-κB activation. 

Retracted: No

PubPeer comments:
 Figure 1 and 2 appear to have repeated control images, but they may be described differently. Could the authors comment? *** ![file] ![file] ,
A novel PAAD-containing protein that modulates NF-kappa B induction by cytokines tumor necrosis factor-alpha and interleukin-1beta
Authors: Maria Eugenia Ariza
John C Reed
Christian Stehlik
Loredana Fiorentino
Vasco Oliveira
Adam Godzik
Journal: Journal of Biological Chemistry (2002)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: PAAD domains; protein interaction modules; PAN2; NF-kappaB; cytokine signaling pathways
Affiliations: Burnham Institute, La Jolla, California 92037, USA.

Abstract:  PAAD domains are found in diverse proteins of unknown function and are structurally related to a superfamily of protein interaction modules that includes death domains, death effector domains, and Caspase activation and recruitment domains. Using bioinformatics strategies, cDNAs were identified that encode a novel protein of 110 kDa containing a PAAD domain followed by a putative nucleotide-binding (NACHT) domain and several leucine-rich repeat domains. This protein thus resembles Cryopyrin, a protein implicated in hereditary hyperinflammation syndromes, and was termed PAN2 for PAAD and NACHT-containing protein 2. When expressed in HEK293 cells, PAN2 suppressed NF-kappaB induction by the cytokines tumor necrosis factor-alpha (TNFalpha) and interleukin-1beta (IL-1beta), suggesting that this protein operates at a point of convergence in these two cytokine signaling pathways. This PAN2-mediated suppression of NF-kappaB was evident both in reporter gene assays that measured NF-kappaB transcriptional activity and electromobility shift assays that measured NF-kappaB DNA binding activity. PAN2 also suppressed NF-kappaB induction resulting from overexpression of several adapter proteins and protein kinases involved in the TNF or IL-1 receptor signal transduction, including TRAF2, TRAF6, RIP, IRAK2, and NF-kappaB-inducing kinase as well as the IkappaB kinases IKKalpha and IKKbeta. PAN2 also inhibited the cytokine-mediated activation of IKKalpha and IKKbeta as measured by in vitro kinase assays. Furthermore, PAN2 association with IKKalpha was demonstrated by co-immunoprecipitation assays, suggesting a direct effect on the IKK complex. These observations suggest a role for PAN2 in modulating NF-kappaB activity in cells, thus providing the insights into the potential functions of PAAD family proteins and their roles in controlling inflammatory responses. 

Retracted: No

PubPeer comments:
 This paper claims to have made an APOBEC3G construct that does not have any editing effect on transcriptome. This claim is flawed since authors failed to address the A3G RNA editing function (specific targets, secondary structure etc.) recently described in PMID: 27974822 and PMID: 30791937. Specifically, PMID: 27974822 showed that W94 and W127 residues had no role in RNA editing when tested against specific transcript targets. In contrast, authors seem to think RNA binding is the same as RNA editing and claim R24A, W94L, Y124A, and W127L abolished RNA editing by just looking at global C T mutation rates. Until the RNA editing ability against specific targets are addressed, conclusion of  ...is also free of global off-target effects on the transcriptome. cannot be supported. ,
Animal personality aligns task specialization and task proficiency in a spider society
Authors: C Tate Holbrook
Colin M Wright
Jonathan N Pruitt
Journal: Proceedings of the National Academy of Sciences of the United States of America (2014)
Discipline: Multidisciplinary
Keywords: Araneae; behavioral syndrome; cooperation; social organization; temperament.
Affiliations: Department of Biological Sciences, University of Pittsburgh, Pittsburgh, PA 15260; and ., Department of Natural Sciences, College of Coastal Georgia, Brunswick, GA 31520., Department of Biological Sciences, University of Pittsburgh, Pittsburgh, PA 15260; and.

