PReD-Bench/PRed-Bench huggingface dataset:
Bee Venom Soluble Phospholipase A2 Exerts Neuroprotective Effects in a Lipopolysaccharide-Induced Mouse Model of Alzheimer’s Disease via Inhibition of Nuclear Factor-Kappa B
Authors: Jaesuk Yun
YangSu Park
Se Hyun Kim
Jin Tae Hong
Ji Hye Han
Hyeon Joo Ham
Shin Kook Kang
Yong Sun Lee
Ki Cheon Kim
Journal: Frontiers in Aging Neuroscience (2019)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Alzheimer’s disease; NF-κB; bee venom phospholipase A2; neuroinflammation; regulatory T cells.
Affiliations: College of Pharmacy and Medical Research Center, Chungbuk National University, Chungbuk, South Korea., INISTst Company Limited, Gyeonggi-do, South Korea.

Abstract:  Neuroinflammation is important in the pathogenesis and development of Alzheimer's disease (AD). In the AD brain, microglial activation and upregulation of pro-inflammatory mediators both induce amyloid beta (Aβ) accumulation. Regulatory T cells (Tregs) and nuclear factor-kappa B (NF-κB) signaling have been implicated in AD development through their effects on neuroinflammation and microglial activation. The bee venom soluble phospholipase A2 (bv-sPLA2) enzyme is known to exert anti-inflammatory and anti-immune effects. Here, we investigated the inhibitory effects of bv-sPLA2 on memory deficiency in a lipopolysaccharide (LPS)-induced mouse model of AD. We examined whether bv-sPLA2 (0.02, 0.2, and 2 mg/kg by i.p. injection three times for 1 week) could inhibit neuroinflammation and memory impairment in LPS-treated mice (250 μg/kg by i.p. injection daily for 1 week). We also assessed the effects of bv-sPLA2 administration (0.01, 0.1, and 1 μg/ml) on LPS (1 μg/ml)-treated microglial BV-2 cells. In the LPS-injected mouse brain, sPLA2 treatment rescued memory dysfunction and decreased Aβ levels, through the downregulation of amyloidogenic proteins, and decreased the expression of inflammatory proteins and pro-inflammatory cytokines. Moreover, the LPS-mediated increase in inflammatory protein expression was attenuated bv-sPLA2 treatment in BV-2 cells. Treatment with bv-sPLA2 also downregulated signaling by NF-κB, which is considered to be an important factor in the regulation of neuroinflammatory and amyloidogenic responses, both in vivo and in vitro. Additionally, co-treatment with NF-κB (5 μM) and bv-sPLA2 (0.1 μg/ml) exerted more marked anti-inflammatory effects, compared to bv-sPLA2 treatment alone. These results indicate that bv-sPLA2 inhibits LPS-induced neuroinflammation and amyloidogenesis via inhibition of NF-κB. 

Retracted: No

PubPeer comments:
 Looking back at this issue, I withdraw my initial concern. I made a mistake on what was being illustrated. Apologies to the authors. However, I did identify a new issue shown below. I will send a note to the journal in hopes that they can address this with the authors. *** ![file] ,
MiR-338-3p inhibits the growth and invasion of non-small cell lung cancer cells by targeting IRS2
Authors: Peng Zhang
Zhiguang Yang
Yunpeng Liu
Guoguang Shao
Xingyu Lin
Journal: American journal of cancer research (2017)
Discipline: CLINICAL MEDICINE
Keywords: IRS2; Non-small cell lung cancer; invasion; miR-338-3p; migration
Affiliations: Department of Thoracic Surgery, The First Hospital of Jilin University #71 Xinmin Street, Chaoyang District, Changchun 130021, Jilin, China.

Abstract:  MicroRNA-338-3p (miR-338-3p) has recently been reported to have anti-cancer efficacy in several types of cancers. However, its biological function and underlying mechanism involved in modulation of human non-small cell lung cancer (NSCLC) remain largely unknown. The present study was designed to investigate the function and underlying mechanism of miR-338-3p in human NSCLC tissues and cell lines. We demonstrated that miR-338-3p was significantly decreased in NSCLC tissues and cell lines, and negatively correlated with advanced and tumor-node-metastasis (TNM) stage and lymph node metastasis (both P&lt;0.01). Transient overexpression of miR-338-3p by transfecting with miR-338-3p mimic significantly suppressed NSCLC cell proliferation, migration, invasion and induced apoptosis and cell cycle at G1 phase. Additionally, insulin receptor substrate 2 (IRS2), a known oncogene, was identified as a potential target gene of miR-338-3p. Subsequent investigations found a negative correlation between the expression of miR-338-3p and IRS2 in NSCLC tissues. Furthermore, overexpression of IRS2 reversed the effects of miR-338-3p in NSCLC cells on cell proliferation, cycle, apoptosis, migration, invasion. These findings suggested that miR-338-3p might act as a tumor suppressor by directly targeting IRS2 in NSCLC. 

