PReD-Bench/PRed-Bench huggingface dataset:
RETRACTED: Uncoupling IL-2 Signals that Regulate T Cell Proliferation, Survival, and Fas-Mediated Activation-Induced Cell Death
Authors: J D Lord
L Van Parijs
D Baltimore
B H Nelson
Y Refaeli
A K Abbas
Journal: Immunity (1999)
Discipline: IMMUNOLOGY
Keywords: IL-2; T lymphocytes; Fas-mediated activation-induced cell death; IL-2 receptor beta; Stat5
Affiliations: Department of Biology, California Institute of Technology, Pasadena 91125, USA.

Abstract:  IL-2 is an important growth and survival factor for T lymphocytes but also sensitizes these cells to Fas-mediated activation-induced cell death (AICD). The molecular basis of these different effects of IL-2 was studied by introducing wild-type and mutant forms of the IL-2 receptor beta (IL-2Rbeta) chain that lacked specific signaling capacities into receptor-deficient T cells by retroviral gene transfer. Activation of Stat5 by IL-2 was found to be involved in T cell proliferation and promoted Fas ligand (FasL) expression and AICD. T cell survival was dependent on a receptor region that activated Akt and the expression of Bcl-2. Thus, distinct IL-2Rbeta chain signaling modules regulate T cell fate by stimulating growth and survival or by promoting apoptosis. 

Retracted: Yes

PubPeer comments:
 The authors in this paper introduced a new notion for decision making called **q-rung orthopair hesitant fuzzy numbers** and defined a series of aggregation operators. However, the results presented are merely symbol manipulation. For example, although the authors claimed that the properties of q-ROHFPGHM operator can be easily proved, **Property 1 (Idempotency) does not hold obviously** because according to Definition 5, the numbers of values may change after the operations of $oplus$ and $otimes$. See also https: pubpeer.com publications FA150232DB1F6F8919598158836BD1 https: pubpeer.com publications 8AF6953436EB17B0E8C3E7238E7BEF ![file] ![file] ![file] ![file] , 
 A typical citation pattern of GW Wei, the third author of this paper. ![file] ,
Effects of Mitofusin2 on astrocytes proliferation in vitro induced by scratch injury
Authors: Jie Xie
Qian Zhang
Yulong Shi
Peng Luo
Chengla Yi
Journal: Neuroscience Letters (2020)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Astrocyte; Mitofusin2; PI3K-Akt; Proliferation; Raf1-ERK1/2
Affiliations: Department of Traumatic Surgery, Tong-Ji Hospital, Tongji Medical College, Jie Fang Avenue 1095, Wuhan, China; Department of Orthopedics, Xinhua Hospital of Hubei Province, Hankou District, Wuhan, China., Department of Orthopedics, Xinhua Hospital of Hubei Province, Hankou District, Wuhan, China., Department of Traumatic Surgery, Tong-Ji Hospital, Tongji Medical College, Jie Fang Avenue 1095, Wuhan, China. Electronic address: ., Department of Traumatic Surgery, Tong-Ji Hospital, Tongji Medical College, Jie Fang Avenue 1095, Wuhan, China.

Abstract:  Reactive astrogliosis, a common phenomenon after central nervous system (CNS) injury, exerts negative effects on neuronal repair and recovery by forming a glial scar. Mitofusin2 (Mfn2), a hyperplasia suppression gene, is a potential target of therapeutics to better control astrogliosis. To simulate traumatic injury of the CNS in vivo, an in vitro scratch injury model was established to investigate the role of Mfn2 in the proliferation of astrocytes in this study. We demonstrated that scratch-injury stimulation upregulated the expression of the markers cyclin D1, PCNA and GFAP and turned quiescent astrocytes into mitotic cells, which may have been via activation of Ras-Raf1-ERK1/2 and PI3K-Akt signaling. Meanwhile, both the gene and protein of Mfn2 were markedly inhibited. Furthermore, overexpression of Mfn2 effectively attenuated astrocyte proliferation and halted the cell cycle, concomitant with marker downregulation and wound healing suppression. Our results demonstrate that overexpression of Mfn2 inhibits the reactive astrogliosis process by blocking the Raf1-ERK1/2 and PI3K-Akt signal pathways. Therapeutic approaches that target Mfn2 may have protective effects against reactive gliosis and glia formation. 

Retracted: No

PubPeer comments:
 Seems that there is image duplication in the western-blots in this paper. Even the the grey backgrounds show same artifacts. Two actin controls in Figure 1 and 3 are the same. I attach a composite picture in which I juxtaposed the 2 images. Figure 1C is supposed to be a time course study of protein phosphorylation. It displays same actin controls (0, 6 and 12 h) as in Figure 3A, which shows expressions under 3 transfection conditions. So not the same experiment. Same kind of duplication in Fig1C, for p-Raf1 blots. Time points 6, 12 and 24 hours similar to blots in Figure 3B, supposed to show 3 conditions of transfections. What do you think? ![file] , 
 I agree with #1. There is an additional finding with respect to the PCNA plots. Here is a comparison of all three possible duplications, marked with boxes of the same color. ![file] , 
 This article has still not been retracted (or at least corrected), despite chasing up Editors. ,
DISC1 Regulates the Proliferation and Migration of Mouse Neural Stem/Progenitor Cells through Pax5, Sox2, Dll1 and Neurog2
Authors: Li Feng
Zhaohui Luo
Yi Shu
Yi Li
Weiting Tang
Zongwei Yue
Qian Wu
Bo Xiao
Journal: Frontiers in Cellular Neuroscience (2017)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: DISC1; Dll1; Neurog2; Pax5; Sox2
Affiliations: Department of Neurology, First Affiliated Hospital, Kunming Medical UniversityKunming, China., Department of Neurology, Xiangya Hospital, Central South UniversityChangsha, China., Department of Neurology, University of Massachusetts Medical SchoolWorcester, MA, United States., Department of Neurology, The Second Xiangya Hospital, Central South UniversityChangsha, China., Department of Neurology, Yale University School of MedicineNew Haven, CT, United States.

