PReD-Bench/PRed-Bench huggingface dataset:
Molecular antagonism and plasticity of regulatory and inflammatory T cell programs
Authors: Chen Dong
Stephanie S Watowich
Xin-Hua Feng
Bhanu P Pappu
Seon Hee Chang
Anton M Jetten
Gustavo J Martinez
Xuexian O Yang
Roza Nurieva
Hong Soon Kang
Kimberly S Schluns
Yeonseok Chung
Bhavin Shah
Journal: Immunity (2008)
Discipline: IMMUNOLOGY
Keywords: Regulatory T cells; T helper 17 cells; differentiation; interleukin-17F; Foxp3
Affiliations: Department of Immunology, M.D. Anderson Cancer Center, Houston, TX 77030, USA.

Abstract:  Regulatory T (Treg) and T helper 17 (Th17) cells were recently proposed to be reciprocally regulated during differentiation. To understand the underlying mechanisms, we utilized a Th17 reporter mouse with a red fluorescent protein (RFP) sequence inserted into the interleukin-17F (IL-17F) gene. Using IL-17F-RFP together with a Foxp3 reporter, we found that the development of Th17 and Foxp3(+) Treg cells was associated in immune responses. Although TGF-beta receptor I signaling was required for both Foxp3 and IL-17 induction, SMAD4 was only involved in Foxp3 upregulation. Foxp3 inhibited Th17 differentiation by antagonizing the function of the transcription factors RORgammat and ROR*. In contrast, IL-6 overcame this suppressive effect of Foxp3 and, together with IL-1, induced genetic reprogramming in Foxp3(+) Treg cells. STAT3 regulated Foxp3 downregulation, whereas STAT3, RORgamma, and ROR* were required for IL-17 expression in Treg cells. Our data demonstrate molecular antagonism and plasticity of Treg and Th17 cell programs. 

Retracted: No

PubPeer comments:
 All FACS figures in Figure 4H has identical background spots, could the authors please show the raw data and explain? ![file] , 
 #1 We donu2019t see these dots in our PDF copy (see attached). Thanks. -Xuexian Yang and Chen Dong ![file] , 
 #2 The manuscript version on NCBI(PMC) has those background dots. This must be a rare technical mistake made by NCBI. Thanks for the clarification! ,
Lysyl Oxidase Is a Strong Determinant of Tumor Cell Colonization in Bone
Authors: Edith Bonnelye
Floriane Pez
Paola Di Mauro
Clémence Thomas
Casina Kan
Philippe Clézardin
Martine Croset
Caroline Reynaud
Laura Ferreras
Antoine E Karnoub
Marie Brevet
Géraldine Aimond
Journal: Cancer Research (2017)
Discipline: CLINICAL MEDICINE
Keywords: Lysyl oxidase; LOX; colorectal cancer; HIF-1; bone metastases
Affiliations: INSERM, UMR1033, Lyon, France.  ., University of Lyon, Villeurbanne, France., INSERM, UMR1033, Lyon, France., CNRS, UMR5305, IBCP, Lyon, France., Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts., Department of Pathology, Groupement Hospitalier Est, Hospices Civils de Lyon, Lyon, France.

Abstract:  Lysyl oxidase (LOX) is a secreted copper-dependent amine oxidase whose primary function is to drive collagen crosslinking and extracellular matrix stiffness. LOX in colorectal cancer synergizes with hypoxia-inducible factor-1 (HIF-1) to promote tumor progression. Here we investigated whether LOX/HIF1 endows colorectal cancer cells with full competence for aggressive colonization in bone. We show that a high LOX expression in primary tumors from patients with colorectal cancer was associated with poor clinical outcome, irrespective of HIF-1 In addition, LOX was expressed by tumor cells in the bone marrow from colorectal cancer patients with bone metastases. In vivo experimental studies show that LOX overexpression in colorectal cancer cells or systemic delivery of the conditioned medium from LOX-overexpressing colorectal cancer cells promoted tumor cell dissemination in the bone marrow and enhanced osteolytic lesion formation, irrespective of HIF-1 Conversely, silencing or pharmacologic inhibition of LOX activity blocked dissemination of colorectal cancer cells in the bone marrow and tumor-driven osteolytic lesion formation. In vitro, tumor-secreted LOX supported the attachment and survival of colorectal cancer cells to and in the bone matrix, and inhibited osteoblast differentiation. LOX overexpression in colorectal cancer cells also induced a robust production of IL6. In turn, both LOX and IL6 were acting in concert to promote RANKL-dependent osteoclast differentiation, thereby creating an imbalance between bone resorption and bone formation. Collectively, our findings show that LOX supports colorectal cancer cell dissemination in the bone marrow and they reveal a novel mechanism through which LOX-driven IL6 production by colorectal cancer cells impairs bone homeostasis. Cancer Res; 77(2); 268-78. ©2016 AACR. 

Retracted: No

PubPeer comments:
 The tissue samples in Figure 1 appear to be from some very closely related patients, although slightly different in coloring. *** ![file] ,
High-mobility group box 1 is essential for mitochondrial quality control
Authors: Rui Kang
Kristen M Livesey
Herbert J Zeh 3rd
Michael T Lotze
Timothy R Billiar
Daolin Tang
Guido Kroemer
Bennett Van Houten
Journal: Cell Metabolism (2011)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Mitochondria; HMGB1; HSPB1; bioenergetics; apoptotic death
Affiliations: Department of Surgery, G.27A Hillman Cancer Center, University of Pittsburgh Cancer Institute, Pittsburgh, PA 15219, USA.

