PReD-Bench/PRed-Bench huggingface dataset:
Inactivation of YAP oncoprotein by the Hippo pathway is involved in cell contact inhibition and tissue growth control
Authors: Weiquan Li
Joe Xie
Georg Halder
Qian Yang
Ryan S Udan
Bin Zhao
Keqiang Ye
Pan Zheng
Zhi-Chun Lai
Arul Chinnaiyan
Tsuneo Ikenoue
Jindan Yu
Xiaomu Wei
Kun-Liang Guan
Joungmok Kim
Li Li
Journal: Genes & Development (2007)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Hippo pathway; cell proliferation; apoptosis; Drosophila; NF2
Affiliations: Life Sciences Institute, University of Michigan, Ann Arbor, Michigan 48109, USA.

Abstract:  The Hippo pathway plays a key role in organ size control by regulating cell proliferation and apoptosis in Drosophila. Although recent genetic studies have shown that the Hippo pathway is regulated by the NF2 and Fat tumor suppressors, the physiological regulations of this pathway are unknown. Here we show that in mammalian cells, the transcription coactivator YAP (Yes-associated protein), is inhibited by cell density via the Hippo pathway. Phosphorylation by the Lats tumor suppressor kinase leads to cytoplasmic translocation and inactivation of the YAP oncoprotein. Furthermore, attenuation of this phosphorylation of YAP or Yorkie (Yki), the Drosophila homolog of YAP, potentiates their growth-promoting function in vivo. Moreover, YAP overexpression regulates gene expression in a manner opposite to cell density, and is able to overcome cell contact inhibition. Inhibition of YAP function restores contact inhibition in a human cancer cell line bearing deletion of Salvador (Sav), a Hippo pathway component. Interestingly, we observed that YAP protein is elevated and nuclear localized in some human liver and prostate cancers. Our observations demonstrate that YAP plays a key role in the Hippo pathway to control cell proliferation in response to cell contact. 

Retracted: No

PubPeer comments:
 Figure 6C. Much more similar than expected. https: imgur.com WCtYv6j ,
Bioinspired Functionalized Melanin Nanovariants with a Range of Properties Provide Effective Color Matched Photoprotection in Skin
Authors: Hemlata Gautam
Vishvabandhu Gotherwal
Sudhir Chandna
Rajkishor Rai
Kanupriya Sharma
Ritika Grover
Prashant Joshi
Manika Vij
Rajesh S Gokhale
Vivek T Natarajan
Munia Ganguli
Naiem Ahmad Wani
Journal: Biomacromolecules (2016)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Melanin; polydopamine; biomimetic approach; peptide-derived; physicochemical properties
Affiliations: CSIR-Institute of Genomics and Integrative Biology , Mathura Road, Delhi 110 020, India., Academy of Scientific and Innovative research , CSIR campus, CSIR Road, Chennai 600113, India., CSIR-Indian Institute of Integrative Medicine , Canal Road, Jammu 180001, India., Institute of Nuclear Medicine and Allied Sciences , Brig. SK Mazumdar Road, Delhi 110054, India., National Institute of Immunology , Aruna Asaf Ali Marg, Delhi 110067, India.

Abstract:  Melanin and related polydopamine hold great promise; however, restricted fine-tunabilility limits their usefulness in biocompatible applications. In the present study, by taking a biomimetic approach, we synthesize peptide-derived melanin with a range of physicochemical properties. Characterization of these melanin polymers indicates that they exist as nanorange materials with distinct size distribution, shapes, and surface charges. These variants demonstrate similar absorption spectra but have different optical properties that correlate with particle size. Our approach enables incorporation of chemical groups to create functionalized polyvalent organic nanomaterials and enables customization of melanin. Further, we establish that these synthetic variants are efficiently taken up by the skin keratinocytes, display appreciable photoprotection with minimal cytotoxicity, and thereby function as effective color matched photoprotective agents. In effect we demonstrate that an array of functionalized melanins with distinct properties could be synthesized using bioinspired green chemistry, and these are of immense utility in generating customized melanin/polydopamine like materials. 

Retracted: No

PubPeer comments:
  , 
 Thank you for pointing this out. It appears after checking the raw data that we have made a mistake during the final figure assembly and inadvertently pasted an incorrect figure. We will get this corrected at the earliest. ,
Geriatric muscle stem cells switch reversible quiescence into senescence
Authors: Esteban Ballestar
Vanessa Ruiz-Bonilla
Eusebio Perdiguero
Antonio L Serrano
Susana Gonz√°lez
Pedro Sousa-Victor
Susana Gutarra
Merc√® Jard√≠
Laura Ortet
Laura Garc√≠a-Prat
Pura Mu√±oz-C√°noves
Javier Rodriguez-Ubreva
Journal: Nature (2014)
Discipline: Multidisciplinary
Keywords: skeletal muscle; satellite cells; ageing; quiescent state; regenerative capacity
Affiliations: 1] Cell Biology Group, Department of Experimental and Health Sciences, Pompeu Fabra University, CIBER on Neurodegenerative diseases, E-08003 Barcelona, Spain [2] Buck Institute for Research on Aging, Novato, California 94945, USA., 1] Cell Biology Group, Department of Experimental and Health Sciences, Pompeu Fabra University, CIBER on Neurodegenerative diseases, E-08003 Barcelona, Spain [2]., Chromatin and Disease Group, Cancer Epigenetics and Biology Programme, Bellvitge Biomedical Research Institute, L'Hospitalet de Llobregat, E-08907 Barcelona, Spain., Cell Biology Group, Department of Experimental and Health Sciences, Pompeu Fabra University, CIBER on Neurodegenerative diseases, E-08003 Barcelona, Spain., Stem Cell Aging Group, Centro Nacional de Investigaciones Cardiovasculares, E-28029 Madrid, Spain., 1] Cell Biology Group, Department of Experimental and Health Sciences, Pompeu Fabra University, CIBER on Neurodegenerative diseases, E-08003 Barcelona, Spain [2] Instituci√≥ Catalana de Recerca i Estudis Avan√ßats, E-08010 Barcelona, Spain.