Abstract:  Background: Disrupted-in-schizophrenia 1 (DISC1) regulates neurogenesis and is a genetic risk factor for major psychiatric disorders. However, how DISC1 dysfunction affects neurogenesis and cell cycle progression at the molecular level is still unknown. Here, we investigated the role of DISC1 in regulating proliferation, migration, cell cycle progression and apoptosis in mouse neural stem/progenitor cells (MNSPCs) in vitro. Methods: MNSPCs were isolated and cultured from mouse fetal hippocampi. Retroviral vectors or siRNAs were used to manipulate DISC1 expression in MNSPCs. Proliferation, migration, cell cycle progression and apoptosis of altered MNSPCs were analyzed in cell proliferation assays (MTS), transwell system and flow cytometry. A neurogenesis specific polymerase chain reaction (PCR) array was used to identify genes downstream of DISC1, and functional analysis was performed through transfection of expression plasmids and siRNAs. Results: Loss of DISC1 reduced proliferation and migration of MNSPCs, while an increase in DISC1 led to increased proliferation and migration. Meanwhile, an increase in the proportion of cells in G0/G1 phase was concomitant with reduced levels of DISC1, but significant changes were not observed in the number MNSPCs undergoing apoptosis. Paired box gene 5 (Pax5), sex determining region Y-box 2 (Sox2), delta-like1 (Dll1) and Neurogenin2 (Neurog2) emerged as candidate molecules downstream of DISC1, and rescue experiments demonstrated that increased or decreased expression of either molecule regulated proliferation and migration in DISC1-altered MNSPCs. Conclusion: These results suggest that Pax5, Sox2, Dll1 and Neurog2 mediate DISC1 activity in MNSPC proliferation and migration. 

Retracted: No

PubPeer comments:
 Fig. 4 contains images that look highly similar: ![file] ,
High-molecular-mass hyaluronan mediates the cancer resistance of the naked mole rat
Authors: Amita Vaidya
Jorge Azpurua
Xiao Tian
Vera Gorbunova
Max Myakishev-Rempel
Zhiyong Mao
Andrei Seluanov
Christopher Hine
Julia Ablaeva
Eviatar Nevo
Journal: Nature (2013)
Discipline: Multidisciplinary
Keywords: Naked mole rat; longevity; cancer resistance; hyaluronan; fibroblasts
Affiliations: Department of Biology, University of Rochester, Rochester, New York 14627, USA.

Abstract:  The naked mole rat (Heterocephalus glaber) displays exceptional longevity, with a maximum lifespan exceeding 30 years. This is the longest reported lifespan for a rodent species and is especially striking considering the small body mass of the naked mole rat. In comparison, a similarly sized house mouse has a maximum lifespan of 4 years. In addition to their longevity, naked mole rats show an unusual resistance to cancer. Multi-year observations of large naked mole-rat colonies did not detect a single incidence of cancer. Here we identify a mechanism responsible for the naked mole rat's cancer resistance. We found that naked mole-rat fibroblasts secrete extremely high-molecular-mass hyaluronan (HA), which is over five times larger than human or mouse HA. This high-molecular-mass HA accumulates abundantly in naked mole-rat tissues owing to the decreased activity of HA-degrading enzymes and a unique sequence of hyaluronan synthase 2 (HAS2). Furthermore, the naked mole-rat cells are more sensitive to HA signalling, as they have a higher affinity to HA compared with mouse or human cells. Perturbation of the signalling pathways sufficient for malignant transformation of mouse fibroblasts fails to transform naked mole-rat cells. However, once high-molecular-mass HA is removed by either knocking down HAS2 or overexpressing the HA-degrading enzyme, HYAL2, naked mole-rat cells become susceptible to malignant transformation and readily form tumours in mice. We speculate that naked mole rats have evolved a higher concentration of HA in the skin to provide skin elasticity needed for life in underground tunnels. This trait may have then been co-opted to provide cancer resistance and longevity to this species. 

Retracted: No

PubPeer comments:
 This article has a Matters Arising related article: https: www.nature.com articles s41586-020-2410-x And a reply from the authors: https: www.nature.com articles s41586-020-2411-9 , 
 Sorry for being late at the party. Already the original article mixed up images where Fig 3 has a partial duplication. ![file] ,
Long noncoding RNA CHL1‐AS1 promotes cell proliferation and migration by sponging miR‐6076 to regulate CHL1 expression in endometrial cancer
Authors: Manzhen Zuo
Huamei Song
Jinfen Zha
Yanmei Shi
Qian Yan
Journal: Journal of Cellular Biochemistry (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: CHL1; CHL1-AS1; endometrial cancer; miR-6076.
Affiliations: Department of Gynecology and ObstetricsYantaishan Hospital Yantai Shandong China, Department of Gynecology and ObstetricsThe People's Hospital of China Three Gorges University Yichang Hubei China