Abstract:  Mitochondria are organelles centrally important for bioenergetics as well as regulation of apoptotic death in eukaryotic cells. High-mobility group box 1 (HMGB1), an evolutionarily conserved chromatin-associated protein which maintains nuclear homeostasis, is also a critical regulator of mitochondrial function and morphology. We show that heat shock protein beta-1 (HSPB1 or HSP27) is the downstream mediator of this effect. Disruption of the HSPB1 gene in embryonic fibroblasts with wild-type HMGB1 recapitulates the mitochondrial fragmentation, deficits in mitochondrial respiration, and adenosine triphosphate (ATP) synthesis observed with targeted deletion of HMGB1. Forced expression of HSPB1 reverses this phenotype in HMGB1 knockout cells. Mitochondrial effects mediated by HMGB1 regulation of HSPB1 expression serve as a defense against mitochondrial abnormality, enabling clearance and autophagy in the setting of cellular stress. Our findings reveal an essential role for HMGB1 in autophagic surveillance with important effects on mitochondrial quality control. 

Retracted: No

PubPeer comments:
 Figure 2A. * Blue vertical line: Most panels show 4 replicates of each condition, so 12 lanes per panel, but the p-S6 S6 b-actin blots in the middle only show 9 lanes. * Red arrows: four lanes in the b-actin blot serving as the loading control for the p-S6 S6 panels appear to look similar to four lanes in the b-actin blot serving as the loading control for the p-4EBP1 4EBP1 panels, if one of the two panels would be in mirror image. Could the authors please show the original, uncropped blots? ![file] , 
 Thanks for your critical comments to our paper. The WB is conducted at different time and use different electrophoresis tanks, we should note n=3 or 4 in context for the better. For the 4 red lane of actin band, all the phospho-protein is normalized by their relative total protein. The actin expression is only the doulble internal standard. It is nonsense for us to modify and mad any modification on actin band. What s more, apart from this *looks similar *4 lane, other lanes are obviously different. I will show the original uncrop pictures once we dig it. , 
 There appear to be some other issues here. Specifically, the 0.5 mM succinate image in Figure 1D is a duplicate from the control untreated image in Figure 1B of this paper... https: www.ncbi.nlm.nih.gov pmc articles PMC6266637 ![file] The other paper was published later (2018 vs. the 2017 here), so maybe FASEBJ would like to request for copyright release from the publishers of Mol Med Reports? ,
The effect of estrogen on prolidase-dependent regulation of HIF-1α expression in breast cancer cells
Authors: Izabela Prokop
Wojciech Miltyk
Jerzy Palka
Arkadiusz Surazynski
Journal: Molecular and Cellular Biochemistry (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: estrogen; breast cancer progression; prolidase activity; HIF-1α; MCF-7 cells
Affiliations: Department of Medicinal Chemistry, Medical University of Bialystok, Bialystok, Poland.

Abstract:  The role of estrogen in breast cancer progression and activation of prolidase activity and HIF-1α led us to study the effect of estrogen on nuclear HIF-1α expression in breast cancer estrogen-dependent MCF-7 and estrogen-independent MDA-MB-231 cells. We have found that in MCF-7 cells (expressing α and β estrogen receptor) cultured without estrogen receptor activator (phenol red, estradiol), HIF-1α was down-regulated, compared to the cells cultured with estrogen receptor activator. This effect was not observed in MDA-MB-231 cells (expressing only β estrogen receptor), suggesting that α estrogen receptor is involved in down-regulation of HIF-1α. However, in MDA-MB-231 cells (expressing high prolidase activity) cultured in the presence of prolidase substrates, Gly-Pro or Gly-HyPro, HIF-1α expression was induced in a dose-dependent manner, independently of estrogen receptor activation. In MCF-7 cells (with constitutively low prolidase activity) the effect of studied iminodipeptides on HIF-1α expression was much less pronounced but it was estrogen-dependent, showing importance of prolidase activity in mechanism of this process. The data were supported by confocal microscopy bio-imaging of HIF-1α in nucleus of MCF-7 and MDA-MB-231 cells that were cultured in the presence and absence of estrogen activator and prolidase substrates. It suggests that estrogen receptor may represent important therapeutic target in pharmacotherapy of estrogen receptor positive breast cancer, while ECM degradation enzymes, including prolidase may represent target in pharmacotherapy of estrogen receptor negative breast cancers. 

Retracted: No

PubPeer comments:
 Figure 4. * Red boxes: Panels A and E appear to show the same sample, albeit shown at different exposures. Reported to the journal in October 2015, with a friendly reminder in 2017, but no response as of today. ![file] , 
 Thank you for this comment and please accept my apologies for not responding early. I haven t observed this post before. You are actually right. Photo a and e are identical. probably this error is due to incorrectly selected images from a huge file. In general, MCF-7 cells grown in estrogen-free conditions showed no response to imidodipeptides, which probably contributed to the failure to notice this error. Thank you for paying attention to this error which will contribute to greater caution in constructing figures. Regards, Jerzy Palka ,
Long noncoding RNA MAGI1-IT1 promoted invasion and metastasis of epithelial ovarian cancer via the miR-200a/ZEB axis
Authors: Jiapo Wang
Hao Gao
Weimin Wu
Guangxi Zhan
Xiaoqing Guo
Xiaofeng Li
Jing Yu
Na Liu
Yong Zhu
Li Li
Journal: Cell Cycle (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Epithelial ovarian cancer; MAGI1-IT1; ZEB1 and ZEB2; invasion and metastasis; miR-200a.
Affiliations: a Department of Obstetrics and Gynecology, Shanghai First Maternity and Infant Hospital , Tongji University School of Medicine , Shanghai , China., b Department of Obstetrics and Gynecology , Central Theater of the Chinese PLA , Wuhan , China., c Department of Pathology, Shanghai First Maternity and Infant Hospital , Tongji University School of Medicine , Shanghai , China.