Abstract:  Classic theory on division of labor implicitly assumes that task specialists are more proficient at their jobs than generalists and specialists in other tasks; however, recent data suggest that this might not hold for societies that lack discrete worker polymorphisms, which constitute the vast majority of animal societies. The facultatively social spider Anelosimus studiosus lacks castes, but females exhibit either a "docile" or "aggressive" phenotype. Here we observed the propensity of individual females of either phenotype to perform various tasks (i.e., prey capture, web building, parental care, and colony defense) in mixed-phenotype colonies. We then measured the performance outcomes of singleton individuals of either phenotype at each task to determine their proficiencies. Aggressive females participated more in prey capture, web building, and colony defense, whereas docile females engaged more in parental care. In staged trials, aggressive individuals were more effective at capturing prey, constructing webs, and defending the colony, whereas docile females were more effective at rearing large quantities of brood. Thus, individuals' propensity to perform tasks and their task proficiencies appear to be adaptively aligned in this system. Moreover, because the docile/aggressive phenotypes are heritable, these data suggest that within-colony variation is maintained because of advantages gleaned by division of labor. 

Retracted: No

PubPeer comments:
  PNAS is publishing an Editorial Expression of Concern regarding the following article: u201cAnimal personality aligns task specialization and task proficiency in a spider society,u201d by Colin M. Wright, C. Tate Holbrook, and Jonathan N. Pruitt, which was first published June 16, 2014; 10.1073 pnas.1400850111 (Proc. Natl. Acad. Sci. U.S.A. 111, 9533u20139537). The editors wish to alert readers of an ongoing investigation by McMaster University into the underlying data of this work. We will await the conclusion of the investigation to determine whether further action is required. https: www.pnas.org content early 2020 05 06 2008526117.long ,
Synergistic interaction between leptin and cholecystokinin in the rat nodose ganglia is mediated by PI3K and STAT3 signaling pathways: implications for leptin as a regulator of short term satiety
Authors: Chung Owyang
Il Song
Gintautas Grabauskas
Andrea Heldsinger
Journal: Journal of Biological Chemistry (2011)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: vagal cholecystokinin-A receptors; leptin receptors; short term satiety; signaling cascades; K(+) channels
Affiliations: Division of Gastroenterology, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109, USA.

Abstract:  Research has shown that the synergistic interaction between vagal cholecystokinin-A receptors (CCKARs) and leptin receptors (LRbs) mediates short term satiety. We hypothesize that this synergistic interaction is mediated by cross-talk between signaling cascades used by CCKARs and LRbs, which, in turn, activates closure of K(+) channels, leading to membrane depolarization and neuronal firing. Whole cell patch clamp recordings were performed on isolated rat nodose ganglia neurons. Western immunoblots elucidated the intracellular signaling pathways that modulate leptin/CCK synergism. In addition, STAT3, PI3K, Src, and MAPK genes were silenced by lentiviral infection and transient Lipofectamine transfection of cultured rat nodose ganglia to determine the effect of these molecules on leptin/CCK synergism. Patch clamp studies showed that a combination of leptin and CCK-8 caused a significant increase in membrane input resistance compared with leptin or CCK-8 alone. Silencing the STAT3 gene abolished the synergistic action of leptin/CCK-8 on neuronal firing. Leptin/CCK-8 synergistically stimulated a 7.7-fold increase in phosphorylated STAT3 (pSTAT3), which was inhibited by AG490, C3 transferase, PP2, LY294002, and wortmannin, but not PD98059. Silencing the Src and PI3K genes resulted in a loss of leptin/CCK-stimulated pSTAT3. We conclude that the synergistic interaction between vagal CCKARs and LRbs is mediated by the phosphorylation of STAT3, which, in turn, activates closure of K(+) channels, leading to membrane depolarization and neuronal firing. This involves the interaction between CCK/Src/PI3K cascades and leptin/JAK2/PI3K/STAT3 signaling pathways. Malfunctioning of these signaling molecules may result in eating disorders. 