Abstract:  Endometrial cancer (EC) is deemed to be the most typical gynecologic malignant tumor. Despite the incidence of EC being lower in Asia than that in western countries, substantial increased incidence has been observed in the past few decades in Asia. Although various molecular testing methods and genomic science have developed, the overall prognosis is still disappointing. LncRNAs have been found to influence the progression of various cancers. CHL1-AS1 has been found to be upregulated in ovarian endometriosis, nevertheless, the molecular mechanism and biological function of CHL1-AS1 in EC have not been explored. In our exploration, both CHL1-AS1 and CHL1 were upregulated in EC cells. Knockdown of CHL1-AS1 or CHL1 inhibited cell proliferation and migration in EC. Furthermore, microRNA-6076 (miR-6076) could bind with CHL1-AS1 or CHL1, and regulate the expression of CHL1. Finally, absence of miR-6076 or overexpression of CHL1 can partially rescue the effect of CHL1-AS1 knockdown or miR-6076 upregulation on cell proliferation and migration, respectively. All in all, our research was the first endeavor to study the underlying mechanism of CHL1-AS1 in EC and confirmed that CHL1-AS1 regulated EC progression via targeting the miR-6076/CHL1 axis, offering new insight into treating EC. 

Retracted: No

PubPeer comments:
 In Figure 4, one of the cell proliferation assay images has been duplicated. Oddly, the two images are slightly differently cropped, showing a few extra cells along the left side. I suggest the authors contact the journal about uploading the correct images. ![file] ,
In vitro effects of imatinib mesylate on radiosensitivity and chemosensitivity of breast cancer cells
Authors: Alexander Strauss
Linda Dahmke
Christoph Mundhenke
Maret Bauer
Katrin Weber
Nicolai Maass
Marion T Weigel
Dirk O Bauerschlag
Walter Jonat
Christian Schem
Peter Niehoff
Journal: BMC Cancer (2010)
Discipline: CLINICAL MEDICINE
Keywords: Breast cancer treatment; Imatinib; Radiotherapy; Chemotherapy; Cell proliferation
Affiliations: Department of Obstetrics and Gynecology, Breast Center, University of Kiel, Arnold-Heller Strasse 3, 24105 Kiel, Germany.

Abstract:  Background: Breast cancer treatment is based on a combination of adjuvant chemotherapy followed by radiotherapy effecting intracellular signal transduction. With the tyrosine kinase inhibitors new targeted drugs are available. Imatinib mesylate is a selective inhibitor of bcr-abl, PRGFR alpha, beta and c-kit. The purpose of this study was to determine whether Imatinib has an influence on the effectiveness of radiotherapy in breast cancer cell lines and if a combination of imatinib with standard chemotherapy could lead to increased cytoreduction. Methods: Colony-forming tests of MCF 7 and MDA MB 231 were used to study differences in cell proliferation under incubation with imatinib and radiation. Changes in expression and phosphorylation of target receptors were detected using western blot. Cell proliferation, migration and apoptosis assays were performed combining imatinib with doxorubicin. Results: The combination of imatinib and radiotherapy showed a significantly stronger inhibition of cell proliferation compared to single radiotherapy. Differences in PDGFR expression could not be detected, but receptor phosphorylation was significantly inhibited when treated with imatinib. Combination of imatinib with standard chemotherapy lead to an additive effect on cell growth inhibition compared to single treatment. Conclusions: Imatinib treatment combined with radiotherapy leads in breast cancer cell lines to a significant benefit which might be influenced through inhibition of PDGFR phosphorylation. Combining imatinib with chemotherapy enhances cytoreductive effects. Further in vivo studies are needed to evaluate the benefit of Imatinib in combination with radiotherapy and chemotherapy on the treatment of breast cancer. 

Retracted: No

PubPeer comments:
 unexpected similarity ![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. ,
Flow shear stress stimulates Gab1 tyrosine phosphorylation to mediate protein kinase B and endothelial nitric-oxide synthase activation in endothelial cells
Authors: Chelsea Wong
Zheng-Gen Jin
Jie Wu
Bradford C Berk
Journal: Journal of Biological Chemistry (2005)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Fluid shear stress; endothelial cell function; intracellular signaling; phosphatidylinositol 3-kinase (PI3K); Akt
Affiliations: Center for Cardiovascular Research and Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA. 

Abstract:  Fluid shear stress generated by blood flow modulates endothelial cell function via specific intracellular signaling events. We showed previously that flow activated the phosphatidylinositol 3-kinase (PI3K), Akt, and endothelial nitric-oxide synthase (eNOS) via Src kinase-dependent transactivation of vascular endothelial growth factor receptor 2 (VEGFR2). The scaffold protein Gab1 plays an important role in receptor tyrosine kinase-mediated signal transduction. We found here that laminar flow (shear stress = 12 dynes/cm2) rapidly stimulated Gab1 tyrosine phosphorylation in both bovine aortic endothelial cells and human umbilical vein endothelial cells, which correlated with activation of Akt and eNOS. Gab1 phosphorylation as well as activation of Akt and eNOS by flow was inhibited by the Src kinase inhibitor PP2 (4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine) and VEGFR2 kinase inhibitors SU1498 and VTI, suggesting that flow-mediated Gab1 phosphorylation is Src kinase-dependent and VEGFR2-dependent. Tyrosine phosphorylation of Gab1 by flow was functionally important, because flow stimulated the association of Gab1 with the PI3K subunit p85 in a time-dependent manner. Furthermore, transfection of a Gab1 mutant lacking p85 binding sites inhibited flow-induced activation of Akt and eNOS. Finally, knockdown of endogenous Gab1 by small interference RNA abrogated flow activation of Akt and eNOS. These data demonstrate a critical role of Gab1 in flow-stimulated PI3K/Akt/eNOS signal pathway in endothelial cells. 