Abstract:  Epithelial ovarian cancer (EOC) is the most lethal gynecologic malignancy, and its vulnerability to metastasis contributes to the poor outcomes of EOC patients. Long noncoding RNAs (lncRNAs) were verified to play a pivotal role in EOC metastasis. However, the potential role of lncRNA membrane-associated guanylate kinase inverted 1 (MAGI1) intronic transcript (MAGI1-IT1) in EOC is largely unknown. In this study, the function and mechanisms of MAGI1-IT1 in EOC metastasis were explored profoundly. First, MAGI1-IT1 expression was found to be significantly decreased in overexpressing miR-200a EOC cells. Second, MAGI1-IT1 expression was remarkably increased in metastatic EOC tissues, and high MAGI1-IT1 was dramatically associated with EOC FIGO III-IV stage; in addition, MAGI1-IT1 might be related to EOC dissemination via epithelial-mesenchymal transition (EMT). Next, a series of gain- and loss-of-function assays verified that, although MAGI1-IT1 has no significant role in EOC proliferation and subcutaneous xenograft growth, the upregulation of MAGI1-IT1 can remarkably facilitate EOC EMT phenotype, cells migration and invasion ability and intraperitoneal metastasis in nude mice, while downregulation of MAGI1-IT1 led to the opposite effect in vitro. Moreover, MAGI1-IT1 was validated to promote EOC metastasis through upregulation of ZEB1 and ZEB2 by competitively binding miR-200a, and the restrictive effects of MAGI1-IT1 depletion on EOC metastasis could be reversed by inhibition of miR-200a and upregulation of ZEB1 and ZEB2. Collectively, these results suggest that MAGI1-IT1 may work as a ceRNA in promoting EOC metastasis through miR-200a and ZEB1/2 and may be a potential therapeutic target for EOC. 

Retracted: No

PubPeer comments:
 Figure 3a: two cases where microscopy data have been duplicated and presented as something else. ![file] , 
 Figure 4a appears to contain an incorrect DAPI image, as the blue features do not appear in the merged image. *** ![file] , 
 Figure 3e does not want to be left out of the fun. ![file] ,
SIRT2 is involved in the modulation of depressive behaviors
Authors: Ying Du
Qiong Zhou
Rui Liu
Wei Dang
Zhaohui Liu
Kai Jiao
Journal: Scientific Reports (2015)
Discipline: Multidisciplinary
Keywords: chronic stress; mood disorders; SIRT2; depression; neurogenesis
Affiliations: Department of Rehabilitation, Tangdu Hospital, Fourth Military Medical University, Xi'an 710032, P.R. China., Department of Psychiatry, Xi'an Mental Health Center, Xi'an 710061, P.R. China., Department of Neurology, Tangdu Hospital, Fourth Military Medical University, Xi'an 710032, P.R. China., Department of Endocrinology, Tangdu Hospital, Fourth Military Medical University, Xi'an 710032, P.R. China.

Abstract:  Exposure to chronic stress produces negative effects on mood and hippocampus-dependent memory formation. SIRT2 alteration has been reported in mood disorders; however, the role of SIRT2 in depression remains unclear. Therefore, we aimed to determine whether SIRT2 can restore stress-induced suppression of neurogenesis in a rat chronic unpredictable stress (CUS) model of depression. Sucrose preference test, home-cage locomotion, forced swim test, and elevated plus maze were used to determine the role of SIRT2 in CUS model. To further determine the hippocampal neurogenesis contributes to the role of SIRT in mediating the antidepressant-like behavior, rats were exposed to X-irradiation to disrupt the process of hippocampal neurogenesis. CUS decreased expression of the SIRT2 protein in the hippocampus. Treatment with the antidepressant fluoxetine reversed the CUS-induced SIRT2 change. Furthermore, inhibiting SIRT2 by tenovin-D3 resulted in depression-like behaviors and impaired hippocampal neurogenesis in rats. Conversely, overexpression of SIRT2 by the intra-hippocampal infusion of recombinant adenovirus vector expressing mouse SIRT2 reversed the CUS-induced depressive-like behaviors, and promoted neurogenesis. Disrupting neurogenesis in the dentate gyrus by X-irradiation abolished the antidepressant-like effect of Ad-SIRT2-GFP. These findings indicate that hippocampal SIRT2 is involved in the modulation of depressant-like behaviors, possibly by regulating neurogenesis. 

Retracted: No

PubPeer comments:
 The loading controls for the western blots in Figures 2 and 3 look more alike than could be expected by chance. ![file] It would appear as if they are the same, only having been slightly stretched for Figure 3. Could the authors check their original data and perhaps provide uncropped scans from these analyses? ,
RETRACTED ARTICLE: Disruption of the Bcr-Abl/Hsp90 protein complex: a possible mechanism to inhibit Bcr-Abl-positive human leukemic blasts by novobiocin
Authors: Q Lin
K Z Zhang
Y Z Chen
L X Wu
X W Huang
J H Xu
C X Wen
Journal: Leukemia (2008)
Discipline: CLINICAL MEDICINE
Keywords: Bcr-Abl fusion gene; Hsp90; novobiocin; leukemia cells; apoptosis
Affiliations: Deparment of Pharmacology, Institute of Clinical Pharmacology, Fujian Medical University, Fuzhou, PR China. 

