PReD-Bench/PRed-Bench huggingface dataset:
Functional interaction of the Ess1 prolyl isomerase with components of the RNA polymerase II initiation and termination machineries
Authors: Shankarling Krishnamurthy
Mohamed A Ghazy
Michael Hampsey
Claire Moore
Journal: Molecular and Cellular Biology (2009)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: RNA polymerase II; C-terminal domain; transcription cycle; phosphorylation; prolyl isomerase
Affiliations: Department of Biochemistry, Division of Nucleic Acids Enzymology, Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA., Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts 02111, Department of Biochemistry, Division of Nucleic Acids Enzymology, Robert Wood Johnson Medical School, 683 Hoes Lane, Piscataway, New Jersey 08854

Abstract:  The C-terminal domain (CTD) of the largest subunit of RNA polymerase II (Pol II) is a reiterated heptad sequence (Tyr1-Ser2-Pro3-Thr4-Ser5-Pro6-Ser7) that plays a key role in the transcription cycle, coordinating the exchange of transcription and RNA processing factors. The structure of the CTD is flexible and undergoes conformational changes in response to serine phosphorylation and proline isomerization. Here we report that the Ess1 peptidyl prolyl isomerase functionally interacts with the transcription initiation factor TFIIB and with the Ssu72 CTD phosphatase and Pta1 components of the CPF 3'-end processing complex. The ess1(A144T) and ess1(H164R) mutants, initially described by Hanes and coworkers (Yeast 5:55-72, 1989), accumulate the pSer5 phosphorylated form of Pol II; confer phosphate, galactose, and inositol auxotrophies; and fail to activate PHO5, GAL10, and INO1 reporter genes. These mutants are also defective for transcription termination, but in vitro experiments indicate that this defect is not caused by altering the processing efficiency of the cleavage/polyadenylation machinery. Consistent with a role in initiation and termination, Ess1 associates with the promoter and terminator regions of the PMA1 and PHO5 genes. We propose that Ess1 facilitates pSer5-Pro6 dephosphorylation by generating the CTD structural conformation recognized by the Ssu72 phosphatase and that pSer5 dephosphorylation affects both early and late stages of the transcription cycle. 

Retracted: No

PubPeer comments:
 Figure 1A. * Red boxes: Two panels in the 30C column appear to look very similar. ![file] Figure 5. * Green circles: The two plates look remarkably similar, but there is no mentioning of replica plating. ![file] Figure 7E. * Blue boxes: The two bottom Rpb3 panels look more similar than expected. ![file] These three issues were reported to the journal in September 2016. No action was taken. This paper was part of a structured search for image duplications in Molecular and Cellular Biology paper, which was published here: https: mcb.asm.org content 38 20 e00309-18.long ,
Knockdown of LINC00657 inhibits ox-LDL-induced endothelial cell injury by regulating miR-30c-5p/Wnt7b/β-catenin
Authors: Tingting Liu
Hong Hou
Haojie Wu
Journal: Molecular and Cellular Biochemistry (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Atherosclerosis; HUVEC; LINC00657; Ox-LDL; Wnt7b/β-catenin
Affiliations: Department of Cardiology, Xi'an No. 1 Hospital, Xi'an, Shaanxi, China., Department of Respiratory Medicine, The Second Medical Center of PLA General Hospital, Beijing, China., Department of Cardiology, Xi'an No. 3 Hospital, No. 10, East Section of Fengcheng Third Road, Weiyang District, Xi'an, 710000, Shaanxi, China. ., Department of Cardiology, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277, West Yanta Road, Xi'an, 710000, Shaanxi, China. .