Retracted: No

PubPeer comments:
 Figure 6B u2013 Very similar to a previous blot published by this same group (Alvarez et al., 2008, doi: 10.1096 fj.07-102715). Could authors check it please? ![file] , 
 Thanks for noting this involuntary mistake. As you pointed-out, Figure 2A of the FASEB J article was partially reproduced in Figure 6B of NBD. This does not modify the conclusions of the NBD article. We contacted the FASEB J and permission to reproduce the figure was granted. An erratum in NBD will be published soon. Alejandra R. Alvarez Andres Klein Silvana Zanlungo ,
Deregulated E2F activity induces hyperplasia and senescence-like features in the mouse pituitary gland
Authors: Kristian Helin
Diego Pasini
Eros Lazzerini Denchi
Claire Attwooll
Journal: Molecular and Cellular Biology (2005)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: RB1; E2F transcription factors; pituitary tumors; transgenic mice; inducible E2F3 protein
Affiliations: Biotech Research and Innovation Center, Fruebjergvej 3, 2100 Copenhagen, Denmark., Department of Experimental Oncology, European Institute of Oncology, Milan, Italy, Biotech Research &amp; Innovation Center, Copenhagen, Denmark

Abstract:  The retinoblastoma gene, RB1, is one of the most frequently mutated genes in human cancer. Rb heterozygous mice develop pituitary tumors with 100% incidence, and the E2F transcription factors are required for this. To assess whether deregulated E2F activity is sufficient to induce pituitary tumors, we generated transgenic mice expressing an inducible E2F3 protein in the intermediate lobe of the pituitary gland. We found that short-term deregulation of E2F activity, similar to the earliest stages of Rb loss, is able to induce abnormal proliferation of otherwise quiescent melanotrophs. However, while long-term exposure to deregulated E2F activity results in hyperplasia of the intermediate lobe, it did not lead to tumor formation. In fact, melanotrophs become insensitive to sustained E2F stimulation and enter an irreversible senescence-like state. Thus, although deregulated E2F activity results in hyperproliferation, it is not sufficient to mimic loss of Rb, sustain proliferation of melanotrophs, and ultimately induce pituitary tumors. Similarly, we found that primary cells in tissue culture become insensitive to sustained E2F3 activation and undergo premature senescence in a pRB-, p16Ink4a-, and p19Arf-dependent manner. Thus, we conclude that deregulated E2F activity is not sufficient to fully mimic loss of Rb due to the engagement of a senescence response. 

Retracted: No

PubPeer comments:
 Figure 6B. Much more similar than expected. ![file] , 
 #1 One more duplicated panel in Fig. 6B, just rotated 180 deg (red boxes): ![file] , 
 Figure 3A and 3B, another duplication: images of WT 3 months samples are the same (orange boxes), but treatments seem to be different (ellipses). Apologies if I misunderstood. ![file] ,
Genetic Variation in the Androgen Receptor and Measures of Plasma Testosterone Levels Suggest Androgen Dysfunction in Alzheimer’s Disease
Authors: Alicia K Morgans
Jennifer S Yokoyama
Jessie S Carr
Charles J Ryan
Luke W Bonham
Ethan G Geier
Alzheimer’s Disease Neuroimaging Initiative
Journal: Frontiers in neuroscience (2018)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Alzheimer’s disease; androgen receptor; biomarker; steroid; testosterone.

Abstract:  Alzheimer's disease (AD) prevalence varies by sex, suggesting that sex chromosomes, sex hormones and/or their signaling could potentially modulate AD risk and progression. Low testosterone levels are reported in men with AD. Further, variation in the androgen receptor (AR) gene has been associated with AD risk and cognitive impairment. We assessed measures of plasma testosterone levels as a biomarker of AD in male participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort. Baseline testosterone levels were significantly different between clinical diagnosis groups [cognitively normal controls, mild cognitive impairment (MCI), or AD], with the lowest testosterone levels in men with AD. Lower baseline testosterone levels were associated with higher baseline clinical severity. Change in testosterone levels between baseline and 1-year follow-up varied by diagnosis; MCI had the greatest decreases in testosterone levels between baseline and 1-year follow-up. Despite differences by clinical diagnosis, there was no association between plasma testosterone and CSF biomarkers of AD pathology. We also tested single nucleotide polymorphisms (SNPs) in AR for association with AD risk in a separate cohort from ADNI and found 26 SNPs associated with risk for AD. The top associated SNP is predicted to be an expression quantitative trait locus for AR in multiple tissues, including brain, with the AD-associated risk allele predicted to confer lower AR expression. Our findings suggest a link between the androgen pathway and AD through Aβ/tau independent pathways. These effects may be most pronounced during conversion from MCI to dementia. 

Retracted: Yes

PubPeer comments:
 2019 retraction. https: www.frontiersin.org articles 10.3389 fnins.2019.01265 full After publication, the authors were made aware of an unfortunate coding error resulting in the data analyzed in this study being inconsistent with the data provided in the Alzheimer s Disease Neuroimaging Initiative repository. Due to this honest error, the authors request that this article be retracted. The retraction of the article was approved by the Chief Editors of Frontiers in Neuroscience, Neurodegeneration and the Editor-in-Chief of Frontiers. ,
Wogonin inhibits LPS-induced vascular permeability via suppressing MLCK/MLC pathway
Authors: Zhiyu Li
Xiaorui Li
Xuwei Luo
Yujie Huang
Qidong You
Libin Wei
Xiuming Song
Qinglong Guo
Na Lu
Journal: Vascular pharmacology (2015)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Lipopolysaccharide (LPS); MLCK/MLC; Vascular permeability; Wogonin; Wogonin (PubChem CID: 5281703)
Affiliations: State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Carcinogenesis and Intervention, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing 210009, PR China., Chia Tai Tianqing Pharmaceutical Group Co., Ltd., PR China., Department of Medicinal Chemistry, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing 210009, PR China., JiangSu Key Laboratory of Drug Design and Optimization, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing 210009, PR China., State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Carcinogenesis and Intervention, China Pharmaceutical University, 24 Tongjiaxiang, Nanjing 210009, PR China. Electronic address: .