Abstract:  Regeneration of skeletal muscle depends on a population of adult stem cells (satellite cells) that remain quiescent throughout life. Satellite cell regenerative functions decline with ageing. Here we report that geriatric satellite cells are incapable of maintaining their normal quiescent state in muscle homeostatic conditions, and that this irreversibly affects their intrinsic regenerative and self-renewal capacities. In geriatric mice, resting satellite cells lose reversible quiescence by switching to an irreversible pre-senescence state, caused by derepression of p16(INK4a) (also called Cdkn2a). On injury, these cells fail to activate and expand, undergoing accelerated entry into a full senescence state (geroconversion), even in a youthful environment. p16(INK4a) silencing in geriatric satellite cells restores quiescence and muscle regenerative functions. Our results demonstrate that maintenance of quiescence in adult life depends on the active repression of senescence pathways. As p16(INK4a) is dysregulated in human geriatric satellite cells, these findings provide the basis for stem-cell rejuvenation in sarcopenic muscles. 

Retracted: No

PubPeer comments:
  Extended Data Fig. 1, part c, the same cells are representing u2018oldu2019 and u2018geriatricu2019 mice, but eMHC staining (green fluorescence) is only shown for the geriatric sample, giving the false impression that this protein is specifically expressed in geriatric mice. The authors even present quantitative scoring to suggest that the differences in expression between the samples is highly significant. ,
Sensory lesioning induces microglial synapse elimination via ADAM10 and fractalkine signaling
Authors: Ana Badimon
Bruce T Lamb
Liwang Liu
Georgia Gunner
Shane M Bemiller
Kasey M Johnson
Sergio A Lira
Erica Mondo
Ki-Wook Kim
M Aurel Nagy
Dorothy P Schafer
Pinar Ayata
Michael E Greenberg
Andrew R Tapper
Anne Schaefer
Lucas Cheadle
Richard M Ransohoff
Journal: Nature neuroscience (2019)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Microglia; synaptic connectivity; neuron-derived molecules; synapse elimination; CX3CR1
Affiliations: Department of Neurobiology, Brudnick Neuropsychiatric Research Institute, University of Massachusetts Medical School, Worcester, MA, USA., Department of Neurobiology, Harvard Medical School, Boston, MA, USA., Fishberg Department of Neuroscience, Department of Psychiatry, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA., Ronald M. Loeb Center for Alzheimer's Disease, Icahn School of Medicine at Mount Sinai, New York, NY, USA., Stark Neurosciences Research Institute, Indiana University, Indianapolis, IN, USA., Department of Pharmacology and Center for Stem Cell and Regenerative Medicine, University of Illinois College of Medicine, Chicago, IL, USA., Precision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA., Third Rock Ventures, Boston, MA, USA., Department of Neurobiology, Brudnick Neuropsychiatric Research Institute, University of Massachusetts Medical School, Worcester, MA, USA. .

Abstract:  Microglia rapidly respond to changes in neural activity and inflammation to regulate synaptic connectivity. The extracellular signals, particularly neuron-derived molecules, that drive these microglial functions at synapses remain a key open question. Here we show that whisker lesioning, known to dampen cortical activity, induces microglia-mediated synapse elimination. This synapse elimination is dependent on signaling by CX3CR1, the receptor for microglial fractalkine (also known as CXCL1), but not complement receptor 3. Furthermore, mice deficient in CX3CL1 have profound defects in synapse elimination. Single-cell RNA sequencing revealed that Cx3cl1 is derived from cortical neurons, and ADAM10, a metalloprotease that cleaves CX3CL1 into a secreted form, is upregulated specifically in layer IV neurons and in microglia following whisker lesioning. Finally, inhibition of ADAM10 phenocopies Cx3cr1-/- and Cx3cl1-/- synapse elimination defects. Together, these results identify neuron-to-microglia signaling necessary for cortical synaptic remodeling and reveal that context-dependent immune mechanisms are utilized to remodel synapses in the mammalian brain. 

Retracted: No

PubPeer comments:
 The single-cell analyses could have been improved by more careful pre-processing. For example, cluster 17 quite obviously consists of cell doublets that should have been removed. On average, these cells have over three times higher counts than other clusters of excitatory neurons and higher counts on average than the remaining 99% of cells. ,
Abnormal expression and function of the E-cadherin‚Äìcatenin complex in gastric carcinoma cell lines
Authors: M J Farthing
A U Jawhari
M Noda
M Pignatelli
Journal: British Journal of Cancer (1999)
Discipline: CLINICAL MEDICINE
Keywords: cadherin-catenin complex; E-cadherin; catenin; gastric carcinoma; cell lines
Affiliations: Digestive Diseases Research Centre, St Bartholomew's and the Royal London School of Medicine and Dentistry, Whitechapel, London, UK.

Abstract:  Dysfunction of the cadherin-catenin complex, a key component of adherens junctions, is thought to confer invasive potential to cells. The aim of this study is to examine the expression and function of the E-cadherin/catenin complex in gastric carcinoma cell lines. Expression of E-cadherin, alpha, beta and gamma-catenin and p120ctn, and of the adenomatous polyposis coli protein (APC), together with function of the cadherin-catenin complex was examined in a panel of gastric carcinoma cell lines, using immunocytochemistry, Western blotting and a cell-cell aggregation assay. Protein interactions were examined by sequential immunoprecipitation and immunoblotting with antibodies to E-cadherin, alpha, beta and gamma-catenin, p120ctn and APC. Abnormalities of E-cadherin, alpha- and beta-catenin expression, were associated with disturbance of E-cadherin-catenin complex composition, loss of membranous localization and loss of calcium-dependent aggregation in six gastric carcinoma cell lines. APC protein expression and interaction with beta-catenin was preserved in five cell lines. We demonstrate frequent abnormalities of expression and function of E-cadherin and catenins, and associated disturbance of E-cadherin-mediated intercellular adhesion in gastric carcinoma cell lines. These findings support the tumour suppressor role of the E-cadherin and its contribution to the development and progression of the neoplastic phenotype in gastric carcinoma. 