Abstract:  Long noncoding RNAs (lncRNAs) play pivotal roles in the pathogenesis, development, and treatment of atherosclerosis (AS). The endothelial cell injury is a feature of AS. However, the role and mechanism of lncRNA LINC00657 in oxidized low-density lipoprotein (ox-LDL)-induced endothelial cell injury remain unclear. The serum samples were collected from 32 AS patients and normal volunteers. Ox-LDL-treated human umbilical vein endothelial cells (HUVEC) were used for the experiments in vitro. The levels of LINC00657, microRNA (miR)-30c-5p and Wnt family member 7B (Wnt7b) were measured by quantitative real-time polymerase chain reaction or western blot. The expression levels of proteins in Wnt7b/β-catenin pathway or endothelial-mesenchymal transition (EndMT) were detected by western blot. The secretion of inflammatory cytokine was examined by enzyme linked immunosorbent assay (ELISA). Cell viability and apoptosis were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide, flow cytometry, and western blot. The target association of miR-30c-5p and LINC00657/Wnt7b was analyzed via dual-luciferase reporter assay and RNA pull-down assay. LINC00657 expression was increased in AS serum and ox-LDL-treated HUVEC cells. LINC00657 knockdown suppressed ox-LDL-induced Wnt7b/β-catenin activation, EndMT, inflammatory response, and apoptosis in HUVEC cells. MiR-30c-5p was bound to LINC00657 and it knockdown reversed the role of LINC00657 inhibition in ox-LDL-induced HUVEC cell injury. MiR-30c-5p targeted Wnt7b to inhibit ox-LDL-induced Wnt7b/β-catenin activation, EndMT, inflammatory response, and apoptosis in HUVEC cells. Silence of LINC00657 repressed ox-LDL-induced injury via inhibiting EndMT, inflammatory response, and apoptosis in HUVEC cells by regulating miR-30c-5p/Wnt7b/β-catenin, indicating a potential target for treatment of AS. 

Retracted: No

PubPeer comments:
 The Western blots in this paper unusually appear to be missing all background noise. Could the authors please post the original uncropped scan of Figure 1D? *** ![file] ,
SOX4 contributes to TGF-β-induced epithelial–mesenchymal transition and stem cell characteristics of gastric cancer cells
Authors: Lang Zha
Hongxia Peng
Anqi Chen
Guangyi Liu
Ziwei Wang
Xudong Peng
Journal: Genes & Diseases (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Epithelial–mesenchymal transition; Gastric cancer; SOX4; Stemness; TGF-β.
Affiliations: Gastrointestinal Surgical Unit, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400000, China., Department of General Surgery, The First People's Hospital, Yibin, Sichuan, 644000 China.

Abstract:  SOX4 is highly expressed in gastric cancer (GC) and is associated with tumor grade, metastasis and prognosis, however the mechanism is not clear. We report herein that SOX4 was upregulated and overexpression of SOX4 was associated with increased expression of the markers of Epithelial-mesenchymal transition (EMT) and stemness in clinic patient samples. In vitro, overexpression of SOX4 promoted the invasion as showed by Transwell assay and stemness of GC cells as assessed by sphere formation assay, which was suppressed by silencing SOX4 with shRNA. Further studies showed that SOX4 up-regulated the expression of EMT transcription factors Twist1, snail1 and zeb1 and stemness transcription factors SOX2 and OCT4, and promoted the nuclear translocation of β-catenin. Moreover, we revealed that TGF-β treatment significantly up-regulated the expression of SOX4 and silencing SOX4 reversed TGF-β induced invasion and sphere formation ability of GC cells. Finally, we showed that SOX4 promoted the lung metastasis and tumor formation ability of gastric cancer cells in nude mice. Our results suggest that SOX4 is a target TGF-β signaling and mediates TGF-β-induced EMT and stem cell characteristics of GC cells, revealing a novel role of TGF-β/SOX4 axis in the regulation of malignant behavior of GC. 

Retracted: No

PubPeer comments:
 Two images in Figure 1A appear to overlap. Color appears differently. *** Closeup (No. 8 left, No. 2 right) ![file] *** Full figure showing location only ![file] , 
 #2 Thank you for your response and for your intent to correct the publication. ,
miR-4454 up-regulated by HPV16 E6/E7 promotes invasion and migration by targeting ABHD2/NUDT21 in cervical cancer
Authors: Zhenzhao Luo
Hui Hu
Jing Wang
Zhongxin Lu
Wangze Wu
Hui Wang
Shuiyi Liu
Man Zhu
Yingle Liu
Journal: Bioscience Reports (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Cervical Cancer; HPV16 E6/E7; NUDT21; miR-4454; α/β-hydrolase domain-containing 2.
Affiliations: Department of Medical Laboratory, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430014, China, Cancer Research Institute of Wuhan, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430014, China, State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, China