Abstract:  Wogonin, a naturally occurring monoflavonoid extracted from the root of Scutellaria baicalensis Georgi, has been shown to have anti-inflammatory and anti-tumor activities and inhibits oxidant stress-induced vascular permeability. However, the influence of wogonin on vascular hyperpermeability induced by overabounded inflammatory factors often appears in inflammatory diseases and tumor is not well known. In this study, we evaluate the effects of wogonin on LPS induced vascular permeability in human umbilical vein endothelial cells (HUVECs) and investigate the underlying mechanisms. We find that wogonin suppresses the LPS-stimulated hyperactivity and cytoskeleton remodeling of HUVECs, promotes the expression of junctional proteins including VE-Cadherin, Claudin-5 and ZO-1, as well as inhibits the invasion of MDA-MB-231 across EC monolayer. Miles vascular permeability assay proves that wogonin can restrain the extravasated Evans in vivo. The mechanism studies reveal that the expressions of TLR4, p-PLC, p-MLCK and p-MLC are decreased by wogonin without changing the total steady state protein levels of PLC, MLCK and MLC. Moreover, wogonin can also inhibit KCl-activated MLCK/MLC pathway, and further affect vascular permeability. Significantly, compared with wortmannin, the inhibitor of MLCK/MLC pathway, wogonin exhibits similar inhibition effects on the expression of p-MLCK, p-MLC and LPS-induced vascular hyperpermeability. Taken together, wogonin can inhibit LPS-induced vascular permeability by suppressing the MLCK/MLC pathway, suggesting a therapeutic potential for the diseases associated with the development of both inflammatory and tumor. 

Retracted: No

PubPeer comments:
 This paper shows photos of naked patients and breast and genital area surgery. Although no faces are visible, they are also not anonymous. Did the patients give consent to have their photos used in this paper? Patients were given informed consent to participate in the research project, but there is no statement on whether they granted permission to have their photos used in this paper. ,
Postnatal development of layer III pyramidal cells in the primary visual, inferior temporal, and prefrontal cortices of the marmoset
Authors: Hirosato Aoi
Tetsuya Sasaki
Tomofumi Oga
Noritaka Ichinohe
Ichiro Fujita
Journal: Frontiers in Neural Circuits (2013)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: area differences; autism; dendritic spine; schizophrenia; spinogenesis.
Affiliations: Department of Ultrastructural Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry Kodaira, Tokyo, Japan ; Laboratory for Cognitive Neuroscience, Graduate School of Frontier Biosciences, Osaka University Toyonaka, Osaka, Japan.

Abstract:  Abnormalities in the processes of the generation and/or pruning of dendritic spines have been implicated in several mental disorders including autism and schizophrenia. We have chosen to examine the common marmoset (Callithrix jacchus) as a primate model to explore the processes. As a first step, we studied the postnatal development of basal dendritic trees and spines of layer-III pyramidal cells in the primary visual sensory cortex (V1), a visual association cortex (inferior temporal area, TE), and a prefrontal cortex (area 12, PFC). Basal dendrites in all three areas were longer in adulthood compared with those in the newborn. In particular, rapid dendritic growth occurred in both TE and PFC around the second postnatal month. This early growth spurt resulted in much larger dendritic arbors in TE and PFC than in V1. The density of the spines along the dendrites peaked at 3 months of age and declined afterwards in all three areas: the degree of spine pruning being greater in V1 than in TE and PFC. The estimates of the total numbers of spines in the basal dendrites of a single pyramidal cell were larger in TE and PFC than in V1 throughout development and peaked around 3 months after birth in all three areas. These developmental profiles of spines and dendrites will help in determining assay points for the screening of molecules involved in spinogenesis and pruning in the marmoset cortex. 

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. ,
Lesion of the subiculum reduces the spread of amyloid beta pathology to interconnected brain regions in a mouse model of Alzheimer’s disease
Authors: Caroline Graff
Fiona Grueninger
Patrik Brundin
Géraldine H Petit
Bengt Winblad
Annica Rönnbäck
Gunnar K Gouras
Sonia George
Journal: Acta Neuropathologica Communications (2014)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Alzheimer's disease; pathology; spatiotemporal pattern; transgenic mouse model; amyloid precursor protein
Affiliations: Neuronal Survival Unit, Department of Experimental Medical Science, Wallenberg Neuroscience Center, Lund University, Lund, Sweden. .

Abstract:  Background: The progressive development of Alzheimer's disease (AD) pathology follows a spatiotemporal pattern in the human brain. In a transgenic (Tg) mouse model of AD expressing amyloid precursor protein (APP) with the arctic (E693G) mutation, pathology spreads along anatomically connected structures. Amyloid-β (Aβ) pathology first appears in the subiculum and is later detected in interconnected brain regions, including the retrosplenial cortex. We investigated whether the spatiotemporal pattern of Aβ pathology in the Tg APP arctic mice to interconnected brain structures can be interrupted by destroying neurons using a neurotoxin and thereby disconnecting the neural circuitry. Results: We performed partial unilateral ibotenic acid lesions of the subiculum (first structure affected by Aβ pathology) in young Tg APParc mice, prior to the onset of pathology. We assessed Aβ/C99 pathology in mice aged up to 6 months after injecting ibotenate into the subiculum. Compared to the brains of intact Tg APP arctic mice, we observed significantly decreased Aβ/C99 pathology in the ipsilateral dorsal subiculum, CA1 region of the hippocampus and the retrosplenial cortex; regions connecting to and from the dorsal subiculum. By contrast, Aβ/C99 pathology was unchanged in the contralateral hippocampus in the mice with lesions. Conclusion: These results, obtained in an animal model of AD, support the notion that Aβ/C99 pathology is transmitted between interconnected neurons in AD. 