Retracted: No

PubPeer comments:
 Figs 5B, 5F. ![file] See e.g. Figs 3C, 4D, 5A, 6D from [Pang et al (2015)] . A few of the other manifestations of these versatile loading controls are linked in that thread. ![] , 
 *[left]* Fig 2D. Cell  apoptosis ... determined in A549 cells after transfection of miR-338-3p or miR-NC . *[right]* Fig 3B from [Wang et al (2017)] .  Cell apoptosis was determined in SKOV3 cells transfected with siu2011AQP1 or siu2011NC by flow cytometry . ![file] Could the authors of either paper comment on the appearance of the same FACS plot in both? , 
 Corrected [15 August 2021] .  In this article, we found that the protein bland of Figure 5B and 5F had some mistake in this paper due to misuse upload. In addition, Figure 2D also has flaw due to cell contaminated during experiments. Thus, we provide corrected Figure 2 and Figure 5. The authors have confirmed that the errors associated with this figure did not have any significant impact on either the results or the conclusions reported in this study. All the authors on this paper wish to correct this paper, and are grateful to the Editor of Am J Cancer Res for allowing them the opportunity to publish this Corrigendum. Furthermore, we apologize to the readership of the Journal for any inconvenience caused. Fig 2: ![] Fig 5: ![] ,
Luteolin-mediated Kv1.3 K+ channel inhibition augments BCG vaccine efficacy against tuberculosis by promoting central memory T cell responses in mice
Authors: Shashi Prakash Singh
Gobardhan Das
Anjna Kumari
Dhiraj Kumar Singh
Saurabh Kumar Sharma
Anand Ranganathan
Ved Prakash Dwivedi
Luc Van Kaer
Journal: PLoS Pathogens (2020)
Discipline: MICROBIOLOGY
Keywords: Tuberculosis; Vaccine efficacy; Memory T cells; Kv1.3 K+ ion channel; Luteolin
Affiliations: Special Centre for Molecular Medicine (SCMM), Jawaharlal Nehru University, New Delhi, India., International Centre for Genetic Engineering and Biotechnology, New Delhi, India., Southwest National Primate Research Center, Texas Biomedical Research Institute, San Antonio, Texas, United States of America., School of Computer & Systems Sciences, Jawaharlal Nehru University, New Delhi, India., Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, United States of America.

Abstract:  Despite the availability of multiple antibiotics, tuberculosis (TB) remains a major health problem worldwide, with one third of the population latently infected and ~2 million deaths annually. The only available vaccine for TB, Bacillus Calmette Guérin (BCG), is ineffective against adult pulmonary TB. Therefore, alternate strategies that enhance vaccine efficacy are urgently needed. Vaccine efficacy and long-term immune memory are critically dependent on central memory T (TCM) cells, whereas effector memory T (TEM) cells are important for clearing acute infections. Recently, it has been shown that inhibition of the Kv1.3 K+ ion channel, which is predominantly expressed on TEM but not TCM cells, profoundly enhances TCM cell differentiation. We exploited this phenomenon to improve TCM:TEM cell ratios and protective immunity against Mycobacterium tuberculosis infection in response to BCG vaccination of mice. We demonstrate that luteolin, a plant-derived Kv1.3 K+ channel inhibitor, profoundly promotes TCM cells by selectively inhibiting TEM cells, and significantly enhances BCG vaccine efficacy. Thus, addition of luteolin to BCG vaccination may provide a sustainable means to improve vaccine efficacy by boosting host immunity via modulation of memory T cell differentiation. 

Retracted: No

PubPeer comments:
 In Figure 6c, a micrograph has been duplicated and presented as something else. ![file] , 
 #1 Please refer to the new version for your query. , 
 There are only two versions on the journal site. Version 1 is the uncorrected copy. Version 2 is the current copy. Version 2 still has the possibly duplicated image. ![file] , 
 An author correction has been posted regarding this issue. https: journals.plos.org plospathogens article?id=10.1371 journal.ppat.1009896 ,
Naringenin inhibits osteoclastogenesis through modulation of helper T cells‐secreted IL‐4
Authors: Chen Xu
Mingjun Li
Mingkui Shen
Genzhong Xu
Ming Luo
Wengang Wang
Yaokun Chen
Lei Xia
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: IL-4; RANKL; T cells; naringenin; osteoclast.
Affiliations: Department of OrthopaedicsThe First Affiliated Hospital of Zhengzhou UniversityZhengzhouHenanP.R. China, Department of OncologyThe First Affiliated Hospital of Zhengzhou UniversityZhengzhouHenanP.R. China

Abstract:  Naringenin (NAR) is a natural predominant flavanone and has a wide range of pharmacological activities. The aim of this study was to investigate the protective mechanisms of NAR on RANKL-induced osteoclastogenesis and osteoclast bone resorption. T cells were divided into four groups under different concentrations of NAR (0, 25, 50, 100 µM). CD4+ T cell subsets in different groups were evaluated by flow cytometry. TRAP staining, pit formation assays and F-actin ring immunofluorescent staining were performed. In addition, gene expression of osteoclast-specific markers was analyzed by qPCR and Western blot. Our results showed that compared with the control group, there were relatively fewer Th1 and Th17 cells and more Th2 cells and Treg cells in the NAR groups. Besides, the number of TRAP-positive multinucleated osteoclasts, the areas of bone resorption pits and the size and number of F-actin rings were notably decreased in the bone marrow macrophages (BMMs) treated with T-cell supernatant containing NAR. Moreover, NAR treatment dramatically reduced the expressions of cathepsin K, c-Fos, DC-STAMP, NFATc1, TRAP, and V-ATPase d2 at mRNA and protein levels. However, these effects were abolished by adding a neutralizing antibody against IL-4. In conclusion, NAR suppressed RANKL-induced osteoclastogenesis and osteoclast bone resorption by promoting the release of IL-4 from T cells. 

Retracted: No

PubPeer comments:
 Figure 1. * Some panels appear to share unexpected similarities, as shown with boxes of the same color. ![file] , 
 Figure 2B: * Red boxes: The 0uM and 25uM panels appear to show an overlap. * Green and blue boxes: cells in the 50 uM panel appear to look similar to panels in Figure 4B. ![file] ,
Mechanism of IL‑8‑induced acute lung injury through pulmonary surfactant proteins A and B
Authors: Yinong Yang
Wu Zhu
Feng Tan
Qing Li
Jun Zhang
Journal: Experimental and Therapeutic Medicine (2019)
Discipline: CLINICAL MEDICINE
Keywords: IL-8; acute lung injury; protein-protein interaction; pulmonary surfactant protein A; pulmonary surfactant protein B.
Affiliations: Medical School, Hunan University of Medicine, Huaihua, Hunan 418000, P.R. China, Nursing School, Hunan University of Medicine, Huaihua, Hunan 418000, P.R. China, School of Stomatology, Hunan University of Medicine, Huaihua, Hunan 418000, P.R. China