Abstract:  The Bcr-Abl fusion gene encodes for the p210(Bcr-Abl) or p185(Bcr-Abl) tyrosine kinase (TK) implicated in the pathogenesis of chronic myelogenous leukemia (CML) or acute lymphoblastic leukemia, respectively. Because Bcr-Abl TK is chaperoned by Hsp90 (90 kDa heat-shock protein), we investigated the effects of novobiocin (NB), an Hsp90 C-terminal inhibitor, on the viability of the Bcr-Abl-positive human leukemia cells HL-60/Bcr-Abl and K562, the expression of Bcr-Abl protein and the interaction between Hsp90 and Bcr-Abl TK. Present studies demonstrate that NB is a potent inhibitor of the growth of Bcr-Abl-positive human leukemia cells. NB induces cytosolic accumulation of cytochrome c and activation of caspase-9 and caspase-3, triggering apoptosis of HL-60/Bcr-Abl and K562 cells. Treatment of cell lines with NB disrupts Bcr-Abl /Hsp90 and Bcr-Abl /Hsp70 interactions, resulting in a decreased amount of intracellular Bcr-Abl protein levels. Co-treatment with the proteasome inhibitor N-acetyl leucyl-leucyl norlucinal increases NB-mediated accumulation of Bcr-Abl in the detergent-insoluble cellular fraction, which demonstrates that NB promotes proteasomal degradation of Bcr-Abl. Moreover, both imatinib-resistant K562/G01 and primary CML CD34(+) cells are sensitive to NB. 

Retracted: Yes

PubPeer comments:
 ![file] , 
 ![file] , 
 ![file] , 
 ![file] , 
 #2 I think you missed one. ![file] , 
 #4 I have added copies of the repeating beta-actin motif from Figure 3, vertically compressed, for comparison with the repeating beta-actin band here. ![file] , 
 2020 retraction. https: www.nature.com articles s41375-020-0823-z The authors have retracted this article [1]. An investigation by Fujian Medical University identified multiple errors in the assembly of the figures, most notably in the duplication of loading controls. All authors agree with this retraction. Reference 1. Wu LX, Xu JH, Zhang KZ, Lin Q, Huang XW, Wen CX, Chen YZ. Disruption of the Bcr-Abl Hsp90 protein complex: a possible mechanism to inhibit Bcr-Abl-positive human leukemic blasts. Leukemia. 2008;22:1402u20139. ,
p73 and p63 sustain cellular growth by transcriptional activation of cell cycle progression genes
Authors: Konstantinos Lefkimmiatis
Beatriz Navarro
Apollonia Tullo
Anna Maria D&#x27;Erchia
Massimo Levrero
Mariano Francesco Caratozzolo
Paola Merlo
Elisabetta Sbisa&#x27;
Journal: Cancer Research (2009)
Discipline: CLINICAL MEDICINE
Keywords: tumor suppressor; p53 protein; p73; p63; cell cycle progression
Affiliations: Istituto di Tecnologie Biomediche CNR-Bari, Universita' degli Studi di Bari, Bari, Italy.

Abstract:  Despite extensive studies on the role of tumor suppressor p53 protein and its homologues, p73 and p63, following their overexpression or cellular stress, very little is known about the regulation of the three proteins in cells during physiologic cell cycle progression. We report a role for p73 and p63 in supporting cellular proliferation through the transcriptional activation of the genes involved in G(1)-S and G(2)-M progression. We found that in MCF-7 cells, p73 and p63, but not p53, are modulated during the cell cycle with a peak in S phase, and their silencing determines a significant suppression of proliferation compared with the control. Chromatin immunoprecipitation analysis shows that in cycling cells, p73 and p63 are bound to the p53-responsive elements (RE) present in the regulatory region of cell cycle progression genes. On the contrary, when the cells are arrested in G(0)-G(1), p73 detaches from the REs and it is replaced by p53, which represses the expression of these genes. When the cells move in S phase, p73 is recruited again and p53 is displaced or is weakly bound to the REs. These data open new possibilities for understanding the involvement of p73 and p63 in cancer. The elevated concentrations of p73 and p63 found in many cancers could cause the aberrant activation of cell growth progression genes and therefore contribute to cancer initiation or progression under certain conditions. 

Retracted: No

PubPeer comments:
null, 
 2020 Editor s Note. https: cancerres.aacrjournals.org content 80 7 1611 The editors are publishing this note to alert readers to a concern about this article (1). The authors made the editors aware of duplicated Western blot bands in Fig. 3. Specifically, the same image was used for the actin loading control Western blot bands for the ADA and FASN experiments. ,
<p>MiR-935 Promotes Clear Cell Renal Cell Carcinoma Migration and Invasion by Targeting IREB2 [Retraction]</p>
Authors: Yuedong Chen
Jinchun Xing
Fei Liu
Bin Chen
Chunxiao Liu
Journal: Cancer Management and Research (2020)
Discipline: CLINICAL MEDICINE
Keywords: Retract; Article; DOI; CMAR; S232380

Abstract:  [This retracts the article DOI: 10.2147/CMAR.S232380.]. 

Retracted: No

PubPeer comments:
 At the authors request, the Editor-in-Chief and Publisher of Cancer Management and Research wish to retract the published article. Following a review of their article the authors found some errors had been made in Figure 4E, specifically images in panels Migration miR-935 inhibitor + si-IREB2 + and Invasion miR-935 inhibitor + si-IREB2 +. After carefully going through the raw data for their study the authors were unable to locate the original images for Figure 4E. The authors were also unable to locate the original images for the western blots shown in the article. Both the editor and authors determined the findings of this study could no longer be supported and agreed for the article to be retracted. The authors wish to apologise for this error. Our decision-making was informed by our policy on publishing ethics and integrity and the COPE guidelines on retraction. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as u201cRetractedu201d. ,
Paeoniflorin inhibits proliferation and promotes apoptosis of multiple myeloma cells via its effects on microRNA‑29b and matrix metalloproteinase‑2
Authors: Wenhua Liu
Shaofeng Wang
Journal: Molecular medicine reports (2016)
Discipline: CLINICAL MEDICINE
Keywords: Multiple myeloma; Paeoniflorin; SKO-007 cells; MMP-2; miR-29b
Affiliations: Department of Orthopedics, The Affiliated Hospital of Weifang Medical College, Weifang, Shandong 261031, P.R. China.