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. ,
Axin gene methylation status correlates with radiosensitivity of lung cancer cells
Authors: En-Hua Wang
Yang Han
Lian-He Yang
Ke Xu
Zheng-Fan Xu
Hong-Tao Xu
Guang Li
Huan-Yu Zhao
Gui-Yang Jiang
Xiu-Peng Zhang
Yuan Miao
Maggie Stoecker
Endi Wang
Journal: BMC Cancer (2013)
Discipline: CLINICAL MEDICINE
Keywords: Axin1; lung cancer; X-ray irradiation; methylation status; gene expression
Affiliations: Department of Pathology, First Affiliated Hospital and College of Basic Medical Sciences, China Medical University, Shenyang, Liaoning, China.

Abstract:  Background: We previously reported that Axin1 (Axin) is down-regulated in many cases of lung cancer, and X-ray irradiation increased Axin expression and inhibited lung cancer cells. The mechanisms, however, were not clear. Methods: Four lung cancer cell lines were used to detect the methylation status of Axin with or without X-ray treatment. Real-time PCR was used to quantify the expression of Axin, and western blot analysis was applied to measure protein levels of Axin, β-catenin, Cyclin D1, MMP-7, DNMTS, MeCP2 and acetylated histones. Flow cytometric analysis, colony formation assay, transwell assay and xenograft growth experiment were used to study the biological behavior of the cells with hypermethylated or unmethylated Axin gene after X-ray treatment. Results: Hypermethylated Axin gene was detected in 2 of 4 cell lines, and it correlated inversely with Axin expression. X-ray treatment significantly up-regulated Axin expression in H446 and H157 cells, which possess intrinsic hypermethylation of the Axin gene (P&lt;0.01), but did not show up-regulation in LTE and H460 cells, which have unmethylated Axin gene. 2Gy X-ray significantly reduced colony formation (from 71% to 10.5%) in H157 cells, while the reduction was lower in LTE cells (from 71% to 20%). After X-ray irradiation, xenograft growth was significantly decreased in H157 cells (from 1.15 g to 0.28 g) in comparison with LTE cells (from 1.06 g to 0.65 g). Significantly decreased cell invasiveness and increased apoptosis were also observed in H157 cells treated with X-ray irradiation (P&lt;0.01). Down-regulation of DNMTs and MeCP2 and up-regulation of acetylated histones could be detected in lung cancer cells. Conclusions: X-ray-induced inhibition of lung cancer cells may be mediated by enhanced expression of Axin via genomic DNA demethylation and histone acetylation. Lung cancer cells with a different methylation status of the Axin gene showed different radiosensitivity, suggesting that the methylation status of the Axin gene may be one important factor to predict radiosensitivity of the tumor. 

Retracted: No

PubPeer comments:
 Two panels in Figure 4A look very similar, but represent different experiments. ![file] , 
 Correction to: BMC Cancer 2013, 13:368 https: doi.org 10.1186 1471-2407-13-368 Following publication of the original article [1], it has been brought to our attention that in Fig. 4a, the panel for LTE 2Gy was identical to the panel for LTE 1Gy. The correct panel for LTE 2Gy is now included in the new version of Fig. 4 shown below. We apologize for any inconvenience caused. ![file] ,
D-Galactose-induced accelerated aging model: an overview
Authors: Khairunnuur Fairuz Azman
Rahimah Zakaria
Journal: Biogerontology (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Aging model; Anti-aging; D-Galactose; Senescence.
Affiliations: Department of Physiology, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, 16150, Kota Bharu, Kelantan, Malaysia. ., Department of Physiology, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, 16150, Kota Bharu, Kelantan, Malaysia.

Abstract:  To facilitate the process of aging healthily and prevent age-related health problems, efforts to properly understand aging mechanisms and develop effective and affordable anti-aging interventions are deemed necessary. Systemic administration of D-galactose has been established to artificially induce senescence in vitro and in vivo as well as for anti-aging therapeutic interventions studies. The aim of this article is to comprehensively discuss the use of D-galactose to generate a model of accelerated aging and its possible underlying mechanisms involved in different tissues/organs. 

Retracted: No

PubPeer comments:
 Galactose oxidase-mediated generation of H2O2 has been referred to as an important pathophysiological mechanism in the context of D-galactose-induced aging in rodents in the text and in Fig.2. However, galactose oxidase is a fungal enzyme so it is hard to understand how it can mediate detrimental effects in rodents? A comment on the topic entitled:  Separating science from science fiction: A non-existent enzyme is a primary driver of pathophysiological processes in galactose-induced rodent models of aging is available here: https: bit.ly 2ZVJMh9 ,
Influence of RT-qPCR primer position on EGFR interference efficacy in lung cancer cells
Authors: Gang Chen
Erik Teugels
Peter Kronenberger
Jacques De Grève
Journal: Biological procedures online (2010)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: RT-qPCR; siRNA efficacy; primer selection; mRNA levels; EGFR gene
Affiliations: Laboratory of Molecular Oncology and Department of Medical Oncology, Universitair Ziekenhuis Brussel, Vrije Universiteit Brussel, Brussels, Belgium.