Retracted: No

PubPeer comments:
 Figure 4c. Splice 2nd panel down, no splice top panel. https: imgur.com R13ssoU ,
Relationship of p215BRCA1 to tyrosine kinase signaling pathways and the cell cycle in normal and transformed cells
Authors: H T Zhang
Q Wang
H B Zhang
X Zhang
J G Davis
B L Weber
H Z Zhao
M I Greene
D M O&#x27;Rourke
Y Kajino
K Kajino
Journal: Oncogene (1997)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: BRCA1; neu; breast cancer; tyrosine phosphorylation; cell growth
Affiliations: Department of Pharmacology, School of Medicine, University of Pennsylvania, Philadelphia 19104, USA.

Abstract:  We have analysed the relationship of the products of two genes, neu and BRCA1, known to be important in human breast cancer. Highly specific antibodies that recognized both the rodent and human form of the BRCA1 gene product (Mr 215 kDa, p215BRCA1) were developed to facilitate these efforts. p215BRCA1 was identified as a tyrosine phosphorylated protein primarily localized in the nucleus of several breast cancer cell lines. In transformed murine and human cells, levels of p215BRCA1 tyrosine phosphorylation were inversely correlated with the activity of the erbB family receptor-tyrosine-kinases and with the transformed growth features of these cells. Regulation of p215BRCA1 tyrosine phosphorylation was also related to events in the cell cycle. Increased levels of p215BRCA1 phosphotyrosine content were observed in NIH3T3 cells arrested at the G2/M transition. These findings indicate that the products of BRCA1, neu, and erbB breast cancer genes participate in a common or shared signaling pathway important in cell growth and its regulation. 

Retracted: No

PubPeer comments:
 Figure 1d. Lanes 1 and 2 much more similar than you would expect. Lanes 5 and 6 much more similar than you would expect. https: imgur.com M8MtlT6 , 
 #1 I agree with the original poster that these two sets of lanes appear to be the same. Understanding that the authors may no longer have the original images, could they address how this might affect the conclusions? False color images below. ***  ***  ,
Inhibition of breast cancer cells by targeting E2F-1 gene and expressing IL15 oncolytic adenovirus
Authors: Jiandong Wang
Xiaohui Du
Xin Wu
Wei Wen
Hu Xu
Yan Liang
Yang Yan
Fengyuan Liu
Lingdi Wang
Journal: Bioscience Reports (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: E2F-1; IL-15; Oncolytic adenovirus; breast cancers.
Affiliations: Department of General Surgery, Chinese People's Liberation Army General Hospital, Beijing 100853, China., Department of General Surgery, Hainan Hospital of Chinese People's Liberation Army General Hospital, Sanya 572013, China., Department of General Surgery, Chinese People's Liberation Army General Hospital, Beijing 100853, China  ., Department of Pediatrics, Chinese People's Liberation Army General Hospital, Beijing 100853, China.

Abstract:  The wide application of oncolytic adenovirus presents a novel therapeutic strategy for breast cancer gene therapy. Application of adenovirus alone achieves little curative effects on breast cancer. In addition, it is worth exploring the synergistic anti-tumor effect by inserting immunomodulatory factor in oncolytic adenovirus genome. By taking the advantage of the highly proliferative property of breast cancer, a novel recombinant adenovirus which could selectively kill tumor cells is established under an E2F-1 promoter. Also by carrying human Interleukin-15 (IL-15) gene, the oncolytic adenovirus exhibits an immunomodulatory effect. The present study proved that the novel oncolytic virus (SG400-E2F/IL-15) exhibits an enhanced anti-tumor activity both in vitro and in vivo, representing an experimental basis for breast cancer "virus-gene" therapy. 

Retracted: No

PubPeer comments:
 Images in figure 2A appear to overlap, although described as being imaged at different times. ***  , 
 https: doi.org 10.1042 BSR-20190384_COR Some substantive corrections are to be made to the original article u201cInhibition of breast cancer cells by targeting E2F-1 gene and expressing IL15 oncolytic adenovirusu201d (Biosci Rep. (2019) 39(7), DOI: 10.1042 BSR20190384). In Figure 2A, the photos of u201872 hours after infectionu2019 in the MDA-MB-231 group and u201824 hours after infectionu2019 in the MRC-5 group are replaced with the correct pictures in this correction article. This change does not affect the conclusion of this article. Corrected Figure  , 
 Several figures have small repeated regions, possibly due to editing during figure labeling. *** Figure 1A  *** Figure 5A and 5E  ,
Dr. Manners
Authors: K Heran Darwin
Journal: EMBO reports (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Good manners; science; social media etiquette; researchers
Affiliations: New York University School of Medicine New York NY USA

Abstract:  Good manners make a difference-in science and elsewhere. This includes our social media etiquette as researchers. 

Retracted: No

PubPeer comments:
null, 
null, 
null, 
null, 
null, 
null, 
null, 
null, 
 Figure 4. Continuation Dystrophin expression RT-PCR panel. Much more similar than expected.  ,
Heat-shock protein 70 binds to a novel sequence in 5' UTR of tumor suppressor SMAR1 and regulates its mRNA stability upon Prostaglandin A2 treatment
Authors: Sandeep Singh
Kadreppa Sreenath
Lakshminarasimhan Pavithra
Samit Chattopadhyay
Journal: FEBS letters (2010)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Prostaglandin A2; HSP70; SMAR1; cell cycle arrest; breast cancers
Affiliations: National Centre for Cell Science, Pune University Campus, Ganeshkhind, Pune, India.