Abstract:  Multiple myeloma (MM) is a type of cancer characterized by the excessive proliferation of malignant plasma cells. In China, the incidence of MM has been increasing annually. Paeoniflorin exerts numerous functions, including coronary vessel expansion, and anti‑inflammation and anticancer activities. The present study aimed to investigate the effects of paeoniflorin on the proliferation and apoptosis of SKO‑007 MM cells, via its effects on the regulation of matrix metalloproteinase‑2 (MMP‑2) and microRNA (miR)‑29b. In the present study, an MTT assay was used to analyze the proliferation of SKO‑007 cells treated with paeoniflorin. Annexin V‑fluorescein isothiocyanate/propidium iodide apoptosis and caspase‑3 activation assays were used to detect the levels of cellular apoptosis. The expression levels of MMP‑2 and miR‑29b were detected using gelatin zymography and quantitative‑polymerase chain reaction, respectively. In addition, miR‑29b and anti‑miR‑29b plasmids were transfected into SKO‑007 cells, and the effects of paeoniflorin on cell proliferation and apoptosis were subsequently detected. The results of the present in vitro studies demonstrated that paeoniflorin was able to inhibit the proliferation of SKO‑007 cells in a dose‑ and time‑dependent manner. Furthermore, paeoniflorin effectively increased cell apoptosis, and augmented the activation of caspase‑3 and caspase‑9 in the SKO‑007 cells. The expression levels of MMP‑2 were suppressed following treatment of the SKO‑007 cells with paeoniflorin. In addition, paeoniflorin was able to induce the expression of miR‑29b. Notably, the results of the present study indicated that miR‑29b expression may control the expression of MMP‑2 in SKO‑007 cells. In conclusion, the present study demonstrated that paeoniflorin was able to inhibit cell proliferation and promote apoptosis of MM cells by suppressing the expression of MMP‑2, via the upregulation of miR‑29b. 

Retracted: No

PubPeer comments:
 Figs 6A,  The effects of paeoniflorin on (A) MMP-2 expression , and 10D,  Anti-miR-29b significantly increased MMP-2 activity in SKO-007 cells following treatment with paeoniflorin (10 u00b5M) for 48 h. Some surprising similarities. ![file] Here the similarities are enhanced by some rescaling of protein blobs. ![file] ,
TMS over the supramarginal gyrus delays selection of appropriate grasp orientation during reaching and grasping tools for use
Authors: Alan Sunderland
Nicholas P Holmes
Tomás McDowell
Martin Schürmann
Journal: Cortex (2018)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Grasp orientation; SMG; TMS; Tool use; Visuomotor control.
Affiliations: School of Psychology, University of Nottingham, Nottingham, UK. Electronic address: ., School of Psychology, University of Nottingham, Nottingham, UK.

Abstract:  Tool use, a ubiquitous part of human behaviour, requires manipulation control and knowledge of tool purpose. Neuroimaging and neuropsychological research posit that these two processes are supported by separate brain regions, ventral premotor and inferior parietal for manipulation control, and posterior middle temporal cortex for tool knowledge, lateralised to the left hemisphere. Action plans for tool use need to integrate these two separate processes, which is likely supported by the left supramarginal gyrus (SMG). However, whether this integration occurs during action execution is not known. To clarify the role of the SMG we conducted two experiments in which healthy participants reached to grasp everyday tools with the explicit instruction to use them directly following their grasp. To study the integration of manipulation control and tool knowledge within a narrow time window we mechanically perturbed the orientation of the tool to force participants to correct grasp orientation 'on-line' during the reaching movement. In experiment 1, twenty healthy participants reached with their left hand to grasp a tool. Double-pulse transcranial magnetic stimulation (TMS) was applied, in different blocks over left or right SMG at the onset of perturbation. Kinematic data revealed delayed and erroneous online correction after TMS over left and right SMG. In Experiment 2 twelve participants reached, in different blocks, with their left or right hand and TMS was applied over SMG ipsilateral to the reaching hand. A similar effect on correction was observed for ipsilateral stimulation when reaching with the left and right hands, and no effect of or interaction with hemisphere was observed. Our findings implicate a bilateral role of the SMG in correcting movements and selection of appropriate grasp orientation during reaching to grasp tools for use. 

Retracted: No

PubPeer comments:
 This paper was criticised as part of a self-reflection posted on Twitter on 2nd-3rd April, 2021 (twitter TheHandLab status 1377760796130869248) Criticism: I ve made much noise about having good control conditions in TMS studies. This paper by Tomas devised some truly ingenious methods analysis that deeply impressed me. But the No-TMS control condition is weak. ,
Infant behavioral inhibition predicts personality and social outcomes three decades later
Authors: Daniel S Pine
Santiago Morales
Nathan A Fox
Alva Tang
Kathryn A Degnan
Haley Crawford
Journal: Proceedings of the National Academy of Sciences of the United States of America (2020)
Discipline: Multidisciplinary
Keywords: behavioral inhibition; lifespan; personality; temperament.
Affiliations: Department of Human Development and Quantitative Methodology, University of Maryland, College Park, MD 20740; ., Department of Human Development and Quantitative Methodology, University of Maryland, College Park, MD 20740., Department of Psychology, Catholic University of America, Washington, DC 20064., Intramural Research Program, National Institutes of Mental Health, Bethesda, MD 20892.