Retracted: No

PubPeer comments:
  [Clistoabdominalis Helluo commented] And now, blots recycled from a different paper:  ![] The parallel paper with Figs 5B, 5D is [Heldsinger et al (2012)] . ,
FOXF2 aggravates the progression of non-small cell lung cancer through targeting lncRNA H19 to downregulate PTEN
Authors: Z-J Liu
J Ding
J-W Lian
Y Fan
J-L Xu
T Hua
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: FOXF2; NSCLC; H19; PTEN; prognosis
Affiliations: Department of Oncology, Xi'an Chest Hospital, Xi'an, China. .

Abstract:  Objective: To illustrate the role of FOXF2 in the aggravation of the progression of non-small cell lung cancer (NSCLC) by targeting long non-coding RNA (lncRNA) H19 to down-regulate the gene of phosphate and tensin homolog deleted on chromosome ten (PTEN). Patients and methods: The relative levels of FOXF2 and H19 in NSCLC tissues and adjacent normal tissues were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The correlation between the expression levels of FOXF2 and H19 was analyzed. Kaplan-Meier curves were depicted for uncovering the prognostic value of FOXF2 in NSCLC patients. The proliferative and migratory abilities of A549 cells influenced by FOXF2 were also assessed. The interaction between FOXF2 and H19 was evaluated through chromatin immunoprecipitation (ChIP) assay and Western blot, so did the association between H19 and PTEN. Finally, rescue experiments were conducted to explore the role of FOXF2/H19/PTEN axis in regulating the viability and migration of A549 cells. Results: FOXF2 and H19 were upregulated in NSCLC and a positive correlation was observed between the two genes. High level of FOXF2 indicated a worse prognosis in NSCLC patients. The knockdown of FOXF2 attenuated the proliferative and migratory abilities of A549 cells. FOXF2 could bind to the promoter region of H19 and accelerated its transcription. Moreover, H19 could recruit EZH2 to bind to PTEN. The overexpression of H19 could reverse the regulatory effects of FOXF2 on the viability and migration of A549 cells. Conclusions: FOXF2 was upregulated in NSCLC. It accelerated the proliferative and migratory abilities of the NSCLC cells by targeting H19 to downregulate PTEN, thus aggravating the progression of NSCLC. 

Retracted: No

PubPeer comments:
 Fig. 3.  miR-142-5p inhibits cell migration and invasion in NSCLC cells. A. Cell migration assay was determined in A549 cells. B. Cell invasion assay was determined in A549 cells. Cells were transfected with miR142-5p mimics, miR-142-5p inhibitors or NC duplex . Control and NC Migration are unlikely to have come from different treatments. ![file] ,
Merging of Kirkendall growth and Ostwald ripening: CuO@MnO2 core-shell architectures for asymmetric supercapacitors
Authors: Zhiyu Wen
Ming Huang
Fei Li
Alamusi
Ning Hu
Qing Liu
Yuxin Zhang
Zhongchang Wang
Journal: Scientific Reports (2014)
Discipline: Multidisciplinary
Keywords: hierarchical core-shell nanostructures; CuO@MnO2; supercapacitors; electrodes; asymmetric supercapacitor
Affiliations: College of Materials Science and Engineering, Chongqing University, Chongqing 400044, China., 1] College of Materials Science and Engineering, Chongqing University, Chongqing 400044, China [2] National Key Laboratory of Fundamental Science of Micro/Nano-Devices and System Technology, Chongqing University, Chongqing 400044, China., 1] WPI, Advanced Institute for Materials Research, Tohoku University, 2-1-1 Katahira, Aoba-ku, Sendai 980-8577, Japan [2] Department of Engineering Mechanics, College of Aerospace Engineering, Chongqing University, Chongqing 400044, China., Department of Engineering Mechanics, College of Aerospace Engineering, Chongqing University, Chongqing 400044, China., National Key Laboratory of Fundamental Science of Micro/Nano-Devices and System Technology, Chongqing University, Chongqing 400044, China.