Abstract:  This study explored how interleukin-8 (IL-8) causes acute lung injury (ALI) through pulmonary surfactant protein A (SP-A) and surfactant protein B (SP-B). Serum was collected from 53 ALI patients and further 56 healthy subjects who underwent physical examination. The IL-8, SP-A, and SP-B levels were determined using enzyme-linked immunosorbent assay (ELISA). An ALI model was constructed using lipopolysaccharide (LSP)-induced normal A549 cells. siRNA was employed to interfere with the expression of IL-8, SP-A and SP-B. Western blot analysis was carried out to determine the protein levels, and MTT assay to determine the cell activity. In addition, co-immunoprecipitation (Co-IP) assay was used to verify the interaction between IL-8, SP-A and SP-B. ALI patients showed high expression of serum IL-8, and low expression of SP-A and SP-B, and IL-8 was negatively correlated with SP-A and SP-B, respectively. LSP-induced normal A549 cells showed increased expression of IL-8 and decreased expression of SP-A and SP-B. Silencing IL-8 led to increased expression levels of SP-A, SP-B and Bcl2, decreased expression levels of caspase-9, caspase-3, Bax, TNF-α, IL-17 and IL-1β, reduced cell apoptosis rate, and enhanced cell viability. Silencing SP-A and SP-B resulted in increased expression of IL-8, caspase-9, caspase-3, Bax, TNF-α, IL-17 and IL-1β, and decreased expression of Bcl2. Co-IP assay revealed that IL-8 could interact with SP-A and SP-B, respectively. IL-8 induces apoptosis by inhibiting SP-A and SP-B, and intensifies cellular inflammatory reaction, leading eventually to ALI. 

Retracted: No

PubPeer comments:
 Figure 6. * Blue boxes: two panels appear to show the same background * The bands appear to hover over the background, and have unnatural shapes Could the authors please show the uncropped blots? ![file] ,
Identification of one critical amino acid that determines a conformational neutralizing epitope in the capsid protein of porcine circovirus type 2
Authors: Chang M Liu
Yue H Lu
Li P Huang
Long J Guo
Yan W Wei
Journal: BMC Microbiology (2011)
Discipline: MICROBIOLOGY
Keywords: Porcine circovirus type 2; PCV2; capsid protein; immunology; monoclonal antibody
Affiliations: Division of Swine Infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, 427 Maduan Street, Nangang District, Harbin, 150001, China.

Abstract:  Background: Porcine circovirus type 2 (PCV2) is associated with post-weaning multisystemic wasting syndrome (PMWS) in pigs. Currently, there is considerable interest in the immunology of PCV2; in particular, the immunological properties of the capsid protein. This protein is involved in PCV2 immunogenicity and is a potential target for vaccine development. In this study, we identified one critical amino acid that determines a conformational neutralizing epitope in the capsid protein of PCV2. Results: One monoclonal antibody (mAb; 8E4), against the capsid protein of PCV2, was generated and characterized in this study. 8E4 reacted with the genotype PCV2a (CL, LG and JF2) strains but not PCV2b (YJ, SH and JF) strains by an immunoperoxidase monolayer assay (IPMA) and a capture ELISA. Furthermore, the mAb had the capacity to neutralize PCV2a (CL, LG and JF2) strains but not PCV2b (YJ, SH and JF) strains. One critical amino acid that determined a conformational neutralizing epitope was identified using mAb 8E4 and PCV2 infectious clone technique. Amino acid residues 47-72 in the capsid protein of PCV2a/CL were replaced with the corresponding region of PCV2b/YJ, and the reactivity of mAb 8E4 was lost. Further experiments demonstrated that one amino acid substitution, the alanine for arginine at position 59 (A59R) in the capsid protein of PCV2a (CL, LG and JF2) strains, inhibited completely the immunoreactivity of three PCV2a strains with mAb 8E4. Conclusions: It is concluded that the alanine at position 59 in the capsid protein of PCV2a (CL, LG and JF2) strains is a critical amino acid, which determines one neutralizing epitope of PCV2a (CL, LG and JF2) strains. This study provides valuable information for further in-depth mapping of the conformational neutralizing epitope, understanding antigenic difference among PCV2 strains, and development of a useful vaccine for control of PCV2-associated disease. 

Retracted: No

PubPeer comments:
 Fig 5c and f show identical image areas ![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. ,
Conversion of vascular endothelial cells into multipotent stem-like cells
Authors: Vitali Y Lounev
Raghu Kalluri
Eileen M Shore
Frederick S Kaplan
Bjorn R Olsen
Damian Medici
Journal: Nature Medicine (2010)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Mesenchymal stem cells; vascular endothelial cells; activin-like kinase-2 (ALK2); fibrodysplasia ossificans progressiva (FOP); heterotopic ossification
Affiliations: Division of Matrix Biology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.

Abstract:  Mesenchymal stem cells can give rise to several cell types, but varying results depending on isolation methods and tissue source have led to controversies about their usefulness in clinical medicine. Here we show that vascular endothelial cells can transform into multipotent stem-like cells by an activin-like kinase-2 (ALK2) receptor-dependent mechanism. In lesions from individuals with fibrodysplasia ossificans progressiva (FOP), a disease in which heterotopic ossification occurs as a result of activating ALK2 mutations, or from transgenic mice expressing constitutively active ALK2, chondrocytes and osteoblasts expressed endothelial markers. Lineage tracing of heterotopic ossification in mice using a Tie2-Cre construct also suggested an endothelial origin of these cell types. Expression of constitutively active ALK2 in endothelial cells caused endothelial-to-mesenchymal transition and acquisition of a stem cell-like phenotype. Similar results were obtained by treatment of untransfected endothelial cells with the ligands transforming growth factor-β2 (TGF-β2) or bone morphogenetic protein-4 (BMP4) in an ALK2-dependent manner. These stem-like cells could be triggered to differentiate into osteoblasts, chondrocytes or adipocytes. We suggest that conversion of endothelial cells to stem-like cells may provide a new approach to tissue engineering. 