Abstract:  The abnormal expression of HPV16 E6/E7 activates oncogenes and/or inactivates tumor suppressor genes, resulting in the selective growth and malignant transformation of cancer cells. miR-4454 was selected by sequencing due to its abnormal high expression in HPV16 E6/E7 positive CaSki cell compared with HPV16 E6/E7 negative C33A cell. Overexpression of miR-4454 enhances cervical cancer cell invasion and migration. ABHD2 and NUDT21 are identified as a target gene of miR-4454.The effects of ABHD2 and NUDT21 on migration and invasion of CaSki and C33A cells were determined. The dual luciferase and RT-qPCR assays confirmed that miR-4454 might regulate its targets ABHD2 and NUDT21 to promote the proliferation, invasion and migration, whereas, inhibit the apoptosis in CaSki and C33A cells. 

Retracted: No

PubPeer comments:
 Much more similar than you could expect. Could the authors please check? ![file] , 
 Dear Dr. Platycheirus Stegnus, I am the first author Fang Xu. Thank you very much for your interest. After carefully checking the original data, I realized that when I preparing Figure 3C with photoshop microsoftware, the immunoblot of the dose-dependent Caspase 9 in RPMI-8226 was inadvertently and incorrectly duplicated. The original data of time-dependent Caspase 9 in LP1 is shown below. The change tendency in Caspase 9 was same, therefore the original conclusion was not impacted. The authors will contact the journal for an erratum. We sincerely apologize for the inconvenience caused by an unconscious mistake, and appreciate your pointing out. Thanks. Fang Xu ![file] ,
Virtual screening and repurposing of FDA approved drugs against COVID-19 main protease
Authors: Mohammed Al-Nazawi
Mahmoud Kandeel
Journal: Life sciences (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: 2019-Novel Coronavirus; COVID-19, 2019-nCoV; Main protease; Molecular modeling; Wuhan Coronavirus.
Affiliations: Department of Biomedical Sciences, College of Veterinary Medicine, King Faisal University, Al-hofuf, 31982, Al-ahsa, Saudi Arabia; Department of Pharmacology, Faculty of Veterinary Medicine, Kafrelshikh University, Kafrelshikh 33516, Egypt. Electronic address: ., Department of Biomedical Sciences, College of Veterinary Medicine, King Faisal University, Al-hofuf, 31982, Al-ahsa, Saudi Arabia.

Abstract:  Aims: In December 2019, the Coronavirus disease-2019 (COVID-19) virus has emerged in Wuhan, China. In this research, the first resolved COVID-19 crystal structure (main protease) was targeted in a virtual screening study by of FDA approved drugs dataset. In addition, a knowledge gap in relations of COVID-19 with the previously known fatal Coronaviruses (CoVs) epidemics, SARS and MERS CoVs, was covered by investigation of sequence statistics and phylogenetics. Materials and methods: Molecular modeling, virtual screening, docking, sequence comparison statistics and phylogenetics of the COVID-19 main protease were investigated. Key findings: COVID-19 Mpro formed a phylogenetic group with SARS CoV that was distant from MERS CoV. The identity% was 96.061 and 51.61 for COVID-19/SARS and COVID-19/MERS CoV sequence comparisons, respectively. The top 20 drugs in the virtual screening studies comprised a broad-spectrum antiviral (ribavirin), anti-hepatitis B virus (telbivudine), two vitamins (vitamin B12 and nicotinamide) and other miscellaneous systemically acting drugs. Of special interest, ribavirin had been used in treating cases of SARS CoV. Significance: The present study provided a comprehensive targeting of the first resolved COVID+19 structure of Mpro and found a suitable save drugs for repurposing against the viral Mpro. Ribavirin, telbivudine, vitamin B12 and nicotinamide can be combined and used for COVID treatment. This initiative relocates already marketed and approved safe drugs for potential use in COVID-treatment. 