Abstract:  Fabricating hierarchical core-shell nanostructures is currently the subject of intensive research in the electrochemical field owing to the hopes it raises for making efficient electrodes for high-performance supercapacitors. Here, we develop a simple and cost-effective approach to prepare CuO@MnO2 core-shell nanostructures without any surfactants and report their applications as electrodes for supercapacitors. An asymmetric supercapacitor with CuO@MnO2 core-shell nanostructure as the positive electrode and activated microwave exfoliated graphite oxide (MEGO) as the negative electrode yields an energy density of 22.1 Wh kg(-1) and a maximum power density of 85.6 kW kg(-1); the device shows a long-term cycling stability which retains 101.5% of its initial capacitance even after 10000 cycles. Such a facile strategy to fabricate the hierarchical CuO@MnO2 core-shell nanostructure with significantly improved functionalities opens up a novel avenue to design electrode materials on demand for high-performance supercapacitor applications. 

Retracted: No

PubPeer comments:
 Figure 1 of 10.1371 journal.pone.0060817 appears to have image overlaps with Figure 4A of 10.1158 1541-7786.MCR-13-0239, after rotation. As the first author appears to have left this lab, perhaps Dr. Morris could investigate that authoru2019s papers. I have found issues which each I have reviewed. *** ![file] *** ![file] ,
NCAPG upregulation mediated by four microRNAs combined with activation of the p53 signaling pathway is a predictor of poor prognosis in patients with breast cancer
Authors: Hanning Li
Menglu Dong
Xiaoqing Cui
Tao Xu
Xingrui Li
Wenfei Xia
Journal: Oncology Letters (2021)
Discipline: CLINICAL MEDICINE
Keywords: breast cancer; cell division cyclin 25 homolog C; microRNAs; non-SMC condensin I complex subunit G; p53 signaling pathway.
Affiliations: Department of Thyroid and Breast Surgery, Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.

Abstract:  The role of non-SMC condensin I complex subunit G (NCAPG) in breast cancer remains unclear. The present study used online databases, reverse transcription-quantitative PCR, flow cytometry and western blotting to determine the expression levels, prognosis and potential molecular mechanisms underlying the role of NCAPG in breast cancer. The association between NCAPG expression and several different clinicopathological parameters in patients with breast cancer was determined, and the results revealed that NCAPG expression was negatively associated with estrogen receptor and progesterone receptor positive status, but was positively associated with HER2 positive status, Nottingham Prognostic Index score and Scarff-Bloom-Richardson grade status. Furthermore, upregulated expression levels of NCAPG resulted in a poor prognosis in patients with breast cancer. A total of 27 microRNAs (miRNAs/miRs) were predicted to target NCAPG, among which four miRNAs (miR-101-3p, miR-195-5p, miR-214-3p and miR-944) were predicted to most likely regulate NCAPG expression in breast cancer. A total of 261 co-expressed genes of NCAPG were identified, including cell division cyclin 25 homolog C (CDC25C), and pathway enrichment analysis indicated that these co-expressed genes were significantly enriched in the p53 signaling pathway. CDC25C expression was downregulated in breast cancer and was associated with a poor prognosis. These findings suggested that upregulated NCAPG expression may be a prognostic biomarker of breast cancer. 

Retracted: No

PubPeer comments:
 In the results section one can clearly see that CDC25C expression is higher in primary tumour vs. normal. The abstract does not agree with this as it says  CDC25C expression was DOWNregulated in breast cancer and was associated with a poor prognosis . I assume this is a wording error and the sentence should be  CDC25C expression was UPregulated in breast cancer and was associated with a poor prognosis , 
 Thank you very much for your reminder. We are very sorry for our mistakes. If there are subsequent articles published, we will checked carefully to avoid such mistakes. ,
Dual role of interleukin-6 in regulating insulin sensitivity in murine skeletal muscle
Authors: Iria Nieto-Vazquez
Cristina de Alvaro
Sonia Fernández-Veledo
Margarita Lorenzo
Journal: Diabetes (2008)
Discipline: CLINICAL MEDICINE
Keywords: Cytokines; interleukin-6; insulin resistance; glucose uptake; protein kinase
Affiliations: Department of Biochemistry and Molecular Biology II, Faculty of Pharmacy, Complutense University, Madrid, Spain.