Abstract:  Here, we report Prostaglandin A2 (PGA2) induced binding of HSP70 to a novel site on phi1 SMAR1 5' UTR which stabilizes the wild type transcript and leads to subsequent increase in SMAR1 protein levels. SMAR1 mediated cell cycle arrest is perturbed in PGA2-treated cells when HSP70 is knocked-down. Contrarily HSP70, unlike SMAR1, is overexpressed in breast cancers. We demonstrate that this is because of the inability of HSP70 to bind to the phi17 SMAR1 UTR variant which is the predominant form in breast cancers. 

Retracted: No

PubPeer comments:
 There is image duplication in figure 4. Panel 4 B and 4 D are same with different stretch and contrast.  , 
 #1 Thank you for pointing this out. The panel represents SMAR1 isoform 1 levels after different treatments, used as a control for panels on the right in the main figure. As can be seen in the attached raw images below, the panel seems to have been repasted during inversion and assembly. The quantifications remain unaltered and this does not in anyway change the conclusions of the study. We are in touch with the journal to remedy this. - Dr. Samit Chattopadhyay ,
MicroRNA-122 inhibits tumorigenic properties of hepatocellular carcinoma cells and sensitizes these cells to sorafenib
Authors: Gerard Nuovo
Shoumei Bai
Kalpana Ghoshal
Shu-Hao Hsu
Jharna Datta
Pawan Kumar
Arti Yadav
Mohd W Nasser
Huban Kutay
Bo Wang
Journal: Journal of Biological Chemistry (2009)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: MicroRNAs; miR-122; hepatocellular carcinomas; tumorigenic properties; ADAM10
Affiliations: Department of Molecular and Cellular Biochemistry, The Ohio State University, Columbus, Ohio 43210, USA.

Abstract:  MicroRNAs are negative regulators of protein coding genes. The liver-specific microRNA-122 (miR-122) is frequently suppressed in primary hepatocellular carcinomas (HCCs). In situ hybridization demonstrated that miR-122 is abundantly expressed in hepatocytes but barely detectable in primary human HCCs. Ectopic expression of miR-122 in nonexpressing HepG2, Hep3B, and SK-Hep-1 cells reversed their tumorigenic properties such as growth, replication potential, clonogenic survival, anchorage-independent growth, migration, invasion, and tumor formation in nude mice. Further, miR-122-expressing HCC cells retained an epithelial phenotype that correlated with reduced Vimentin expression. ADAM10 (a distintegrin and metalloprotease family 10), serum response factor (SRF), and insulin-like growth factor 1 receptor (Igf1R) that promote tumorigenesis were validated as targets of miR-122 and were repressed by the microRNA. Conversely, depletion of the endogenous miR-122 in Huh-7 cells facilitated their tumorigenic properties with concomitant up-regulation of these targets. Expression of SRF or Igf1R partially reversed tumor suppressor function of miR-122. Further, miR-122 impeded angiogenic properties of endothelial cells in vitro. Notably, ADAM10, SRF, and Igf1R were up-regulated in primary human HCCs compared with the matching liver tissue. Co-labeling studies demonstrated exclusive localization of miR-122 in the benign livers, whereas SRF predominantly expressed in HCC. More importantly, growth and clonogenic survival of miR-122-expressing HCC cells were significantly reduced upon treatment with sorafenib, a multi-kinase inhibitor clinically effective against HCC. Collectively, these results suggest that the loss of multifunctional miR-122 contributes to the malignant phenotype of HCC cells, and miR-122 mimetic alone or in combination with anticancer drugs can be a promising therapeutic regimen against liver cancer. 

Retracted: No

PubPeer comments:
 https: imgur.com QQtSlc7 , 
 I came across this independently and agree. First author appears to currently be affiliated with University of Pittsburgh, and has the unfortunate distinction of appearing as coauthor of multiple papers with similar image concerns while at different institutions: https: pubpeer.com search?q=Shoumei+Bai  ,
miR-302d Competitively Binding with the lncRNA-341 Targets TLE4 in the Process of SSC Generation
Authors: Wenhui Zhang
Bichun Li
Yingjie Wang
Cai Hu
Yi Li
Man Wang
Ahmed Kamel Elsayed
Yani Zhang
Qisheng Zuo
Journal: Stem Cells International (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: miRNAs; poultry; differentiation; embryonic stem cells; spermatogonia stem cells
Affiliations: College of Animal Science and Technology, Yangzhou University, Jiangsu Province Key Laboratory of Animal Breeding and Molecular Design, Yangzhou, 225009 Jiangsu, China, Faculty of Veterinary Medicine, Suez Canal University, 41522 Ismailia, Egypt, College of Computer Science and Technology, Wenzhou-Kean University, Wenzhou, 325035 Zhejiang, China

Abstract:  MicroRNAs (miRNAs) are essential factors in the reproductive process of poultry. Here, we found miR-302d is a potential differentiation and negative factor of chicken embryonic stem cells (ESCs) into spermatogonia stem cells (SSCs). The competition mechanism was carried out for the preliminary exploration to determine the relationship among miR-302d, lncRNA-341(interacting with miR-302d), and target gene TLE4. The results showed that lncRNA-341 can competitively bind to miR-302d to decrease the targeted binding of miR-302d and TLE4 which promotes the differentiation of chicken SSCs. Moreover, it is suggested that miR-302d may participate in the Wnt signaling pathway through TLE4. 