Retracted: No

PubPeer comments:
 Nat. Med. 16, 1400u20131406 (2010); published online 21 November 2010; corrected after print 7 April 2011 In the version of this article initially published, the flow cytometry plot in Figure 4b corresponding to the condition HCMEC and TGF-u03b22 was incorrect. This plot has been replaced with the correct one in the HTML and PDF versions of the article. , 
 Supplemental Figure 5. Should the two images marked with magenta appear so similar? Apologies if I am misunderstanding something. *** ![file] , 
 Others on social media agree that there may be other similar issues throughout this paper, but find the presentation confusing. See below. Could the senior author comment? It seems others may have had some concern with the first authoru2019s research in the past. I do not know the veracity of those concerns. https: www.leagle.com decision infdco20190612707 *** ![file] *** ![file] , 
 #3 More on Figure 1C by other readers. ![file] ,
Mycophenolate mofetil and FK506 have different effects on kidney allograft fibrosis in rats that underwent chronic allograft nephropathy
Authors: Zhaolin Sun
Guangheng Luo
Weidong Wu
Lei Luo
Journal: BMC Nephrology (2012)
Discipline: CLINICAL MEDICINE
Keywords: Tacrolimus; Mycophenolatemofetil; renal fibrosis; chronic allograft nephropathy; fibrosis-associated genes
Affiliations: Department of Research and Education, Guizhou Province People's Hospital, Guiyang, China.

Abstract:  Background: Tacrolimus (FK506) is associated with renal fibrosis in long-term use. Mycophenolatemofetil (MMF) can also inhibit or attenuate the progression of renal fibrosis. This study aimed to determine the different effects of FK506 and MMF on fibrosis-associated genes in the kidney in rats that underwent chronic allograft nephropathy (CAN). Methods: Fisher (F344) kidneys were orthotopically transplanted into Lewis rat recipients. All recipients were given Cyclosporin A (CsA) 10 mg/kg-1.d-1 × 10 day and were then randomly divided into three oral treatment groups (n = 9 in each group): (1) the vehicle group was given vehicle orally; (2) the FK506 group was given 0.15 mg/kg-1.d-1 FK506; and (3) the MMF group was given 20 mg/kg-1.d-1 MMF. At 4, 8, and 12 weeks post-transplantation, serum creatinine (SCr), collagen deposition, Connective tissue growth factor (CTGF), alpha smooth muscle actin (α-SMA) and E-cadherin expressions were determined and hematoxylin-eosin (HE) and Periodic acid-Schiff (PAS) stains were performed. Results: Renal function progressively deteriorated and showed typical CAN morphology in the vehicle and FK506 groups, while SCr and inflammatory infiltration (Banff score) showed a significant decrease in the MMF group after 8 weeks post-transplantation compared with those in the other groups (p &lt; 0.05). Furthermore, expression levels of CTGF and α-SMA in the MMF group were significantly reduced, and the down-regulated expression of E-cadherin was abated (p &lt; 0.05). Conclusions: MMF showed favorable effects on renal interstitial fibrosis, thus efficiently retarding the progression of CAN. 

Retracted: No

PubPeer comments:
 The authors proposed a new notion for decision making in Definition 5, called **picture fuzzy linguistic sets** and proposed some operations in Definition 6 with some illustrations in Example 1 and Example 2. However, some operations defined are not legitimate. For example, let $$pl_1 = (s, 0,1,0)$$ $$pl_2 = (s, 0,0,1)$$ Then, according to eq.(15) and eq.(19), the linguistic term is not well defined and the picture fuzzy term is $$(0, 1,1)$$ This means that the operation $$pl_1 otimes pl_2$$ is not well defined. A decision making method based on such operations are not sound. Can the authors kindly address these issues? ![file] ![file] ![file] ,
Expression of FLR1 transporter requires phospholipase C and is repressed by Mediator
Authors: Nicholas DeLillo
Ales Vancura
Parima Desai
Carlos Romero
Journal: Journal of Biological Chemistry (2006)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Phosphoinositide-specific phospholipase C; PLC1 gene; kinetochores; benomyl sensitivity; chromatin structure
Affiliations: Department of Biological Sciences, St. John's University, 8000 Utopia Parkway, Queens, NY 11439, USA.

Abstract:  In budding yeast, phosphoinositide-specific phospholipase C (Plc1p encoded by PLC1 gene) is important for function of kinetochores. Deletion of PLC1 results in benomyl sensitivity, alterations in chromatin structure of centromeres, mitotic delay, and a higher frequency of chromosome loss. Here we intended to utilize benomyl sensitivity as a phenotype that would allow us to identify genes that are important for kinetochore function and are downstream of Plc1p. However, our screen identified SIN4, encoding a component of the Mediator complex of RNA polymerase II. Deletion of SIN4 gene (sin4Delta) does not suppress benomyl sensitivity of plc1Delta cells by improving the function of kinetochores. Instead, benomyl sensitivity of plc1Delta cells is caused by a defect in expression of FLR1, and the suppression of benomyl sensitivity in plc1Delta sin4Delta cells occurs by derepression of FLR1 transcription. FLR1 encodes a plasma membrane transporter that mediates resistance to benomyl. Several other mutations in the Mediator complex also result in significant derepression of FLR1 and greatly increased resistance to benomyl. Thus, benomyl sensitivity is not a phenotype exclusively associated with mitotic spindle defect. These results demonstrate that in addition to promoter-specific transcription factors that are components of the pleiotropic drug resistance network, expression of the membrane transporters can be regulated by Plc1p, a component of a signal transduction pathway, and by Mediator, a general transcription factor. The results thus suggest another layer of complexity in regulation of pleiotropic drug resistance. 