Abstract:  Objective: Cytokines are elevated in various insulin-resistant states, including type 2 diabetes and obesity, although the contribution of interleukin-6 (IL-6) in the induction of these diseases is controversial. Research design and methods: We analyzed the impact of IL-6 on insulin action in murine primary myocytes, skeletal muscle cell lines, and mice (wild type and protein-tyrosine phosphatase 1B [PTP1B] deficient). Results: IL-6 per se increased glucose uptake by activating serine/threonine protein kinase 11 (LKB1)/AMP-activated protein kinase/protein kinase B substrate of 160 kDa (AS160) pathway. A dual effect on insulin action was observed when myotubes and mice were exposed to this cytokine: additive with short-term insulin (increased glucose uptake and systemic insulin sensitivity) but chronic exposure produced insulin resistance (impaired GLUT4 translocation to plasma membrane and defects in insulin signaling at the insulin receptor substrate 1 [IRS-1] level). Three mechanisms seem to operate in IL-6-induced insulin resistance: activation of c-Jun NH(2)-terminal kinase 1/2 (JNK1/2), accumulation of suppressor of cytokine signaling 3 (socs3) mRNA, and an increase in PTP1B activity. Accordingly, silencing JNK1/2 with either small interfering RNA or chemical inhibitors impaired phosphorylation of IRS-1 (Ser307), restored insulin signaling, and normalized insulin-induced glucose uptake in myotubes. When using a pharmacological approach, liver X receptor agonists overcome IL-6-induced insulin resistance by producing downregulation of socs3 and ptp1b gene expression. Finally, the lack of PTP1B confers protection against IL-6-induced insulin resistance in skeletal muscle in vitro and in vivo, in agreement with the protection against the IL-6 hyperglycemic effect observed on glucose and insulin tolerance tests in adult male mice. Conclusions: These findings indicate the important role of IL-6 in the pathogenesis of insulin resistance and further implicate PTP1B as a potential therapeutic target in the treatment of type 2 diabetes. 

Retracted: Yes

PubPeer comments:
 ![file] , 
null, 
 2020 retraction. https: diabetes.diabetesjournals.org content early 2020 09 04 db20-rt10c ![file] ,
Angiopoietin-1 Modified Human Umbilical Cord Mesenchymal Stem Cell Therapy for Endotoxin-Induced Acute Lung Injury in Rats
Authors: Zhi Wei Huang
Yi Liu
Dong Li
Hai Yan Zhang
Xiu Li Ju
Le Ling Zhang
Ning Liu
Ying Wang
Journal: Yonsei Medical Journal (2017)
Discipline: CLINICAL MEDICINE
Keywords: Angiopoietin-1; acute lung injury; human umbilical cord mesenchymal stem cell.
Affiliations: Department of Hematology, The Qilu Childrens' Hospital, Shandong University, Jinan, Shandong Province, P.R. China., Department of Pediatrics, The Qilu Hospital of Shandong University, Jinan, Shandong Province, P.R. China.

Abstract:  Purpose: Angiopoietin-1 (Ang1) is a critical factor for vascular stabilization and endothelial survival via inhibition of endothelial permeability and leukocyte- endothelium interactions. Hence, we hypothesized that treatment with umbilical cord mesenchymal stem cells (UCMSCs) carrying the Ang1 gene (UCMSCs-Ang1) might be a potential approach for acute lung injury (ALI) induced by lipopolysaccharide (LPS). Materials and methods: UCMSCs with or without transfection with the human Ang1 gene were delivered intravenously into rats one hour after intra-abdominal instillation of LPS to induce ALI. After the rats were sacrificed at 6 hours, 24 hours, 48 hours, 8 days, and 15 days post-injection of LPS, the serum, the lung tissues, and bronchoalveolar lavage fluid (BALF) were harvested for analysis, respectively. Results: Administration of fluorescence microscope confirmed the increased presence of UCMSCs in the injured lungs. The evaluation of UCMSCs and UCMSCs-Ang1 actions revealed that Ang1 overexpression further decreased the levels of the pro-inflammatory cytokines TNF-α, TGF-β₁, and IL-6 and increased the expression of the anti-inflammatory cytokine IL-10 in the injured lungs. This synergy caused a substantial decrease in lung airspace inflammation and vascular leakage, characterized by significant reductions in wet/dry ratio, differential neutrophil counts, myeloperoxidase activity, and BALF. The rats treated by UCMSCs-Ang1 showed improved survival and lower ALI scores. Conclusion: UCMSCs-Ang1 could improve both systemic inflammation and alveolar permeability in ALI. UC-derived MSCs-based Ang1 gene therapy may be developed as a potential novel strategy for the treatment of ALI. 