Retracted: No

PubPeer comments:
 How can the authors claim that curumin is an approved SARS Mpro inhibitor? ![file] , 
 The  diagonal panels probably refer to the sets of numbers bottom left and top right of the diagonal. ,
Loss of the novel mitochondrial protein FAM210B promotes metastasis via PDK4-dependent metabolic reprogramming
Authors: Qingqing Mo
Beibei Wang
Qinglei Gao
Peng Wu
Shujuan Sun
Yuan Tian
Yingyan Han
Pingbo Chen
Jia Liu
Gang Chen
Yong Fang
Meisong Zhao
Jianfeng Zhou
Ding Ma
Journal: Cell death & disease (2017)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: tumor metabolism; metabolic reprogramming; cancer metastasis; FAM210B; human cancer cells
Affiliations: The Key Laboratory of Cancer Invasion and Metastasis of the Ministry of Education of China, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China., Department of hematology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, P.R. China.

Abstract:  Recent advances in tumor metabolism have revealed that metabolic reprogramming could dramatically promote caner metastasis. However, the relation and mechanism between metastasis and metabolic reprogramming are not thoroughly explored. Cell proliferation, colony formation, and invasion analysis were performed to evaluate the role of FAM210B in human cancer cells. Human ovarian cancer xenograft model was used to determine the effects of inhibiting FAM210B by shRNA on tumor metastasis. Microarray analysis was used to determine the target genes of FAM210B. FAM210B cellular localization was performed by mitochondria isolation and mitochondria protein extraction. To detect FAM210B-mediated metabolic reprogramming, oxygen consumption rate and extracellular acidification rate were measured. Our previous study screened a novel cancer progression-suppressor gene, FAM210B, which encodes an outer mitochondrial membrane protein, by the suppression of mortality by antisense rescue technique (SMART). Here we demonstrated that FAM210B loss was significantly associated with cancer metastasis and decreased survival in a clinical setting. Additionally, it was found that low expression of FAM210B was significantly correlated with decreased survival and enhanced metastasis in vivo and in vitro, and the loss of FAM210B led to an increased mitochondrial respiratory capacity and reduced glycolysis through the downregulation of pyruvate dehydrogenase kinase 4 (PDK4), which activated the EMT program and enhanced migratory and invasive properties. Collectively, our data unveil a potential metabolic target and mechanism of cancer metastasis. 

Retracted: No

PubPeer comments:
 In figure 7E, some of the panels appear to show an overlap, although they represent different experiments. ![file] , 
 #1 Corrected, [23 September 2019] :  Following publication of this article [1], the authors became aware of an error in Fig. 7e which requires correction. The images do not currently match the correct treatment and or control conditions. Specifically, the images of siNC+AD-ctr (the top left panel) and siPDK4+AD-PDK4 (the bottom right panel) were incorrect. The corrected figure is provided below. The error does not impact the conclusions of the article. They sincerely apologize for the mistakes in the article and any inconvenience caused. ![] ,
Exploiting the biological efficacy of benzimidazole based Schiff base complexes with l-Histidine as a co-ligand: Combined molecular docking, DNA interaction, antimicrobial and cytotoxic studies
Authors: Ponnukalai Ponya Utthra
Ganesan Kumaravel
Natarajan Raman
Journal: Bioorganic Chemistry (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Cytotoxicity; DNA binding studies; Gel electrophoresis; Molecular docking; Schiff base metal complexes.
Affiliations: Research Department of Chemistry, VHNSN College, Virudhunagar 626 001, India., Research Department of Chemistry, VHNSN College, Virudhunagar 626 001, India. Electronic address: .

Abstract:  Four new metal complexes were synthesized and screened for their cytotoxic activity after sufficient assertion from the preliminary DNA binding studies. The metal complexes could bind to CT-DNA through intercalation binding mode. This has also been confirmed by the molecular docking studies. The DNA cleavage efficiencies of these complexes with pBR322 DNA were investigated by gel electrophoresis. The complexes were found to promote the cleavage of pBR322 DNA from the supercoiled form I to the open circular form II in the presence of an oxidizing agent (H2O2). The in vitro chemosensitivity of the studied complexes exhibits significant cytotoxic effects, compared to those reported for cisplatin. These findings represent a prompting to search for the probable interaction of these complexes with other cellular elements of fundamental consequence in cell proliferation. The in vitro anticancer activities indicate that the Cu(II) complex is active against the selected human tumor cell lines, and the order of in vitro anticancer activities is consistent with the DNA-binding affinities. Towards noncancerous cell line, Cu(II) complex exhibits very low toxicity. On the other hand all the complexes have been found to exhibit cytotoxic effects against cancerous cell lines with potency more than that of the widely used drug cisplatin and hence they have the potential to act as promising anticancer agents. Captivatingly, they are non-toxic to normal cell lymphocytes revealing that they are selective in killing only the cancer cells. 