Retracted: No

PubPeer comments:
 Same Flow Cytometry dotplot in two different treatment ,
RNA-Mediated Control of Metal Nanoparticle Shape
Authors: Lina A Gugliotti
Daniel L Feldheim
Bruce E Eaton
Journal: Journal of the American Chemical Society (2005)
Discipline: CHEMISTRY
Keywords: RNA sequences; palladium particle growth; pyridyl-modified RNA; hexagonal plates; cubic particles

Abstract:  RNA sequences previously isolated by in vitro selection were further characterized for their ability to control palladium particle growth. Five pyridyl-modified RNA sequences (Pdases) representing each of the different evolved families were found to form hexagonal plates with a high degree of shape specificity. However, a sixth nonrelated pyridyl-modified RNA sequence was found to form exclusively cubic particles under identical conditions. Replacing pyridyl-modified RNA with native RNA resulted in a complete loss of RNA function. Removing the 3'-fixed sequence region from the Pdase had little effect on particle growth; however, further truncations into the variable region resulted in a significant loss of activity and particle shape control. These Pdases were selected using the organometallic precursor complex tris(dibenzylideneacetone) dipalladium(0) ([Pd2(DBA)3]). Changing the metal center and ligand of the group VIII organometallic precursor complex revealed a strong dependence of particle growth and shape on the DBA ligands. Changing the metal center from Pd to Pt while retaining the DBA ligands gave predominantly hexagonal Pt, but with a decrease in shape control. Taken together, the results of this study suggest that the full-length Pdases contain active sites capable of highly specific molecular recognition of organometallic complexes as particle formation reagents. 

Retracted: No

PubPeer comments:
 The results of this article are based on the article published in Science  RNA-Mediated Metal-Metal Bond Formation in the Synthesis of Hexagonal Palladium Nanoparticles in 2004. This article was retracted and it was later proved that RNA did not catalyze the formation of Palladium Hexagons and the particles were infact just precursor particles. The big question arise how results of this article correct when the result of base paper in science has been proved incorrect. The authors must answer this very important question or the journal must retract this also. ,
Tanshinone IIA protects hypoxia-induced injury by preventing microRNA-28 up-regulation in PC-12 cells
Authors: Yibin Zeng
Nan Tang
Jian Chang
Jin Zheng
Journal: European Journal of Pharmacology (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Cerebral ischemia; Hypoxia; Sp1/suvivin; Tanshinone IIA; microRNA-28.
Affiliations: Department of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, Hubei, China., Department of Pancreatic Surgery, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei, China., Department of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, Hubei, China. Electronic address: .

Abstract:  This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Editor-in-Chief. Given the comments of Dr Elisabeth Bik regarding this article ‚ÄúThis paper belongs to a set of over 400 papers (as per February 2020) that share very similar Western blots with tadpole-like shaped bands, the same background pattern, and striking similarities in title structures, paper layout, bar graph design, and - in a subset - flow cytometry panels‚Ä? the journal requested the authors to provide the raw data. However, the authors were not able to fulfil this request and therefore the Editor-in-Chief decided to retract the article. 

Retracted: No

PubPeer comments:
 (a) The u201c**quality**u201d of information defined in eq.(7) of Definition 3 has nothing to do with the quality of information as it is supposed to be in Definition 3. As a consequence, the term in eq.(8) of Definition 4 makes no sense for ranking. (b) eq.(9) of Definition 5 is not well defined because no order relation between the so-called trapezoidal intuitionistic fuzzy values in introduced. As a consequence, Proposition 2 is not interpretable. (c) See also the comment for the thermodynamic approach to decision making on https: pubpeer.com publications B6D42E184850FF2F52FC1F3ECF1A5D      ,
The C-terminal domain of CENP-C displays multiple and critical functions for mammalian centromere formation
Authors: Giovanni Perini
Stefania Trazzi
Andrea Musacchio
Giuliano Della Valle
Monica Zoli
Joseph C Reese
Roberto Bernardoni
Journal: PloS one (2009)
Discipline: Multidisciplinary
Keywords: CENP-C; centromeres; structure-function relationship; centromeric DNA; kinetochore proteins
Affiliations: Department of Biology, University of Bologna, Bologna, Italy.

Abstract:  CENP-C is a fundamental component of functional centromeres. The elucidation of its structure-function relationship with centromeric DNA and other kinetochore proteins is critical to the understanding of centromere assembly. CENP-C carries two regions, the central and the C-terminal domains, both of which are important for the ability of CENP-C to associate with the centromeric DNA. However, while the central region is largely divergent in CENP-C homologues, the C-terminal moiety contains two regions that are highly conserved from yeast to humans, named Mif2p homology domains (blocks II and III). The activity of these two domains in human CENP-C is not well defined. In this study we performed a functional dissection of C-terminal CENP-C region analyzing the role of single Mif2p homology domains through in vivo and in vitro assays. By immunofluorescence and Chromatin immunoprecipitation assay (ChIP) we were able to elucidate the ability of the Mif2p homology domain II to target centromere and contact alpha satellite DNA. We also investigate the interactions with other conserved inner kinetochore proteins by means of coimmunoprecipitation and bimolecular fluorescence complementation on cell nuclei. We found that the C-terminal region of CENP-C (Mif2p homology domain III) displays multiple activities ranging from the ability to form higher order structures like homo-dimers and homo-oligomers, to mediate interaction with CENP-A and histone H3. Overall, our findings support a model in which the Mif2p homology domains of CENP-C, by virtue of their ability to establish multiple contacts with DNA and centromere proteins, play a critical role in the structuring of kinethocore chromatin. 

Retracted: No

PubPeer comments:
 An unexpected similarity between two images published seven years apart  ,
RETRACTED ARTICLE: Accelerated oral wound healing using a pre-vascularized mucosal cell sheet
Authors: Jaewang Lee
Eun Hye Kim
Daiha Shin
Jong-Lyel Roh
Journal: Scientific Reports (2017)
Discipline: Multidisciplinary
Keywords: Cell sheets; pre-vascularization; oral wound healing; mucosal cell sheets; keratinocytes
Affiliations: Department of Otolaryngology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea., Department of Otolaryngology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea. .