Retracted: No

PubPeer comments:
 ![file] In Figure 3B, ACT1 panel, lanes 1 and 2 appear to share unexpected similarities to lanes 3 and 4. There is one visible vertical transition in the ACT1 panel in Figure 2A. Could authors provide an explanation, please? , 
 ![file] In Figure 4 I found duplicated spot dilution images in the 0 and 20 ug mL benomyl plates. ,
Synthesis and biological evaluation of hybrids from farnesylthiosalicylic acid and hydroxylcinnamic acid with dual inhibitory activities of Ras-related signaling and phosphorylated NF-κB
Authors: Ying Zhao
Zhiqiang Wang
Xuemin Wang
Wei Zhang
Yong Ling
Li Chen
Yihua Zhang
Zhangjian Huang
Xinyang Wang
Journal: Organic & Biomolecular Chemistry (2014)
Discipline: CHEMISTRY
Keywords: Hybrids; Antiproliferative activity; Cancer cell lines; Apoptosis; Ras-related signaling
Affiliations: School of Pharmacy, Nantong University, Nantong, 226001, PR China.

Abstract:  A series of hybrids (5a–r) of farnesylthiosalicylic acid (FTS) and hydroxylcinnamic acid were designed and synthesized. Most of the hybrids displayed potent antiproliferative activity against seven cancer cell lines in vitro, superior to FTS as well as sorafenib. The most potent compound 5f selectively inhibited cancer cells but not non-tumor liver cell proliferation in vitro, and significantly induced SMMC-7721 cell apoptosis. Interestingly, 5f could simultaneously inhibit not only Ras-related signaling but also phosphorylated NF-κB, which may synergetically contribute to the cell growth inhibition and apoptosis induction. Moreover, 5f showed low acute toxicity to mice and significantly inhibited the hepatoma tumor growth. 

Retracted: No

PubPeer comments:
 A western blot has been duplicated (Figure 5; Actin vs Figure 6; Akt). ![file] ,
Mammalian target of rapamycin complex 1 (mTORC1) enhances bortezomib-induced death in tuberous sclerosis complex (TSC)-null cells by a c-MYC-dependent induction of the unfolded protein response
Authors: Hoa B Nguyen
Jeremiah W Hendricks
Lawrence A Quilliam
Justin T Babcock
Yujun He
Ronald C Wek
Journal: Journal of Biological Chemistry (2013)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: ATF4; Apoptosis; Bortezomib; Myc; Rapamycin
Affiliations: Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana 46202,, USA.

Abstract:  Many factors, including duration and intensity of the unfolded protein response (UPR), dictate whether cells will adapt to endoplasmic reticulum stress or undergo apoptosis. In tuberous sclerosis (TSC), elevation of mammalian target of rapamycin complex 1 (mTORC1) activity has been proposed to compound the induction of UPR transcription factors ATF4 and CHOP, suggesting that the UPR could be targeted to eradicate TSC1/2-null cells during patient therapy. Here we report that control of c-MYC translation by mTORC1 plays a key role in determining whether TSC2-null Elt3 rat leiomyoma cells apoptose in response to UPR induction by the proteasome inhibitor bortezomib. Although bortezomib induces eukaryotic initiating factor 2α phosphorylation, mTORC1 activity was also required for downstream induction of the UPR transcription factors ATF4 and CHOP by a mechanism involving increased expression of c-MYC. Although bortezomib-induced c-MYC transcription was resistant to rapamycin treatment, mTORC1 activity was required for efficient c-MYC translation. c-MYC subsequently bound to the ATF4 promoter, suggesting direct involvement of an mTORC1/c-MYC-driven signaling pathway in the activation of the UPR. Consistent with this notion, exogenously expressed c-MYC reversed the ability of rapamycin to prevent bortezomib-induced CHOP and ATF4 expression as well as apoptosis. These findings indicate that the induction of ATF4/CHOP expression occurs via mTORC1 regulation of c-MYC and that this signaling pathway is a major determinant in the ability of bortezomib to induce apoptosis. 

Retracted: No

PubPeer comments:
 Figure 8C u2013 more similar than expected ![file] ,
Comparison of botulinum toxin type A and aprotinin monotherapy with combination therapy in healing of burn wounds in an animal model
Authors: Ahmad Oryan
Esmat Alemzadeh
Journal: Molecular biology reports (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Aprotinin; Basic fibroblast growth factor; Botulinum toxin type A; Burn wound; Histopathology
Affiliations: Department of Pathology, School of Veterinary Medicine, Shiraz University, Shiraz, Iran. ., Department of Biotechnology, School of Veterinary Medicine, Shiraz University, Shiraz, Iran.

Abstract:  Burns are one of the most common injuries that are complicated by many challenges including infection, severe inflammatory response, excessive expression of proteases, and scar formation. The aim of this study was to investigate the effect of botulinum toxin type A (BO) and aprotinin (AP) separately or in combination (BO-AP) in healing process. Four burn wounds were created in each rat and randomly filled with silver sulfadiazine (SSD), BO, AP and BO-AP. The rats were euthanized after 7, 14, and 28 days, and their harvested wound samples were evaluated by gross pathology, histopathology, gene expression, biochemical testing, and scanning electron microscopy. Both BO and AP significantly reduced expression of interleukin-1β (IL-1β) and transforming growth factor-β1 (TGF-β1) at the 7th post wounding day. Moreover, they inhibited scar formation by reducing the TGF-β1 level and increasing basic fibroblast growth factor (bFGF) at the 28th day. AP by decreasing protease production showed more effective role than BO in wound regeneration. AP increased tissue organization and maturation and improved cosmetic appearance of wounds, at 28 days. The best results gained when combination of BO and AP were used in healing of burn wounds. Treatment by BO-AP significantly subsided inflammation compared to the BO, AP, and SSD treated wounds. Treatment with BO-AP also reduced collagen density and led to minimal scar formation. Combination of botulinum toxin type A and aprotinin considerably increased structural and functional properties of the healing wounds by reducing scar formation and decreasing production of proteases. 