Abstract:  Background: Real-time quantitative RT-PCR (RT-qPCR) is a "gold" standard for measuring steady state mRNA levels in RNA interference assays. The knockdown of the epidermal growth factor receptor (EGFR) gene with eight individual EGFR small interfering RNAs (siRNAs) was estimated by RT-qPCR using three different RT-qPCR primer sets. Results: Our results indicate that accurate measurement of siRNA efficacy by RT-qPCR requires careful attention for the selection of the primers used to amplify the target EGFR mRNA. Conclusions: We conclude that when assessing siRNA efficacy with RT-qPCR, more than one primer set targeting different regions of the mRNA should be evaluated and at least one of these primer sets should amplify a region encompassing the siRNA recognition sequence. 

Retracted: No

PubPeer comments:
 Figure 2D * Marked in yellow: Panels  s1247 and  s1608 appear to show an area of overlap. Could the authors check, please? ![file] , 
 Dear Dr. Elisabeth M Bik: Thank you very much for pointing out this error. Figure 2D was indeed incorrectly prepared. We have rechecked all the raw data of these experiments and found that the mistakes occurred during the process of re-naming the files. The published results and conclusions remain unchanged. Please check the results from one experiment as an example. ![file] ![](http: )![file] The correct Figure 2D was prepared as follows. ![file] A corrigendum has been submitted to the journal of Biol Proced Online. We regret that we did not find this error during the submission procedure, also during the later revisions and proof examinations. As the first author of the paper, I take full responsibility for the error. And I apologize to other co-authors, the journal of Biol Proced Online, and all the readers. Dr. Elisabeth M Bik, thank you very much again. Great job. Best regards Gang Chen , 
 Hard to  check results with such a low resolution image. Please post full resolution. , 
 #2 Dr. Chen: I appreciate your response here and on several other papers. Could you also address the very similar concerns expressed at the links below? https: pubpeer.com publications 27A4AE50994CE93015E2E95A8E43EC#1 https: pubpeer.com publications D968863E7D4DA40BBC4E4B35AB4CEC ,
Human immunodeficiency virus type 1 protease cleaves procaspase 8 in vivo
Authors: David J Schnepple
Sarah Warren
Mona R Loutfy
Gary D Bren
Colin M Kovacs
Andrew D Badley
Stacey R Vlahakis
Sergey A Trushin
Daniel C Douek
Alicia Algeciras Schimnich
Zilin Nie
Jason M Brenchley
Journal: Journal of Virology (2007)
Discipline: MICROBIOLOGY
Keywords: HIV-1; apoptosis; casp8p41; CD4 T cells; protease
Affiliations: Division of Infectious Diseases, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA.

Abstract:  Human immunodeficiency virus type 1 (HIV-1) infection causes apoptosis of infected CD4 T cells as well as uninfected (bystander) CD4 and CD8 T cells. It remains unknown what signals cause infected cells to die. We demonstrate that HIV-1 protease specifically cleaves procaspase 8 to create a novel fragment termed casp8p41, which independently induces apoptosis. casp8p41 is specific to HIV-1 protease-induced death but not other caspase 8-dependent death stimuli. In HIV-1-infected patients, casp8p41 is detected only in CD4(+) T cells, predominantly in the CD27(+) memory subset, its presence increases with increasing viral load, and it colocalizes with both infected and apoptotic cells. These data indicate that casp8p41 independently induces apoptosis and is a specific product of HIV-1 protease which may contribute to death of HIV-1-infected cells. 

Retracted: No

PubPeer comments:
 Fig. 4A: more similar than expected. Could authors check please? ![file] ,
The amino-terminal domain of the vacuolar proton-translocating ATPase a subunit controls targeting and in vivo dissociation, and the carboxyl-terminal domain affects coupling of proton transport and ATP hydrolysis
Authors: T H Stevens
T Nishi
K Bowers
M Forgac
S Kawasaki-Nishi
Journal: Journal of Biological Chemistry (2001)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: V-ATPase; vacuolar proton-translocating ATPase; subunit a; Vph1; Stv1
Affiliations: Department of Physiology, Tufts University School of Medicine, 136 Harrison Ave., Boston, MA 02111, USA.

Abstract:  The 100-kDa "a" subunit of the vacuolar proton-translocating ATPase (V-ATPase) is encoded by two genes in yeast, VPH1 and STV1. The Vph1p-containing complex localizes to the vacuole, whereas the Stv1p-containing complex resides in some other intracellular compartment, suggesting that the a subunit contains information necessary for the correct targeting of the V-ATPase. We show that Stv1p localizes to a late Golgi compartment at steady state and cycles continuously via a prevacuolar endosome back to the Golgi. V-ATPase complexes containing Vph1p and Stv1p also differ in their assembly properties, coupling of proton transport to ATP hydrolysis, and dissociation in response to glucose depletion. To identify the regions of the a subunit that specify these different properties, chimeras were constructed containing the cytosolic amino-terminal domain of one isoform and the integral membrane, carboxyl-terminal domain from the other isoform. Like the Stv1p-containing complex, the V-ATPase complex containing the chimera with the amino-terminal domain of Stv1p localized to the Golgi and the complex did not dissociate in response to glucose depletion. Like the Vph1p-containing complex, the V-ATPase complex containing the chimera with the amino-terminal domain of Vph1p localized to the vacuole and the complex exhibited normal dissociation upon glucose withdrawal. Interestingly, the V-ATPase complex containing the chimera with the carboxyl-terminal domain of Vph1p exhibited a higher coupling of proton transport to ATP hydrolysis than the chimera containing the carboxyl-terminal domain of Stv1p. Our results suggest that whereas targeting and in vivo dissociation are controlled by sequences located in the amino-terminal domains of the subunit a isoforms, coupling efficiency is controlled by the carboxyl-terminal region. 