Abstract:  Does infant temperament predict adult personality and life-course patterns? To date, there is scant evidence examining relations between child temperament and adult outcomes, and extant research has relied on limited methods for measuring temperament such as maternal report. This prospective longitudinal study followed a cohort of infants (n = 165) for three decades to examine whether infant behavioral inhibition, a temperament characterized by cautious and fearful behaviors to unfamiliar situations, shapes long-term personality, social relationships, vocational/education, and mental health outcomes in adulthood. At age 14 mo, behavioral inhibition was assessed using an observation paradigm. In adolescence (15 y; n = 115), error monitoring event-related potentials were measured in a flanker task. In adulthood (26 y; n = 109), personality, psychopathology, and sociodemographics were self-reported using questionnaires. We found that infants with higher levels of behavioral inhibition at 14 mo grew up to become more reserved and introverted adults (β = 0.34) with lower social functioning with friends and family (β = -0.23) at age 26. Infant behavioral inhibition was also a specific risk factor for adult internalizing (i.e., anxiety and depression, β = 0.20) psychopathology, rather than a transdiagnostic risk for general and externalizing psychopathology. We identified a neurophysiologic mechanism underlying risk and resilience for later psychopathology. Heightened error monitoring in adolescence moderated higher levels of adult internalizing psychopathology among behaviorally inhibited individuals. These findings suggest meaningful continuity between infant temperament and the development of adult personality. They provide the earliest evidence suggesting that the foundation of long-term well-being is rooted in individual differences in temperament observed in infancy. 

Retracted: No

PubPeer comments:
 Note: This article has been corrected. Please see the link below: https: www.oncotarget.com article 27512 ,
Inhibition of cell growth and invasion by epidermal growth factor-targeted phagemid particles carrying siRNA against focal adhesion kinase in the presence of hydroxycamptothecin
Authors: Xiu-Mei Cai
Ming-Zhu Liu
Hai-Long Xie
Xi-Liang Zha
Journal: BMC Biotechnology (2008)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: EGF-targeted phagemid particles; siRNA; Akt; hydroxycamptothecin; cell growth inhibition
Affiliations: Department of Biochemistry and Molecular Biology, Shanghai Medical College, Fudan University, Shanghai, PR China. 

Abstract:  Background: Previous studies demonstrated the EGF-targeted phagemid particles carrying siRNA against Akt could be expressed efficiently in the presence of hydroxycamptothecin (HCPT). However, no significant cell growth inhibition was obtained. This study was to further investigate whether the EGF-targeted phagemid particles carrying siRNA would be a promising tool for anti-cancer siRNA delivery. Results: We found that pSi4.1-siFAK phagemid particles could significantly inhibit the expression of focal adhesion kinase in the HCPT-treated cells. Moreover, we also observed that the particles could potently suppress cell growth and cell invasion. Conclusion: These results indicated that EGF-targeted phagemid particles might be a promising tool for anti-cancer siRNA delivery in the presence of HCPT. 

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. ,
CREB regulates hepatic gluconeogenesis through the coactivator PGC-1
Authors: R Quinn
B Spiegelman
U S Jhala
S Herzig
F Long
M Montminy
S Hedrick
A Bauer
D Rudolph
C Yoon
G Schutz
P Puigserver
Journal: Nature (2001)
Discipline: Multidisciplinary
Keywords: glucose homeostasis; gluconeogenic genes; CREB; PGC-1; fasting hypoglycaemia
Affiliations: Peptide Biology Laboratories, Salk Institute for Biological Studies, 10010 N Torrey Pines Road, La Jolla, California 92037-1002, USA.

Abstract:  When mammals fast, glucose homeostasis is achieved by triggering expression of gluconeogenic genes in response to glucagon and glucocorticoids. The pathways act synergistically to induce gluconeogenesis (glucose synthesis), although the underlying mechanism has not been determined. Here we show that mice carrying a targeted disruption of the cyclic AMP (cAMP) response element binding (CREB) protein gene, or overexpressing a dominant-negative CREB inhibitor, exhibit fasting hypoglycaemia [corrected] and reduced expression of gluconeogenic enzymes. CREB was found to induce expression of the gluconeogenic programme through the nuclear receptor coactivator PGC-1, which is shown here to be a direct target for CREB regulation in vivo. Overexpression of PGC-1 in CREB-deficient mice restored glucose homeostasis and rescued expression of gluconeogenic genes. In transient assays, PGC-1 potentiated glucocorticoid induction of the gene for phosphoenolpyruvate carboxykinase (PEPCK), the rate-limiting enzyme in gluconeogenesis. PGC-1 promotes cooperativity between cyclic AMP and glucocorticoid signalling pathways during hepatic gluconeogenesis. Fasting hyperglycaemia is strongly correlated with type II diabetes, so our results suggest that the activation of PGC-1 by CREB in liver contributes importantly to the pathogenesis of this disease. 

Retracted: No

PubPeer comments:
 ![file] , 
 Thanks for bringing this to my attention. This panel shows CRE-binding activity in liver extracts in control (WT) and liver A-CREB transgenic (A-CREB) mice. CRE-binding activity was decreased in extracts from A-CREB relative to WT mice. The presence of endogenous CREB protein in the shifted complexes was confirmed by the ability for CREB antiserum to supershift the CREB-DNA band. We compared activities of two different liver A-CREB mouse strains (Tg1, Tg2). Extracts from Tg2 mice had lower CRE binding activity compared to Tg1 extracts, prompting us to perform remaining functional studies using the Tg2 line. We removed the data corresponding to Tg1 in the published panel 1a (left). ![file] On the right, we provide data from the original autoradiogram, which we re-scanned and labeled; all lanes are shown, including lanes 4 and 5, corresponding to Tg1 mouse extract. ,
Phenol Reduces Nitrite to NO at Copper(II): Role of a Proton-Responsive Outer Coordination Sphere in Phenol Oxidation
Authors: Aditesh Mondal
Jeffery A Bertke
Subrata Kundu
Kiran P Reddy
Journal: Journal of the American Chemical Society (2020)
Discipline: CHEMISTRY
Keywords: physiological significance; transition-metal-mediated routes; nitrite; nitric oxide; phenol oxidation
Affiliations: School of Chemistry , Indian Institute of Science Education and Research Thiruvananthapuram (IISER-TVM) , Thiruvananthapuram 695551 , India., Department of Chemistry , Georgetown University , Box 571227-1227, Washington , D.C. 20057 , United States.