Retracted: No

PubPeer comments:
 Could the authors comment on what appear to be some repeated features? Fig. 6.Gel electrophoresis pattern showing the cleavage of pBR322 supercoiled DNA (10lM) by the complexes. Lane 1: DNA control (10lM); Lane 2: DNA + H2O2 (20lM); Lane 3: DNA + H2O2+ [L] (50lM); Lane 4: DNA + H2O2+1(50lM); Lane 5: DNA + H2O2+2(50lM); Lane 6: DNA + H2O2+3(50lM); Lane 7: DNA + H2O2+ 4(50lM) ![file] , 
 #1 Fig 6 again: ![file] Now marked up for comparison with Fig 6 of [Raman et al (2020)] : ![] ,
Downregulation of miR-122 in the rodent and human hepatocellular carcinomas
Authors: Shoumei Bai
Tasneem Motiwala
Kalpana Ghoshal
Jharna Datta
Wendy Frankel
Igor Pogribny
Samson T Jacob
Huban Kutay
Journal: Journal of Cellular Biochemistry (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: MicroRNAs; gene expression regulation; hepatocellular carcinomas; miR profiles; microarray analysis
Affiliations: Department of Molecular and Cellular Biochemistry, Ohio State University, Columbus, Ohio 43210, USA.

Abstract:  MicroRNAs (miRs) are conserved small non-coding RNAs that negatively regulate gene expression. The miR profiles are markedly altered in cancers and some of them have a causal role in tumorigenesis. Here, we report changes in miR expression profile in hepatocellular carcinomas (HCCs) developed in male Fisher rats-fed folic acid, methionine, and choline-deficient (FMD) diet. Comparison of the miR profile by microarray analysis showed altered expression of some miRs in hepatomas compared to the livers from age-matched rats on the normal diet. While let-7a, miR-21, miR-23, miR-130, miR-190, and miR-17-92 family of genes was upregulated, miR-122, an abundant liver-specific miR, was downregulated in the tumors. The decrease in hepatic miR-122 was a tumor-specific event because it did not occur in the rats switched to the folate and methyl-adequate diet after 36 weeks on deficient diet, which did not lead to hepatocarcinogenesis. miR-122 was also silent in a transplanted rat hepatoma. Extrapolation of this study to human primary HCCs revealed that miR-122 expression was significantly (P = 0.013) reduced in 10 out of 20 tumors compared to the pair-matched control tissues. These findings suggest that the downregulation of miR-122 is associated with hepatocarcinogenesis and could be a potential biomarker for liver cancers. 

Retracted: No

PubPeer comments:
 ![file] , 
 Second author appears to currently be affiliated with University of Pittsburgh, and has the unfortunate distinction of appearing as coauthor of multiple papers with similar image concerns while at different institutions: https: pubpeer.com search?q=Shoumei+Bai ![file] , 
 https: retractionwatch.com 2022 07 25 exclusive-osu-investigation-finds-dishonesty-and-permissive-culture-of-data-manipulation-in-cancer-research-lab ,
Neuroprotective effects of Kukoamine A against cerebral ischemia via antioxidant and inactivation of apoptosis pathway
Authors: Yajun Zhang
Weihong Meng
Qingchun Zhao
Xiaowen Jiang
Jia Liu
Qiao Zhang
Jun Zhu
Sen Lin
Xiaolong Hu
Jiabao Du
Journal: Neurochemistry International (2017)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Antioxidant; Cerebral ischemia; Kukoamine A; Mitochondrial apoptosis.
Affiliations: Department of Pharmacy, General Hospital of Shenyang Military Area Command, Shenyang 110840, China; Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang 110016, China., Department of Traditional Chinese Medicine, Shenyang Pharmaceutical University, Shenyang 110016, China., Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang 110016, China., Department of Radiology, General Hospital of Shenyang Military Area Command, Shenyang 110840, China., Department of Pharmacy, General Hospital of Shenyang Military Area Command, Shenyang 110840, China., Department of Pharmacy, General Hospital of Shenyang Military Area Command, Shenyang 110840, China. Electronic address: .