Retracted: No

PubPeer comments:
 Figure 3 appears to have a repeated image. *** ![file] , 
 Two images in Figure 1 appear unexpectedly similar to images in Figure 3 of 10.1007 s00441-019-03015-9 (Cell and Tissue Research 2019), but seem to be described differently. Could the authors please comment? *** Figure 1 Molecular Biology Reports (2020) ![file] *** Figure 3 Cell and Tissue Research (2019) ![file] ,
Impaired in vivo binding of MeCP2 to chromatin in the absence of its DNA methyl-binding domain
Authors: David P Stuss
Juan Ausió
Manel Esteller
Alexia Martinez de Paz
Joel D Cosman
David McPhee
Marlee K Ng
Brad Williamson
Michael Hendzel
Manjinder Cheema
Kristal Missiaen
Kerry Delaney
Journal: Nucleic Acids Research (2013)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: MeCP2; chromatin association; MBD; Rett syndrome; mutant mice
Affiliations: Department of Biology, University of Victoria, British Columbia, V8W 2Y2, Canada.

Abstract:  MeCP2 is a methyl-CpG-binding protein that is a main component of brain chromatin in vertebrates. In vitro studies have determined that in addition to its specific methyl-CpG-binding domain (MBD) MeCP2 also has several chromatin association domains. However, the specific interactions of MeCP2 with methylated or non-methylated chromatin regions and the structural characteristics of the resulting DNA associations in vivo remain poorly understood. We analysed the role of the MBD in MeCP2-chromatin associations in vivo using an MeCP2 mutant Rett syndrome mouse model (Mecp2(tm1.1Jae)) in which exon 3 deletion results in an N-terminal truncation of the protein, including most of the MBD. Our results show that in mutant mice, the truncated form of MeCP2 (ΔMeCP2) is expressed in different regions of the brain and liver, albeit at 50% of its wild-type (wt) counterpart. In contrast to the punctate nuclear distribution characteristic of wt MeCP2, ΔMeCP2 exhibits both diffuse nuclear localization and a substantial retention in the cytoplasm, suggesting a dysfunction of nuclear transport. In mutant brain tissue, neuronal nuclei are smaller, and ΔMeCP2 chromatin is digested faster by nucleases, producing a characteristic nuclease-resistant dinucleosome. Although a fraction of ΔMeCP2 is found associated with nucleosomes, its interaction with chromatin is transient and weak. Thus, our results unequivocally demonstrate that in vivo the MBD of MeCP2 together with its adjacent region in the N-terminal domain are critical for the proper interaction of the protein with chromatin, which cannot be replaced by any other of its protein domains. 

Retracted: No

PubPeer comments:
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 08 March 2022 correction. https: academic.oup.com nar advance-article doi 10.1093 nar gkac169 6544631 Figure 2, Figure 5A and 5C show multiple signs of splicing. Different lanes of gels were brought together to make final figures. The splicing was done for cosmetic reason, without intent to deceive, and is visible to the naked eye. New figures are provided below. These corrections do not affect the interpretation of the results and conclusions of the article. ,
Pyrene Based Fluorescent Turn-on Chemosensor for Sequential Detection of Fe3+ and Fe2+ Ions and its Application in Live Cell Imaging
Authors: Asaithambi Gomathi
Rajasekaran Dhivya
Periasamy Viswanathamurthi
Journal: Journal of Fluorescence (2019)
Discipline: CHEMISTRY
Keywords: Cell imaging; Fluorescence probe; Iron ions; Schiff base.
Affiliations: Department of Chemistry, Periyar University, Salem, 636 011, India., Department of Chemistry, Periyar University, Salem, 636 011, India. .

Abstract:  A simple pyrene-based "turn-on" chemosensor bearing isonizide namely 3-(pyren-1-yl methylene) pentane-2,4-diyldene di(isonicotinohydrazide) (PMPD) was designed and synthesized for detecting Fe3+and Fe2+ ions in HEPES buffer solution at pH 7.4 (DMSO: H2O (1:9 v/v)) medium. The probe shows conducive selectivity for Fe2+ and Fe3+ ions over the other competitive metal cations. The detection limit was found to be 1.67 μM for Fe3+ and 2.02 μM for Fe2+. The recognition mechanism of PMPD towards Fe3+ and Fe2+ has been examined in detail by absorption, emission, and ESI-MS studies. Moreover, "turn-on" fluorescence behavior of the probe was used to track iron ions in living cells. 

Retracted: No

PubPeer comments:
 I think there is more cause for concern with Figure 5, where three of the NMR signals are the same over much of the range. ![file] ,
Single-walled carbon nanotube supported Pt-Ru bimetallic superb nanocatalyst for the hydrogen generation from the methanolysis of methylamine-borane at mild conditions
Authors: Esra Kuyuldar
Yasar Karatas
Mehmet Gulcan
Eda Gokirmak Sogut
Hilal Acidereli
Fatih Sen
Journal: Scientific Reports (2019)
Discipline: Multidisciplinary
Keywords: metal nanoparticle; catalyst; hydrogen production; methylamine-borane; methanolysis
Affiliations: Chemistry Department, Faculty of Science, Van Yüzüncü Yıl University, Zeve Campus, 65080, Van, Turkey., Sen Research Group, Biochemistry Department, Faculty of Arts and Science, Dumlupınar University, Evliya Çelebi Campus, 43100, Kütahya, Turkey., Chemistry Department, Faculty of Science, Van Yüzüncü Yıl University, Zeve Campus, 65080, Van, Turkey. ., Sen Research Group, Biochemistry Department, Faculty of Arts and Science, Dumlupınar University, Evliya Çelebi Campus, 43100, Kütahya, Turkey. .