Retracted: No

PubPeer comments:
 ![file] In Fig.7, there is a slice site (indicated with red arrow). The panel were assembled together from different images ,
RIF1 is essential for 53BP1-dependent nonhomologous end joining and suppression of DNA double-strand break resection
Authors: Simon J Boulton
Patricia Barral
Martin Steger
Alessandro A Sartori
Ian R Adams
Antonia Tomas-Loba
Facundo D Batista
Valérie Borel
J Ross Chapman
Jean-Baptiste Vannier
Journal: Molecular Cell (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: DNA double-strand break repair; 53BP1; BRCA1; Rif1; class switch recombination
Affiliations: DNA Damage Response Laboratory, London Research Institute, Cancer Research UK, Clare Hall, South Mimms, London, UK.

Abstract:  The appropriate execution of DNA double-strand break (DSB) repair is critical for genome stability and tumor avoidance. 53BP1 and BRCA1 directly influence DSB repair pathway choice by regulating 5' end resection, but how this is achieved remains uncertain. Here we report that Rif1(-/-) mice are severely compromised for 53BP1-dependent class switch recombination (CSR) and fusion of dysfunctional telomeres. The inappropriate accumulation of RIF1 at DSBs in S phase is antagonized by BRCA1, and deletion of Rif1 suppresses toxic nonhomologous end joining (NHEJ) induced by PARP inhibition in Brca1-deficient cells. Mechanistically, RIF1 is recruited to DSBs via the N-terminal phospho-SQ/TQ domain of 53BP1, and DSBs generated by ionizing radiation or during CSR are hyperresected in the absence of RIF1. Thus, RIF1 and 53BP1 cooperate to block DSB resection to promote NHEJ in G1, which is antagonized by BRCA1 in S phase to ensure a switch of DSB repair mode to homologous recombination. 

Retracted: No

PubPeer comments:
 Fig 4 ![file] The a-Actin band for Fig 4 D [lower panel, NAC and Thea treated, NF-kB (cytosol)and Histone H1] looks identical and seems to be reused in Fig 4 F of MMP2 and MMP9 Western blot (lower panel). Could authors check? ,
In vitro interaction and biocompatibility of titanate nanotubes with microglial cells
Authors: J Boudon
L Maurizi
P V Mohanan
A Loiseau
N Millot
G Lizard
F Sallem
S Sruthi
Journal: Toxicology and Applied Pharmacology (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Apoptosis; Lysosomal integrity; Microglial activation; Mitochondrial hyperpolarisation; Reactive oxygen species
Affiliations: Toxicology Division, Biomedical Technology Wing, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram 695 012, Kerala, India; Nanosciences Department, Laboratoire Interdisciplinaire Carnot de Bourgogne, UMR 6303, CNRS/Université Bourgogne Franche-Comté, 9 av. A. Savary BP 47 870, 21 078 Dijon, France., Nanosciences Department, Laboratoire Interdisciplinaire Carnot de Bourgogne, UMR 6303, CNRS/Université Bourgogne Franche-Comté, 9 av. A. Savary BP 47 870, 21 078 Dijon, France., Toxicology Division, Biomedical Technology Wing, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram 695 012, Kerala, India., Faculté des Sciences Gabriel, Laboratoire Bio-PeroxIL, EA7270, Université Bourgogne Franche-Comté/Inserm, 6 Bd Gabriel, 21 000 Dijon, France. Electronic address: ., Nanosciences Department, Laboratoire Interdisciplinaire Carnot de Bourgogne, UMR 6303, CNRS/Université Bourgogne Franche-Comté, 9 av. A. Savary BP 47 870, 21 078 Dijon, France. Electronic address: .

Abstract:  Titanate nanotubes (TiONts) are promising agents for biomedical applications. Microglial activation and associated oxidative burst are major challenges in drug delivery applications across the brain. Here, TiONts were designed for drug delivery systems by functionalizing them with (3-aminopropyl) triethoxysilane (APTES), their interactions and biocompatibility were studied in vitro using murine microglial BV-2 cells. TiONts-APTES exposure resulted in increased ROS production and transient mitochondrial hyperpolarization. However, there was no indication of microglial proliferation in BV-2 cells as suggested by cell cycle analysis and morphology evaluation. The endocytosis as well as passive diffusion mediated TiONts-APTES internalization were proved by transmission electron microscopy (TEM) with and without amiloride, an endocytosis inhibiting agent. In addition, the TiONts-APTES exhibited good biocompatibility on microglial BV-2 cells as revealed by the plasma membrane integrity, lysosmal membrane integrity, morphology and viability analysis. 

Retracted: No

PubPeer comments:
 Could authors explain why the blots look edited? Figure 12. PARP cleavage assay in BV-2 cells exposed to TiONts-APTES for 24 h. Lane 1: protein marker, Lane 2: control cells, Lane3: control cells pre-treated with Z- Fa-FMK, lane 4: TiONts-APTES (80 u03bcg mL), lane 5: 80 u03bcg mL TiONts-APTES pre- treated with Z-Fa-FMK. ![file] , 
 Figure 12 immunoblot images have unusual editing. The area in yellow highlights the possible additional pasting. Could the authors clarify? ![file] ,