Retracted: No

PubPeer comments:
 In Figure 4, a micrographs has been duplicated and presented as something else (MSCs vs MSCs-Ang1, 48h). ![file] , 
 Thank you for pointing out the mistakes in our paper. This paper was verified by the author after checking the original picture. lt is true that the micrographs of MSCs and MSCs-Ang1 groups are overlaped .There were many lung tissue specimens in the research. When selecting photos, the author copied mistakenly the photo of the MSCs-Ang1 group into the MSCs group, and the mistake led to the misuse of the pictures. The completeness of the whole research was not affected and the conclusion remained unchanged. We have informed Yonsei Medical Journal and they just agreed to erratum. ,
The function of Cav-1 in MDA-MB-231 breast cancer cell migration and invasion induced by ectopic ATP5B
Authors: Wenzhe Kang
Xinjie Dong
Yilei Li
Wei Li
Ziyi Xing
Rong Tang
Lijuan Zhou
Wenyi Wu
Journal: Medical Oncology (2021)
Discipline: CLINICAL MEDICINE
Keywords: Breast cancer; Cav-1; Ectopic ATP5B; Invasion; Migration.
Affiliations: Department of Pathology, The First Hospital of Jilin University, Changchun, Jilin, 130021, China., The Key Laboratory of Pathobiology, Ministry of Education, The College of Basic Medical Sciences, Jilin University, Changchun, Jilin, 130021, China., The Key Laboratory of Pathobiology, Ministry of Education, The College of Basic Medical Sciences, Jilin University, Changchun, Jilin, 130021, China. ., Electron Microscopy Laboratory of Renal Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, China. .

Abstract:  Ectopic ATP5B, which is located in a unique type of lipid raft caveolar structure, can be upregulated by cholesterol loading. As the structural component of caveolae, Cav-1 is a molecular hub that is involved in transmembrane signaling. In a previous study, the ATP5B-specific binding peptide B04 was shown to inhibit the migration and invasion of prostate cancer cells, and the expression of ATP5B on the plasma membrane of MDA-MB-231 cells was confirmed. The present study investigated the effect of ectopic ATP5B on the migration and invasion of MDA-MB-231 cells and examined the involvement of Cav-1. Cholesterol loading increased the level of ectopic ATP5B and promoted cell migration and invasion. These effects were blocked by B04. Ectopic ATP5B was physically colocalized with Cav-1, as demonstrated by double immunofluorescence staining and coimmunoprecipitation. After Cav-1 knockdown, the migration and invasion abilities of MDA-MB-231 cells were significantly decreased, suggesting that Cav-1 influences the function of ectopic ATP5B. Furthermore, these effects were not reversed after treatment with cholesterol. We concluded that Cav-1 may participate in MDA-MB-231 cell migration and invasion induced by binding to ectopic ATP5B. 

Retracted: No

PubPeer comments:
 Figure 2A: More similar than expected after flip the image horizontally. Could authors check please? ![file] ,
Developmental evidence for serial homology of the vertebrate jaw and gill arch skeleton
Authors: J Andrew Gillis
Clare V H Baker
Melinda S Modrell
Journal: Nature Communications (2013)
Discipline: Multidisciplinary
Keywords: Gegenbaur; jaw-gill arch serial homology; palaeontological evidence; developmental genetic data; Dlx genes
Affiliations: Department of Physiology, Development and Neuroscience, University of Cambridge, Anatomy Building, Downing Street, Cambridge CB2 3DY, UK. 