Abstract:  Several metal nanoparticle based catalysts have been synthesized for catalyzing the hydrogen production process by hydrolysis of methylamine-borane (MeAB). However, there was only one study that catalyzes the producing of hydrogen via the methanolysis of MeAB, and it was carried out by our research group. For this reason, in this work, a new catalyst system entitled by single-walled carbon nanotube (SWCNT) supported bimetallic platinum-ruthenium nanoparticles were developed and called as PtRu@SWCNT. These NPs were characterized by several techniques (XRD, XPS, Raman, and TEM), and they were performed for the methanolysis of MeAB with high catalytic activity. The prepared PtRu@SWCNT NPs were also tested in the methanolysis of MeAB at different parameters including different temperatures, catalyst and substrate concentrations, and reusability performance. Experimental results revealed that the new PtRu@SWCNT NPs had excellent catalytic activity and reusability for removing of hydrogen from the methanolysis of MeAB at ambient conditions. According to the obtained data, the turnover frequency is 136.25 mole H2/mole PtRu × min, and the activation energy (Ea) is 17.29 kJ/mole. More than 99% of conversion was observed at room temperature. 

Retracted: No

PubPeer comments:
 Figure 2. XRD analysis of Pt@SWCNT and PtRu@SWCNT nanocatalysts. Some parts of XRD patterns are unexpectedly similar. Intensity of major peaks are different. ![file] , 
 Thanks for your interest. I have asked original files, if related person does not give a original files, then I will apply for correction. I am so sorry for the case. Thanks again... , 
 Under closer look the XRD pattern shows some similar fragments: ![file] ,
PRSS8 suppresses colorectal carcinogenesis and metastasis
Authors: Ming Yuan
Yongmeng Zhang
Yiqiong Yang
Yonghua Bao
Xiaonan Wei
Dongli Guo
Wei Zhang
Wancai Yang
Yongchen Guo
Xiangdong Zhu
Virgilia Macias
Shanshan Zhang
Kai Li
Journal: Oncogene (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: PRSS8; cancer initiation; cancer progression; conditional knockout; mouse model
Affiliations: Department of Pathology and Institute of Precision Medicine, Jining Medical University, Jining, 272067, China., Department of Pathology, Xinxiang Medical University, Xinxiang, 453003, China., Department of Gastrointestinal Surgery, Affiliated Hospital, Jining Medical University, Jining, 272067, China., Department of Pathology, University of Illinois, Chicago, IL, 60612, USA., Department of Emergency Medicine, University of Illinois, Chicago, IL, 60612, USA., Department of Preventive Medicine, Northwestern University, Chicago, IL, 60611, USA., Department of Pathology and Institute of Precision Medicine, Jining Medical University, Jining, 272067, China. ., Department of Pathology, University of Illinois, Chicago, IL, 60612, USA. .

Abstract:  The serine protease PRSS8 has shown important physiological and pathological functions, but its roles in cancer initiation and progression are unclear. We developed and dynamically characterized a conditional knockout Prss8fl/fl, p-Villin-Cre+ mouse model. We found that genetic deficiency of the Prss8 gene caused spontaneous colitis and an inflamed rectum at an early age and caused intestinal tumors at a late age, which were linked to increased intestinal cell proliferation and migration but decreased cell differentiation. Increased PRSS8 expression inhibited cancer cell growth and metastasis in nude mice and inhibited cancer cell migration, invasion, colony formation and tumor sphere formation in vitro, but decreased PRSS8 expression facilitated malignancies in vivo and in vitro. Gene profiling on manipulated cancer cells and intestinal epithelial cells of Prss8 mouse models, gene set enrichment analysis and mechanistic studies revealed that PRSS8 targeted the Wnt/β-catenin, epithelial-mesenchymal transition, and stem cell signaling pathways, which were further supported by the results from the TCGA data mining and validated by immunohistochemical staining on colorectal cancer tissue microarrays. In conclusion, PRSS8 is a novel tumor suppressor that plays critical roles in the suppression of colorectal carcinogenesis and metastasis. 

Retracted: No

PubPeer comments:
 Figure 1E and 1I u2013 In blue, more similar than expected ![file] ,
Inhibition of microRNA-21-3p suppresses proliferation as well as invasion and induces apoptosis by targeting RNA-binding protein with multiple splicing through Smad4/extra cellular signal-regulated protein kinase signalling pathway in human colorectal cancer HCT116 cells
Authors: Guiqing Jia
Gaoping Zhao
Xiaogang Shen
Bin Luo
Yifeng Bai
Nengyi Hou
Zhiyi Guo
Journal: Clinical and Experimental Pharmacology and Physiology (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: RNA-binding protein with multiple splicing; SMAD family member 4; colorectal cancer; extra cellular signal-regulated protein kinase; microRNA-21-3p.
Affiliations: Departments of Gastrointestinal Surgery, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu, China., Departments of Oncology, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu, China.

Abstract:  MicroRNA-21-3p (miR-21-3p), the passenger strand of pre-mir-21, has been found to be high-expressing in various cancers and to be associated with tumour malignancy, which is proposed as a novel focus in malignant tumours. Colorectal cancer (CRC), currently known as one of the most prevalent malignancy, is a leading cause of cancer death. This study aimed to investigate the key role of miR-21-3p in CRC by inhibiting its expression using transfection with miR-21-3p inhibitors into human CRC HCT116 cells. Results showed that the expression of miR-21-3p was higher than other CRC cells used in the study including Lovo, HT29, Colo320 and SW480 cells, inhibition of which suppressed the proliferation and induced cell cycle arrest in HCT116 cells. Besides, transfection with miR-21-3p inhibitors also attenuated cell migration and invasion, and induced apoptosis as well. Moreover, luciferase assay confirmed RBPMS as a direct target of miR-21-3p in HCT116 cells. Further, miR-21-3p inhibitors increased the nuclear accumulation of Smad4 and reduced phosphorylation of ERK. Interestingly, we found that silence of RBPMS using RNA interference (siRNA) not only elevated the cell viability but also increased the phosphorylation of ERK and reversed the nuclear accumulation of Smad4 induced by miR-21-3p inhibitors in HCT116 cells. Data suggest that inhibition of miR-21-3p suppresses cell proliferation, invasion as well as migration and induces apoptosis by directly targeting RBPMS through Smad4/ERK signalling pathway in HCT116 cells. Our study demonstrates miR-21-3p as a potent target for suppressing tumour progression of CRC which may have implications in CRC therapy in the future. 