Abstract:  Cell sheets with pre-vascularization have recently been developed but remain relatively untested in oral wound healing. Therefore, we examined the potential utility of our newly developed pre-vascularized mucosal cell sheets in oral wound healing. Mucosal keratinocytes, fibroblasts, and endothelial progenitor cells were primarily cultured for in vitro cell expansion from mucosa and blood of Sprague-Dawley rats. Mucosal cell sheets were generated using cultured keratinocytes and plasma fibrin (K sheet) or keratinocytes and a mixture of fibrin, fibroblasts, and endothelial cells (PV sheet). Autologous sheets were transplanted on deep wounds in the buccal region of rats. The gross and histological characteristics of wound healing were compared among control wound, K sheet, and PV sheet groups. We successfully cultured and expanded keratinocytes, fibroblasts, and endothelial progenitor cells in vitro for generating mucosal cell sheets with or without pre-vascularization. In the in vivo oral wound model, compared with the control wound, the PV sheet group exhibited rapid wound closure more prominently than the K sheet group. The histological healing in the PV sheet group was similar to that in rat normal buccal mucosa without fibrosis. The pre-vascularized mucosal cell sheet exhibited in vivo efficacy in oral wound healing by promoting accelerated healing. 

Retracted: Yes

PubPeer comments:
 2021 retraction. https: www.nature.com articles s41598-021-82919-5 The Editors have retracted this Article. An institutional investigation found evidence that the images used for Figures 3C, 3D, 3F, 5D and 6E, originated from a different set of experiments to those listed. The Editors therefore no longer have confidence in the integrity of the data presented. Authors Jaewang Lee and Daiha Shin agree to this retraction. Authors Eun Hye Kim and Jong-Lyel Roh have not responded to any correspondence from the Editors about this retraction. ,
Connexin 43 reduces susceptibility to sympathetic atrial fibrillation
Authors: Jinyi Li
Zhengnan Zhang
Jiangtao Wu
Yifei Yan
Zhiyu Zeng
Beibei Luo
Hao Liu
Yan He
Haide Liu
Weiqiang Huang
Journal: International journal of molecular medicine (2018)
Discipline: CLINICAL MEDICINE
Keywords: Atrial fibrillation; Connexin 43; Sympathomimetic; Gene-specific small interfering RNA; Animal model
Affiliations: Department of Geriatric Cardiology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530000, P.R. China., Department of Cardiology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530000, P.R. China.

Abstract:  Atrial fibrillation (AF) is the most common arrhythmia reported in clinical practice. Connexin 43 (Cx43) is a member of the connexin protein family, which serves important roles in signal transduction in vivo. The aim of the present study was to investigate the role of Cx43 in the induction and maintenance of atrial fibrillation by using an animal model of sympathomimetic atrial fibrillation. Cx43 was successfully knocked down in the myocardium with gene‚Äëspecific small interfering (si)RNA via lentiviral infection. A total of 25 dogs were randomly and evenly divided into five groups: Normal (N), rapid atrial pacing (RAP), isoproterenol (ISO) + RAP, RAP + Cx43 siRNA and ISO + RAP + Cx43 siRNA. The mRNA and protein levels, as well as the distribution of Cx43 on the cell membrane, were gradually decreased in each group compared with the N group following treatment (P&lt;0.05). The induction rate of the atrial effective refractory period was not significantly affected in the RAP and RAP + Cx43 siRNA groups, whereas it was significantly reduced in the ISO + RAP and ISO + RAP + Cx43 siRNA groups compared with the N group (P&lt;0.05). The induction rate of AF was gradually increased in the RAP + Cx43 siRNA, ISO + RAP and ISO + RAP + Cx43 siRNA groups compared with the N group (P&lt;0.05). The expression of nerve growth factor (NGF) and tyrosine hydroxylase (TH) was gradually increased in the ISO + RAP and ISO + RAP + Cx43 siRNA groups compared with their respective controls (RAP and RAP + Cx43 siRNA groups, respectively). However, no significant difference in the levels of NGF and TH was observed between the RAP, RAP + Cx43 siRNA, ISO + RAP and ISO + RAP + Cx43 siRNA groups. The mitochondrial morphology in each group was notably altered compared with the N group. The mitochondrial reactive oxygen species production and apoptotic index were gradually increased in each group compared with the N group (P&lt;0.05). The results of the present study suggest that Cx43 reduces susceptibility to AF. Downregulation of Cx43 mediates the induction and maintenance of sympathetic AF. 

Retracted: No

PubPeer comments:
 Figure 3B: ECG was reused from previous paper (DOI:10.14744 AnatolJCardiol.2017.7602).  ,
Leptin induces CD40 expression through the activation of Akt in murine dendritic cells
Authors: Liwei Lu
Queenie Lai Kwan Lam
Xuetao Cao
Dong-Yan Jin
Bo-Jian Zheng
Journal: Journal of Biological Chemistry (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: leptin; dendritic cell; CD40 expression; immunostimulatory function; T cell proliferation
Affiliations: Department of Pathology, The University of Hong Kong, China.