Abstract:  Gegenbaur's classical hypothesis of jaw-gill arch serial homology is widely cited, but remains unsupported by either palaeontological evidence (for example, a series of fossils reflecting the stepwise transformation of a gill arch into a jaw) or developmental genetic data (for example, shared molecular mechanisms underlying segment identity in the mandibular, hyoid and gill arch endoskeletons). Here we show that nested expression of Dlx genes--the 'Dlx code' that specifies upper and lower jaw identity in mammals and teleosts--is a primitive feature of the mandibular, hyoid and gill arches of jawed vertebrates. Using fate-mapping techniques, we demonstrate that the principal dorsal and ventral endoskeletal segments of the jaw, hyoid and gill arches of the skate Leucoraja erinacea derive from molecularly equivalent mesenchymal domains of combinatorial Dlx gene expression. Our data suggest that vertebrate jaw, hyoid and gill arch cartilages are serially homologous, and were primitively patterned dorsoventrally by a common Dlx blueprint. 

Retracted: No

PubPeer comments:
 image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
Stabilization of p53 by p14ARF without relocation of MDM2 to the nucleolus
Authors: S Llanos
G Peters
P A Clark
J Rowe
Journal: Nature Cell Biology (2001)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: p14ARF; tumour suppressor; MDM2; p53; nucleolus
Affiliations: Imperial Cancer Research Fund, 44 Lincoln's Inn Fields, London WC2A 3PX, UK.

Abstract:  The alternative product of the human INK4a/ARF locus, p14ARF, has the potential to act as a tumour suppressor by binding to and inhibiting the p53 antagonist MDM2. Current models propose that ARF function depends on its ability to sequester MDM2 in the nucleolus. Here we describe situations in which stabilization of MDM2 and p53 occur without relocalization of endogenous MDM2 from the nucleoplasm. Conversely, forms of ARF that do not accumulate in the nucleolus retain the capacity to stabilize MDM2 and p53. We therefore propose that nucleolar localization is not essential for ARF function but may enhance the availability of ARF to inhibit MDM2. 

Retracted: No

PubPeer comments:
 Figure 8c. Much more similar than expected. ![file] , 
 Figure 6. Much more similar than expected. ![file] , 
 #1 The figures analyzed here look indeed identical. However they are not like the figures published. I assume there must be some mistake. ![file] ![file] , 
 #3 I agree with respect to comment #2. Fig. 6b looks fine and not like shown in #2. I do, however, also agree with comment #1: the band at the indicated ++ position has been pasted in. After somewhat enhancing the contrast the rectangular copy-paste imprint is more clearly visible. And the source may indeed have been the p14ARF(65u2013132)u2013GFP ++ position. [ Fig. 8c, contrast-enhanced. Click for larger (but not more sharp) version] ![file] [ Click to animate. Comparison of the ++ and p14ARF(65u2013132)u2013GFP ++ bands ] ![file] , 
 Figure 6. Much more similar than expected. ![file] , 
 Figure 1a (.pdf version). ![file] ,
Chronic valproic acid administration impairs contextual memory and dysregulates hippocampal GSK-3β in rats
Authors: Silvia Sintoni
Marilyn Scandaglia
Antonio Contestabile
Barbara Monti
Ewelina Kurtys
Journal: Pharmacology Biochemistry and Behavior (2013)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Valproic acid; neuroprotection; learning; memory; hippocampus
Affiliations: Department of Pharmacy and BioTechnology, University of Bologna, Italy.