Abstract:  Kukoamine A (KuA) is a bioactive compound, which is known for a hypotensive effect. Recent studies have shown that KuA has anti-oxidative effect and anti-apoptosis stress in vitro. However, its neuroprotective effect in rats with cerebral ischemia is still unclear. In the study, we investigated whether KuA could attenuate cerebral ischemia induced by permanent middle cerebral artery occlusion (pMCAO) in rats. Results revealed that KuA could significantly reduce infarct volume both pre-treatment and post-treatment, and increase corresponding Garcia neurological scores. Acute KuA postconditioning not only significantly reduced cerebral infarct volume, brain water content and improved neurological deficit scores, but also decreased the number of TUNEL-positive cells. Moreover, it markedly increased the activities of Cu/Zn-SOD and Mn-SOD, reduced levels of MDA and H2O2. Increased expressions of caspase-3, cytochrome c and the ratio of Bax/Bcl-2 were significantly alleviated with KuA treatment. These findings demonstrated that KuA was able to protect the brain against injury induced by pMCAO via mitochondria mediated apoptosis signaling pathway. 

Retracted: No

PubPeer comments:
 Two images in Figure 4A appear to overlap. This group seems to have a difficult time keeping their laboratory results organized. *** Enhanced brightness and contrast ![file] *** Original ![file] ,
Hepatitis B surface protein docked vesicular carrier for site specific delivery to liver
Authors: Suresh P Vyas
Sunil Mahor
Prem N Gupta
Kapil Khatri
Amit Rawat
Journal: Journal of Drug Targeting (2005)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: liposomes; hepatotropic elements; hepatitis B virus; HBsAg; targeting
Affiliations: Drug Delivery Research Laboratory, Department of Pharmaceutical Sciences, Dr. Hari Singh Gour Vishwavidyalaya, Sagar, India., Drug Delivery Research Laboratory, Department of Pharmaceutical Sciences Dr. Hari Singh Gour Vishwavidyalaya

Abstract:  The intrinsic liver tropism of liposomes can be augmented by the addition of targeting features such as the incorporation of hepatotropic elements of the hepatitis viruses. Hepatitis B virus is known to infect hepatocytes after viremia by asialoglycoprotein receptor mediated uptake. However, the specificity of hepatitis B virus surface protein (HBsAg) towards hepatocytes has confronting reports. In the present study, we evaluated the functional ability of HBsAg to be employed as a ligand for targeting hepatocytes. We prepared (14)C labeled small unilamellar vesicles (SUVs) composed of egg PC/Cholesterol/N-glutarylphosphatidylethanolamine (NGPE) in a 60:30:10 molar ratio. HBsAg was covalently linked to SUVs using a water-soluble carbodiimide (EDC) mediated conjugation with NGPE. In vitro cell binding and uptake studies revealed that bioprotein docked carrier system was efficiently taken up by HepG2 cells by the receptor mediated endocytosis. The biodistribution behaviour of plain and HBsAg coated liposomes was also examined followed by intravenous injection. The study revealed that almost 75% of the radioactivity was recovered in the liver after 4 h of injection that was nearly three-fold greater in magnitude than the plain liposomes. Further, fractionation of liver into liver parenchymal cells (PC) and non-parenchymal cells confirmed the preferential localization of the HBsAg coated liposomal carrier in the parenchymal cells. 

Retracted: No

PubPeer comments:
 The alpha-tubulin panel in Figure 2B looks unexpectedly similar to the GAPDH panel in Figure 5G. Note a small wave under the second band. ![file] , 
 Note: This article has been corrected. Please see the link below: https: www.oncotarget.com article 27253 ,
Multigene antiviral vectors inhibit diverse human immunodeficiency virus type 1 clades
Authors: A Gervaix
F Wong-Staal
G Kraus
X Li
Journal: Journal of Virology (1997)
Discipline: MICROBIOLOGY
Keywords: HIV; gene therapy; RNA decoy; ribozyme; antiviral vectors
Affiliations: Department of Medicine, University of California, San Diego, La Jolla 92093-0665, USA.