Abstract:  Increasing evidence suggests a regulatory role for leptin, an adipocyte-derived hormone, in immunity. Although recent studies indicated an essential role of leptin signaling in dendritic cell (DC) maturation, the molecular mechanisms by which leptin modulates DC functional maturation remained unclear. In this study, we showed that leptin induced CD40 expression in murine DC and significantly up-regulated their immunostimulatory function in driving T cell proliferation. Moreover, leptin markedly enhanced lipopolysaccharide-mediated DC activation. Using pharmacological inhibitors for Akt, STAT-1alpha, or NF-kappaB and the dominant negative forms of Akt and IkappaB kinase alpha/beta/gamma, as well as small interfering RNA for STAT-1alpha, we showed that Akt, STAT-1alpha, and NF-kappaB were important for the leptinor lipopolysaccharide-induced CD40 expression. Coimmunoprecipitation analysis revealed that leptin promoted immune complex formation between Akt and the IkappaB kinase subunits as well as STAT-1alpha. Blocking the activity of Akt demonstrated a crucial role for Akt in translocation of STAT-1alpha and NF-kappaB to the nucleus and activation of the CD40 promoter. Further analysis with chromatin immunoprecipitation assay confirmed that leptin recruited STAT-1alpha, NF-kappaBp65, and RNA polymerase II to the CD40 promoter and enhanced histone 4 acetylation in a time-dependent manner. Thus, our results have elucidated the molecular mechanisms underlying leptin-induced CD40 expression and DC maturation. 

Retracted: Yes

PubPeer comments:
 Posting a concern by another reader. In Figure 2, The GAPDH panel shown in Figure 1A appears to look similar to the GAPDH panel belonging to the MEK1 2 expression. Note the different incubation times.  , 
 #1   , 
 #1  , 
 retraction on Aug 21, 2020 : http: m.jbc.org content 295 34 12329  This article has been withdrawn by Bo-Jian Zheng, Dong-Yan Jin, Xuetao Cao, and Liwei Lu. Queenie Lai Kwan Lam could not be reached. The JAK2 immunoblot in Fig. 2A was duplicated as STAT-1u03b1 in Fig. 2B. The GAPDH immunoblot in Fig. 2A was duplicated in Fig. 2B in the MEK1 2 panel. In Fig. 2B, the GAPDH immunoblots in the NF-u03baB and STAT-1u03b1 panels are the same. In Fig. 2C, the Akt, mTOR, STAT-1u03b1, and MEK1 2 immunoblots are the same. The withdrawing authors apologize for not detecting the duplicated panels at the submission and publication of this article. When this issue was brought to their attention, the original data obtained 15 years ago could not be located. However, the withdrawing authors state that they have repeated the experiments shown in Fig. 2 (B and C) and that they were able to confirm the results shown in these two panels. ,
Humoral immune response to native eukaryotic prion protein correlates with anti-prion protection
Authors: Burkhard Becher
Gino Miele
Eduard Urich
Magdalini Polymenidou
Franziska Wopfner
Nathalie Braun
Adriano Aguzzi
Hermann M Sch√§tzl
Frank L Heppner
Erica C Pellicioli
Journal: Proceedings of the National Academy of Sciences of the United States of America (2004)
Discipline: Multidisciplinary
Keywords: Prion diseases; PrP(Sc); PrP(C); antibodies; anti-prion therapy
Affiliations: Institute of Neuropathology, Neuroimmunology Unit, University Hospital, Schmelzbergstrasse 12 and Frauenklinikstrasse 10, CH-8091 Zurich, Switzerland.

Abstract:  Prion diseases are characterized by the deposition of an abnormal form (termed PrP(Sc)) of the cellular prion protein (PrP(C)). Because antibodies to PrP(C) can antagonize deposition of PrP(Sc) in cultured cells and mice, they may be useful for anti-prion therapy. However, induction of protective anti-prion immune responses in WT animals may be hindered by host tolerance. Here, we studied the cellular and molecular basis of tolerance to PrP(C). Immunization of Prnp(o/o) mice with bacterially expressed PrP (PrP(REC)) resulted in vigorous humoral immune responses to PrP(REC) and native cell-surface PrP(C). Instead, WT mice yielded antibodies that failed to recognize native PrP(C) despite immunoreactivity with PrP(REC), even after immunization with PrP-PrP polyprotein and/or upon administration of anti-OX40 antibodies. Consequently, immunized WT mice experienced insignificantly delayed prion pathogenesis upon peripheral prion challenge. Anti-PrP immune responses in Prnp(o/o) mice were completely abrogated by transgenic expression of PrP(C) in B cells, T cells, neurons, or hepatocytes, but only moderately reduced by expression in myelinating cells, despite additional thymic Prnp transcription in each case. We conclude that tolerance to PrP(C) can coexist with immunoreactivity to PrP(REC) and does not depend on thymic PrP(C) expression. Its circumvention might represent an important step toward the development of effective anti-prion immunotherapy. 

Retracted: No

PubPeer comments:
 Fig. 2 u2013 more similar than expected. Could the authors kindly check it please?  ,
Honokiol regulates mitochondrial substrate utilization and cellular fatty acid metabolism in diabetic mice heart
Authors: Anand Chellappan Reghuvaran
Raji Sasikala Rajendran
Nandini Ravikumar Jayakumari
Harikrishnan Vijayakumar Sreelatha
Ashok Sivasailam
Sulfath Thottungal Parambil
Srinivas Gopala
Journal: European Journal of Pharmacology (2021)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Diabetes; Fatty acid metabolism; High resolution respirometry; Honokiol; Mitochondria.
Affiliations: Department of Biochemistry, Sree Chitra Tirunal Institute for Medical Sciences & Technology, Thiruvananthapuram, Kerala, India., Division of Laboratory Animal Sciences, Sree Chitra Tirunal Institute for Medical Sciences & Technology, Thiruvananthapuram, Kerala, India., Department of Biochemistry, Sree Chitra Tirunal Institute for Medical Sciences & Technology, Thiruvananthapuram, Kerala, India. Electronic address: .