Abstract:  Valproic acid (VPA), a long-standing anti-epileptic and anti-manic drug, exerts multiple actions in the nervous system through various molecular mechanisms. Neuroprotective properties have been attributed to VPA in different models of neurodegeneration, but contrasting results on its improvement of learning and memory have been reported in non-pathologic conditions. In the present study, we have tested on a hippocampal-dependent learning test, the contextual fear conditioning, the effect of chronic VPA administration through alimentary supplementation that allows relatively steady concentrations to be reached by a drug otherwise very rapidly eliminated in rodents. Contextual fear memory was significantly impaired in rats chronically treated with VPA for 4 weeks. To understand the cellular and molecular correlates of this amnesic effect with particular regard to hippocampus, we addressed three putatively memory-related targets of VPA action in this brain area, obtaining the following main results: i) chronic VPA promoted an increase of post-translational modifications of histone H3 (acetylation and phosphorylation) known to favor gene transcription; ii) adult neurogenesis in the dentate gyrus, which has been controversially reported to be affected by VPA, was unchanged; and iii) GSK-3β, a kinase playing a key role in hippocampal plasticity, as well as in learning and memory, was dysregulated by VPA treatment. These results point at GSK-3β dysregulation in the hippocampus as an important parameter in the amnesic effect of VPA. The VPA amnesic effect in the animal model here reported is also supported by some observations in patients and, therefore, it should be taken into account and monitored in VPA-based therapies. 

Retracted: No

PubPeer comments:
 Figure 2C may include an undisclosed splice. Image shown below in inverse. Could the authors please provide the uncropped original scan? *** ![file] ,
Taurine prevents cardiomyocyte apoptosis by inhibiting the calpain-1/cytochrome c pathway during RVH in broilers
Authors: Gaofeng Wu
Shumei Lin
Qunhui Yang
Qiufeng Lyu
Jianmin Hu
Weiwei Li
Jiancheng Yang
Journal: Amino acids (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Apoptosis; Broiler; Calpain-1; Cytochrome c; Right ventricular hypertrophy
Affiliations: Liaoning Provincial Key Laboratory of Zoonosis, College of Animal Science and Veterinary Medicine, Shenyang Agricultural University, Shenyang, 110866, Liaoning, People's Republic of China., Liaoning Provincial Key Laboratory of Zoonosis, College of Animal Science and Veterinary Medicine, Shenyang Agricultural University, Shenyang, 110866, Liaoning, People's Republic of China. .

Abstract:  The calpain-1-activated apoptotic pathway plays a key role in right ventricular hypertrophy (RVH). Taurine has been shown to attenuate apoptosis by inhibiting calpain activity. This experiment aimed to determine whether taurine could prevent RVH by inhibiting the calpain-1/cytochrome c apoptotic pathway. The broilers were given 1% taurine dissolved in drinking water and were raised at 10 °C ~ 12 °C from day 21 to day 42. At 21 d, 28 d, 35 d and 42 d, the right ventricular (RV) tissues were collected. Increased RVH index, angiotensin II, norepinephrine and atrial natriuretic peptide mRNA expression were reduced by taurine in the broiler RVs. Taurine obviously inhibited cardiomyocyte apoptosis via maintaining the mitochondrial membrane potential and decreased the activation of caspase-9 and caspase-3 in the broiler RVs. The antioxidant assay demonstrated that taurine enhanced the activities of superoxide dismutase, total antioxidant capacity and glutathione peroxidase and the glutathione/glutathione disulfide ratio. Western blot results revealed that taurine also downregulated the expression of calpain-1 and cytosolic cytochrome c while upregulating the expression of Bcl-2/Bax and mitochondrial cytochrome c in broiler cardiomyocytes during RVH. In summary, we found that taurine could enhance cardiomyocyte antioxidant ability and further prevented cardiomyocyte apoptosis by inhibiting the calpain-1/cytochrome c pathway during RVH in broilers. 

Retracted: No

PubPeer comments:
 The  tadpole style of Western blots in this paper (Figures 3 and 5) are of a very similar nature to those reported by Elizabeth Bik and others. Moreover, the ORCID account of the submitting author also has a similar trend, i.e., no information. , 
 #1 I do not see a great resemblance to performing tadpoles. The WBs here seem plausible enough to my untutored eyes. Fig 3(c): ![file] ,