Abstract:  The chronicity of infection by the human immunodeficiency virus (HIV) calls for therapeutic regimens that offer sustained antiviral effects, such as gene therapy. Recent studies have demonstrated that expression of HIV mutant transdominant proteins, RNA decoys, and ribozymes efficiently inhibited HIV replication. We have previously shown that an RNA decoy (stem-loop II of the Rev response element of HIV type 1 [HIV-1], named SL2) and a ribozyme (Rz) targeting the U5 region of the HIV-1 5' long terminal repeat (LTR), combined in a fusion molecule, was more efficient in inhibiting HIV-1 replication than the ribozyme or the decoy alone. In this study, we expressed this fusion molecule in a retrovirus-based double-copy vector to obtain higher expression of this molecule. Furthermore, we inserted a sequence internally to drive expression of another fusion molecule with a ribozyme targeting the env/rev region linked to SL2 to obtain a triple-copy vector. These multigene antiviral vectors were subsequently transduced or transfected into human CD4+ T cells (Molt-4). Results showed that the translocation of the SL2-Rz cassette from the 3' to the 5' LTR occurred in 80% of the transduced cells. The numbers of ribozyme RNA transcripts, estimated by competitive-quantitative reverse transcription (RT)-PCR, were 1.2 x 10(5), 1.2 x 10(4), and 1.5 x 10(3) copies per cell for the triple-copy, double-copy, and single-copy vectors, respectively. Cell challenge with multiple subtypes of HIV-1 (clades A to E) showed commensurate levels of virus inhibition for the three vectors. This study suggests that the combination of multiple anti-HIV genes, such as ribozymes and decoys, targeting multiple sites of HIV RNA and expressed at high levels are promising for the treatment of HIV-1 infection. 

Retracted: No

PubPeer comments:
null, 
null, 
null, 
null, 
 Figure 4. Much more similar than you would expect. https: imgur.com uPFxbCi ,
How Corona Formation Impacts Nanomaterials as Drug Carriers
Authors: Ipsita Roy
Munishwar Nath Gupta
Journal: Molecular pharmaceutics (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Vroman effect; biocorona; drug delivery; drug targeting; nanoparticles
Affiliations: Former Professor, Department of Chemistry, Indian Institute of Technology, Hauz Khas, New Delhi 110016, India., Department of Biotechnology, National Institute of Pharmaceutical Education and Research (NIPER), Sector 67, S.A.S. Nagar, Punjab 160062, India.

Abstract:  As drugs/drug carriers, upon encountering physiological fluids, nanoparticles adsorb biological molecules almost immediately to form a biocorona, which is often simply called a corona. Once the corona is formed, it dictates the subsequent fate of the drug nanoparticle as a therapeutic agent. Protein adsorption on micron-size or even bigger particles was originally described by the Vroman effect. It has served as a useful framework to understand the corona formation. Proteins that are irreversibly adsorbed on nanoparticles form what is called a hard corona. Beyond that is the exchangeable population of proteins, which constitute the dynamic structure called a soft corona. More than the abundance, the affinity of the proteins toward the nanoparticles decides which ones end up in the corona. For example, the more common serum albumin, which is deposited initially, is displaced by fibrinogen, which has a higher affinity for gold nanoparticles. The curvature of the particle is a crucial parameter with bigger particles generally able to bind a more diverse population of proteins from the physiological milieu. The earlier perception of the corona formation being a challenge for drug targeting, etc. has been turned into an opportunity by engineering corona to manipulate properties like circulating half-lives, capacity to evade the immune system, and targeting or even overcoming the blood-brain barrier. The most commonly used techniques for particle characterization, including dynamic light scattering (DLS), differential sedimentation centrifugation, transmission electron microscopy (TEM), and SDS-PAGE, have been adopted to study corona formation in the past. Many newer tools, for example, a combination of capillary electrophoresis with mass spectrometry, are being used to study the corona composition. The comparison of interlaboratory results is a problem because of the lack of standard protocols. This has hindered the ability to obtain more precise information about the corona composition. That, in turn, affects our prospects to use nanoparticles as drugs/drug carriers. This overview is an attempt to assess our understanding of corona formation critically and to outline the complexities involved in gaining precise information. The discussion is largely focused on findings of the last year or so. 