Abstract:  In the view of physiological significance, the transition-metal-mediated routes for nitrite (NO2-) to nitric oxide (NO) conversion and phenol oxidation are of prime importance. Probing the reactivity of substituted phenols toward the nitritocopper(II) cryptate complex [mC]Cu(κ2-O2N)(ClO4) (1a), this report illustrates NO release from nitrite at copper(II) following a proton-coupled electron transfer (PCET) pathway. Moreover, a different protonated state of 1a with a proton hosted in the outer coordination sphere, [mCH]Cu(κ2-O2N)(ClO4)2 (3), also reacts with substituted phenols via primary electron transfer from the phenol. Intriguingly, the alternative mechanism operative because of the presence of a proton at the remote site in 3 facilitates an unusual anaerobic pathway for phenol nitration. 

Retracted: No

PubPeer comments:
 Being able to see formation of NO in a 1:10 rxn does not necessarily mean NO is also formed in a 1:1 rxn A has a similar EPR spectrum to B does not necessarily mean the metal center in A has similar coord. environment to that in B. Following the authors using EPR to assign gemoetry of the Cu center, their 5-coordinate [mC]CuCl(ClO4)2 would be distorted octahedral. The reported NO stretch of NO(Et2dtc)2Fe (the Fe(dtc) they used) is 1673 cm-1, not 1707 cm-1 (reported in SI), see: Butcher, R. J.; Sinn, E. Proof of a linear Fe-N-O linkage, perpendicular to the S4 plane in Fe(NO)(S2CN{CH(CH3)2}2)2. A new (aerobic) synthesis of the complex and its crystal structure. Inorg. Chem. 1980, 19, 3622-3626. The EA result of the proposed [mC]Cu(OH)(ClO4) has 0.55 eq. of H2O. Based on their rxn, there would not be enough H atoms provided by the reagents to form the 0.55 eq. H2O. The assignment of this product is better supported by analyzing the [mC]Cu(OD)(ClO4) that is possibly formed when phenol-D is used. The result of the reaction between [mCH]Cu(O2N)(ClO4)2 does not relate to a  proton-responsive outer coordination sphere . Rather, I would love to see if same reactivity is observed if the H+ in the ligand is replaced by Li+, Na+ or K+. ,
Experimental investigation on the effectiveness of MHTHS using different metal oxide-based nanofluids
Authors: Sriharan, G.
Harikrishnan, S.
Ali, H. M.
Journal: Journal of Thermal Analysis and Calorimetry (2021)
Discipline: CHEMISTRY
Keywords: mini heat sink; thermal performance; hexagonal tube; nanofluids; deionized water

Abstract: In recent times, the mini heat sink is suggested for cooling the miniature components employed in several engineering applications. In the present work, the thermal performance of the mini hexagonal tube heat sink (MHTHS) was investigated experimentally. Nanofluids and deionized water (DIW) were made to flow through the hexagonal tube side and mini-passage side, respectively. For the preparation of different nanofluids of 0.01 volume fraction, DIW was considered to be a base fluid; Al2O3, CuO, and SiO2 nanoparticles were reckoned to be the supporting materials. Experiments were run under two different conditions in order to ascertain the enhanced thermal performance of the MHTHS. They are as follows: (1) keeping the flow rate of hot DIW constant at 30&nbsp;L&nbsp;h\u22121 in the mini-passage side, the flow rates of nanofluids in the hexagonal tube were varied such as 15, 20, 25, 30, 35, 40, 45, and 50&nbsp;L&nbsp;h\u22121; (2) keeping the flow rate of nanofluids constant at 30&nbsp;L&nbsp;h\u22121 in the hexagonal tube side, the flow rates of hot DIW in the mini-passage side were varied such as 15, 20, 25, 30, 35, 40, 45, and 50&nbsp;L&nbsp;h\u22121. From the experimental results, it divulges that the heat transfer coefficient and effectiveness were found to be higher for Al2O3–DIW nanofluid, while comparing other nanofluids. A further improvement in the thermal performance of MHTHS could be achieved at higher volume flow rates of nanofluids in the hexagonal tube side and constant volume flow rate of hot DIW in the mini-passage side.

Retracted: No

PubPeer comments:
 DUPLICATIONS! ![file] , 
 Harder situation with regarding to the **authenticity** of the images and so the paper itself! ![file] ![file] , 
 No references and legends for the SEM and TEM images! The source reference for one of the TEM images in Fig. 2 (C) for SiO2 nanoparticles is linked below: [Link] After duplication, a heavy image distortion could be seen. Inconsistent data: See the claimed particle size (20 nm) for Al2O3 in Table 1, and compare with the imaged mean sizes in Figure 2 (a) and its marker bar of 200 nm! ![file] ![file] ![file] , 
 The source reference for one of the TEM images in Fig. 2 (C) for SiO2 nanoparticles is linked below: [Link] After duplication, a heavy image manipulation and distortion could be seen. ![file] ![file] ,
Functional characterization of core promoter elements: the downstream core element is recognized by TAF1
Authors: Ilya P Ioshikhes
Naum Gershenzon
Dong-Hoon Lee
Danny Reinberg
Brian A Lewis
Malavika Gupta
Journal: Molecular and Cellular Biology (2005)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Downstream elements; core promoter elements; RNA polymerase II; DCE; TATA motif
Affiliations: Department of Biochemistry, Robert Woods Johnson Medical School, 683 Hoes Lane, Piscataway, NJ 08854, USA., Department of Biomedical Informatics, The Ohio State University, 3184 Graves Hall, 333 W. 10th Ave., Columbus, Ohio 43210, Department of Biochemistry, Howard Hughes Medical Institute, Division of Nucleic Acids Enzymology, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, 683 Hoes Lane, Piscataway, New Jersey 08854