Retracted: No

PubPeer comments:
 Figure 3 has what appears to be a duplicated element. I also annotated some similar elements. ![file] , 
 More duplicated element ![file] ,
Pyk2 activates the NLRP3 inflammasome by directly phosphorylating ASC and contributes to inflammasome-dependent peritonitis
Authors: Hsin-Pai Li
Yu-Sun Chang
I-Che Chung
Yu-Jen Chen
Ching-Liang Chu
Lih-Chyang Chen
Hui-Ru Shieh
Jau-Song Yu
David M Ojcius
Chun-Nan OuYang
Jeng-Ting Chen
Sheng-Ning Yuan
Journal: Scientific Reports (2016)
Discipline: Multidisciplinary
Keywords: ASC; inflammasome; FAK; Pyk2; NLRP3
Affiliations: Molecular Medicine Research Center, Chang Gung University, 333 Taoyuan, Taiwan., Department of Microbiology and Immunology, Chang Gung University, 333 Taoyuan, Taiwan., Graduate Institute of Biomedical Sciences, Chang Gung University, 333 Taoyuan, Taiwan., Division of Hematology-Oncology, Chang Gung Memorial Hospital at Lin-Kuo, 333 Taoyuan, Taiwan., Department of Medical Research Mackay Memorial Hospital, 251 New Taipei City, Taiwan., Department of Radiation Oncology, Mackay Memorial Hospital, 251 New Taipei City, Taiwan., Department of Biomedical Sciences, University of the Pacific Arthur A. Dugoni School of Dentistry, San Francisco, CA 94103, USA., Graduate Institute of Immunology, College of Medicine, National Taiwan University, 100 Taipei, Taiwan., Proteomics Core Laboratory, Chang Gung University, 333 Taoyuan, Taiwan., Liver Research Center, Chang Gung Memorial Hospital at Lin-Kou, 333 Taoyuan, Taiwan., Department of Otolaryngology, Chang Gung Memorial Hospital at Lin-Kuo, 333 Taoyuan, Taiwan., Department of Medicine, Mackay Medical College, 252 New Taipei City, Taiwan.

Abstract:  The inflammasome adaptor protein, ASC, contributes to both innate immune responses and inflammatory diseases via self-oligomerization, which leads to the activation of the protease, caspase-1. Here, we report that the cytosolic tyrosine kinases, FAK and Pyk2, are differentially involved in NLRP3 and AIM2 inflammasome activation. The inhibition of FAK and Pyk2 with RNA interference or chemical inhibitors dramatically abolished ASC oligomerization, caspase-1 activation, and IL-1β secretion in response to NLRP3 or AIM2 stimulation. Pyk2 is phosphorylated by the kinase Syk and relocalizes to the ASC specks upon NLRP3 inflammasome activation. Pyk2, but not FAK, could directly phosphorylate ASC at Tyr146, and only the phosphorylated ASC could participate in speck formation and trigger IL-1β secretion. Moreover, the clinical-trial-tested Pyk2/FAK dual inhibitor PF-562271 reduced monosodium urate-mediated peritonitis, a disease model used for studying the consequences of NLRP3 activation. Our results suggest that although Pyk2 and FAK are involved in inflammasome activation, only Pyk2 directly phosphorylates ASC and brings ASC into an oligomerization-competent state by allowing Tyr146 phosphorylation to participate ASC speck formation and subsequent NLRP3 inflammation. 

Retracted: No

PubPeer comments:
 Figure 3C. Two panels are very similar despite different treatment in one column. ![file] Zoom in: ![file] ,
The interaction between self – assembling peptides and emodin and the controlled release of emodin from in-situ hydrogel
Authors: Wenbin Du
Fushan Tang
Hong Song
Hongfang Li
Yanfei Liu
Cui Meng
Yuhe Wang
Weipeng Wei
Yongsheng Huang
Journal: Artificial Cells Nanomedicine and Biotechnology (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: hydrogel; Self-assembling peptide; drug delivery; emodin; suspension.
Affiliations: Department of Clinical Pharmacy, School of Pharmacy, Zunyi Medical University, Zunyi, China;, Pharmacy Department, Affiliated Hospital of Zunyi Medical University, Zunyi, China;, Peking Union Medical College, Chinese Academy of Medical Sciences, Institute of Basic Medical Sciences, Beijing, China;, State Key Laboratory of Microbial Resources, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China;, Key Laboratory of Cell Engineering of Guizhou Province, Affiliated Hospital of Zunyi Medical University, Zunyi, China;, College of Basic Medicine, Zunyi Medical University, Zunyi, China

Abstract:  Ion-complementary self-assembling peptides have potential in delivering hydrophobic drugs. This study involved two self-assembling peptides, RADA16-I and RVDV16-I, of which RVDV16-I was a novel self-assembling peptide with different hydrophobic side chains designed from RADA16-I. The purpose of this study was to observe the interaction between different self-assembling peptides and emodin through fluorescence spectrophotometry, CD, SEM and AFM; to construct a preliminary suspension in-situ hydrogel delivery system for emodin with the self-assembling peptides; and to investigate the drug-loading and drug-releasing properties of the self-assembling peptides on emodin. The results showed that both peptides can interact with emodin and the interaction was dominated by hydrophobic interaction. The aqueous solutions of both self-assembling peptides can form relatively stable suspensions with emodin under mechanical stirring, and the suspension can form in-situ hydrogel under physiological condition. In vitro release of emodin from the hydrogels showed a manner of sustained release to some extent. Cell viability studies showed inherent proliferation inhibiting effects of emodin on tumor cells was maintained or enhanced through the in-situ hydrogels. The self-assembling peptides RADA16-I and RVDV16-I had showed promising drug-loading and drug-releasing performance for hydrophobic drugs. It is reasonable to exploit self-assembling peptides as drug carriers for their great potential to improve delivery of hydrophobic drugs. 

Retracted: No

PubPeer comments:
 In Figure 17 (!) two micrographs have been duplicated and presented as something else. ![file] ,