Abstract:  Type 2 diabetes mellitus is strongly associated with cardiac mitochondrial dysfunction, which is one of the main reasons for cardiovascular diseases. Among the mitochondrial metabolic changes, fatty acid metabolism is of great importance as cardiac tissues depend primarily on fatty acids. Honokiol, a constituent of Magnolia tree bark extract, is reported to strongly influence cardiac mitochondrial functions, via various mechanisms. The current study showed that honokiol decreased fatty acid-mediated complex I respiration and increased carbohydrate-mediated complex I and II respiration in diabetic C57BL/6 mice cardiac mitochondria. It was also found that honokiol treatment decreased expression of Cluster of Differentiation 36, AMP-activated kinases and nuclear transcription factors like, Peroxisome proliferator-activated receptor Œ≥ co-activator 1Œ±/Œ≤ and Peroxisome proliferator-activated receptor Œ±, surrogating the evidence of decreased fatty acid-mediated complex I respiration. Honokiol treatment also reduced the levels of mitochondrial acetylated proteins, suggesting the possible action of honokiol via acetylation/deacetylation mechanism of regulation of protein functions in diabetic mitochondria. The antioxidant effect of honokiol is evidenced by the augmented expression of Manganese super oxide dismutase. In conclusion, honokiol imparts beneficial effect on diabetic cardiac mitochondria by decreasing the oxidant burden via regulating mitochondrial fatty acid respiration and expression of oxidant response factors. 

Retracted: No

PubPeer comments:
 Figure 5B appears to have a set of repeated bands. There may be more. *** Closeup   ***  ,
shRNA-mediated downregulation of Œ±-N-Acetylgalactosaminidase inhibits migration and invasion of cancer cell lines
Authors: Samad Nadri
Ehsan Saburi
Yousef Mortazavi
Seyed Abbas Mirzaei
Jalil Tavakolafshari
Alireza Biglari
Journal: Iranian journal of basic medical sciences (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Alpha-N-Acetylgalactosamini-; Cancer; Extracellular matrix; Invasion; Migration
Affiliations: Department of Molecular Medicine & Genetics, Zanjan University of Medical Sciences, Zanjan, Iran., Department of Immunogenetics, Buali Institute, Mashhad University of Medical Sciences, Mashhad, Iran., Department of Medical Biotechnology and Nanotechnology, Zanjan University of Medical Sciences, Zanjan, Iran., Cancer Gene Therapy Research Center, Zanjan University of Medical Sciences, Zanjan, Iran., Cellular and Molecular Research Center, Basic Health Sciences Institute, Shahrekord University Of Medical Sciences, Shahrekord, Iran.

Abstract:  Objectives: Extracellular matrix (ECM) is composed of many kinds of glycoproteins containing glycosaminoglycans (GAGs) moiety. The research was conducted based on the N-Acetylgalactosamine (GalNAc) degradation of ECM components by Œ±-N-acetylgalactosaminidase (Nagalase) which facilitates migration and invasion of cancer cells. This study aims to investigate the effects of Naga-shRNA downregulation on migration and invasion of cancer cell lines. Materials and methods: In this study, MCF-7 cell line (human mammary carcinoma cell line) and A2780 (human ovarian carcinoma cell line) were used. The level of normalized Naga expression and Nagalase protein were evaluated by quantitative polymerase chain reaction and enzyme-linked immunosorbent assay/western blotting, respectively. Migration and invasion were determined using transwell assays, and statistical analysis was carried out by ANOVA test. Results: Response to transduction by shRNA compared to the control group, migrative and invasive properties of the transfected cells were significantly inhibited. Conclusion: These results indicate that Nagalase may have an important role in migration and invasion of cancer cells and can be considered as a candidate for further studies. 

Retracted: No

PubPeer comments:
 Figure 5 has 2 images with unexpected similarities (marked in red). Could the authors review and comment? ***  ,
Systemic Delivery of CRISPR/Cas9 Targeting HPV Oncogenes Is Effective at Eliminating Established Tumors
Authors: Luqman Jubair
Nigel A J McMillan
Sora Fallaha
Journal: Molecular Therapy (2019)
Discipline: CLINICAL MEDICINE
Keywords: CRISPR; HPV; gene editing.
Affiliations: School of Medical Sciences, Griffith University, Gold Coast, QLD 4222 Australia; Menzies Health Institute Queensland, Griffith University, Gold Coast, QLD 4222 Australia., School of Medical Sciences, Griffith University, Gold Coast, QLD 4222 Australia; Menzies Health Institute Queensland, Griffith University, Gold Coast, QLD 4222 Australia. Electronic address: .

Abstract:  The recent advancements in CRISPR/Cas9 engineering have resulted in the development of more targeted and potentially safer gene therapies. The challenge in the cancer setting is knowing the driver oncogenes responsible, and the translation of these therapies is hindered by effective and safe delivery methods to target organs with minimal systemic toxicities, on-target specificity of gene editing, and demonstrated lack of long-term adverse events. Using a model system based on cervical cancer, which is driven by the ongoing expression of the human papillomavirus E6 and E7 proteins, we show that CRISPR/Cas9 delivered systemically in vivo using PEGylated liposomes results in tumor elimination and complete survival in treated animals. We compared treatment and editing efficiency of two Cas9 variants, wild-type (WT) Cas9 and the highly specific FokI-dCas9, and showed that the latter was not effective. We also explored high-fidelity repair but found that repair was inefficient, occurring in 6%-8% of cells, whereas non-homologous end joining (NHEJ) was highly efficient, occurring in ‚à?0% of the cells. Finally, we explored the post gene-editing events in tumors and showed that cell death is induced by apoptosis. Overall, our work demonstrates that in vivo CRISPR/Cas editing treatment of preexisting tumors is completely effective despite the large payloads. 

Retracted: No

PubPeer comments:
 In Fig. 1D, the tubulins for the CasKi cells has some unexpected similarities to those from the HeLa cells. , 
 I will look into this ASAP as I can see exactly what you are saying. ,