Abstract:  Downstream elements are a newly appreciated class of core promoter elements of RNA polymerase II-transcribed genes. The downstream core element (DCE) was discovered in the human beta-globin promoter, and its sequence composition is distinct from that of the downstream promoter element (DPE). We show here that the DCE is a bona fide core promoter element present in a large number of promoters and with high incidence in promoters containing a TATA motif. Database analysis indicates that the DCE is found in diverse promoters, supporting its functional relevance in a variety of promoter contexts. The DCE consists of three subelements, and DCE function is recapitulated in a TFIID-dependent manner. Subelement 3 can function independently of the other two and shows a TFIID requirement as well. UV photo-cross-linking results demonstrate that TAF1/TAF(II)250 interacts with the DCE subelement DNA in a sequence-dependent manner. These data show that downstream elements consist of at least two types, those of the DPE class and those of the DCE class; they function via different DNA sequences and interact with different transcription activation factors. Finally, these data argue that TFIID is, in fact, a core promoter recognition complex. 

Retracted: No

PubPeer comments:
 Figure 2A. ![file] , 
 Correction unrelated to above concern. Volume 25, no. 21, p. 9674-9686, 2005. Page 9674, column 1, footnotes, line 4: u201clewisba@umdnj.eduu201d should read u201clewlisba@umdnj.edu.u201d Copyright u00a9 2005 American Society for Microbiology ,
The Polycomb group proteins bind throughout the INK4A-ARF locus and are disassociated in senescent cells
Authors: Kim Theilgaard-Mönch
Kristian Helin
Daniela Kleine-Kohlbrecher
Saverio Minucci
Nikolaj Dietrich
Gaetano Gargiulo
Diego Pasini
Chantal Beekman
Bo T Porse
Jean-Christophe Marine
Klaus H Hansen
Adrian P Bracken
Journal: Genes & Development (2007)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: p16INK4A; p14ARF; cellular senescence; oncogene BMI1; INK4A-ARF locus
Affiliations: Centre for Epigenetics, Biotech Research and Innovation Centre (BRIC), University of Copenhagen, Copenhagen 2200, Denmark. 

Abstract:  The p16INK4A and p14ARF proteins, encoded by the INK4A-ARF locus, are key regulators of cellular senescence, yet the mechanisms triggering their up-regulation are not well understood. Here, we show that the ability of the oncogene BMI1 to repress the INK4A-ARF locus requires its direct association and is dependent on the continued presence of the EZH2-containing Polycomb-Repressive Complex 2 (PRC2) complex. Significantly, EZH2 is down-regulated in stressed and senescing populations of cells, coinciding with decreased levels of associated H3K27me3, displacement of BMI1, and activation of transcription. These results provide a model for how the INK4A-ARF locus is activated and how Polycombs contribute to cancer. 

Retracted: No

PubPeer comments:
 Human BMI1 blots in Figure 4A look surprisingly similar to those of mouse Bmi1 in Figure 3A. Could the authors please check? ![file] ,
Disturbed Yin–Yang balance: stress increases the susceptibility to primary and recurrent infections of herpes simplex virus type 1
Authors: Zhuo Luo
Hiroshi Kurihara
Chang Yan
Rong-Rong He
Wen Li
Robert Dallmann
Yi-Fang Li
Xue Li
Journal: Acta Pharmaceutica Sinica B (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: 4E-BP, eIF4E-binding protein; AD, Alzheimer's disease; AKT, protein kinase B; AMPK, AMP-dependent kinase; BCL-2, B-cell lymphoma 2
Affiliations: Guangdong Engineering Research Center of Chinese Medicine & Disease Susceptibility, Jinan University, Guangzhou 510632, China., Institute of Atmospheric Environmental Safety and Pollution Control, Jinan University, Guangzhou 510632, China., Warwick Medical School, University of Warwick, Coventry CV4 7AL, UK.

Abstract:  Herpes simplex virus type 1 (HSV-1), a neurotropic herpes virus, is able to establish a lifelong latent infection in the human host. Following primary replication in mucosal epithelial cells, the virus can enter sensory neurons innervating peripheral tissues via nerve termini. The viral genome is then transported to the nucleus where it can be maintained without producing infectious progeny, and thus latency is established in the cell. Yin-Yang balance is an essential concept in traditional Chinese medicine (TCM) theory. Yin represents stable and inhibitory factors, and Yang represents the active and aggressive factors. When the organism is exposed to stress, especially psychological stress caused by emotional stimulation, the Yin-Yang balance is disturbed and the virus can re-engage in productive replication, resulting in recurrent diseases. Therefore, a better understanding of the stress-induced susceptibility to HSV-1 primary infection and reactivation is needed and will provide helpful insights into the effective control and treatment of HSV-1. Here we reviewed the recent advances in the studies of HSV-1 susceptibility, latency and reactivation. We included mechanisms involved in primary infection and the regulation of latency and described how stress-induced changes increase the susceptibility to primary and recurrent infections. 

Retracted: No

PubPeer comments:
  Stress increases the susceptibility of HSV-1 infection by disturbing host inner Yinu2013Yang balance is a very extraordinary claim to make ,