Retracted: No

PubPeer comments:
 Figure 6 appears to have several small overlaps ![file] ![file] ,
Temperature-Alternated Electrochemical Aptamer-Based Biosensor for Calibration-Free and Sensitive Molecular Measurements in an Unprocessed Actual Sample
Authors: Zhi-Min Chen
Jian-Jun Sun
Yi Wang
Xing-Yuan Du
Sen Yang
Journal: Analytical Chemistry (2021)
Discipline: CHEMISTRY
Keywords: Electrochemical biosensors; Calibration-free operation; Temperature-alternated; Aptamer-based sensor; Peak currents
Affiliations: Ministry of Education Key Laboratory for Analytical Science of Food Safety and Biology, Fujian Provincial Key Laboratory of Analysis and Detection Technology for Food Safety, College of Chemistry, Fuzhou University, Fuzhou, Fujian 350108, China, Key Laboratory of Targeting Therapy and Diagnosis for Critical Diseases Collaborative Innovation Center of New Drug Research and Safety Evaluation, School of Pharmaceutical Sciences, Zhengzhou University, Zhengzhou 450001, China

Abstract:  Frequently calibrating electrochemical biosensors (ECBs) to obtain acceptable accuracy can be cumbersome for the users. Thus, the achievement of calibration-free operation would effectively lead to commercial applications for ECBs in the real world. Herein, we fabricated a temperature-alternated electrochemical aptamer-based (TAEAB) sensor, producing a cycle of "enhanced-responsive and ∼nonresponsive" state at rapidly alternated interface temperatures (5 and 30 °C, respectively). The ratio of peak currents collected at two temperatures overcomes sensor-to-sensor fabrication variations, obviating sensor calibration prior to use due to its good reproducibility. We then demonstrated the capability of TAEAB sensors for improved, sensitive, and calibration-free measurement of different targets within 7 min, which respectively achieved a detection limit of 0.5 μM procaine in undiluted urine and 1.0 μM adenosine triphosphate in undiluted serum. This generalizable approach ameliorates sensitivity without the complicated amplification step, thus simplifying the operation procedure and reducing the detection time, which will effectively improve the clinical utility of biosensors. 

Retracted: No

PubPeer comments:
 Figure 3A. * Red boxes: The top parts of these 2 panels (representing gels with or without SDS) appear to look very similar. ![file] Reported to the journal in September 2016. It was addressed with a June 2017 Correction, which reads:  *Page 1612, column 1, line 24: The following sentence should be added after u201cu2026with 0.02% SDS.u201d u201cFirst the gel was incubated with substrate without SDS, and then the same gel was incubated with substrate with 0.02% SDS to reveal the latent activity of CP (see Fig. 3A).u201d* This paper was part of a structured search for image duplications in Molecular and Cellular Biology paper, which was published here: https: mcb.asm.org content 38 20 e00309-18.long ,
DASH diet, insulin resistance, and serum hs-CRP in polycystic ovary syndrome: a randomized controlled clinical trial
Authors: Z Asemi
A Esmaillzadeh
Journal: Hormone and Metabolic Research (2014)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Dietary Approaches to Stop Hypertension (DASH); insulin resistance; serum hs-CRP; overweight; obese women
Affiliations: Research Center for Biochemistry and Nutrition in Metabolic Diseases, Kashan University of Medical Sciences, Kashan, Iran, Food Security Research Center, Isfahan University of Medical Sciences, Isfahan, Iran

Abstract:  This study was designed to assess the effects of Dietary Approaches to Stop Hypertension (DASH) eating plan on insulin resistance and serum hs-CRP in overweight and obese women with PCOS. This randomized controlled clinical trial was done on 48 women diagnosed with PCOS. Subjects were randomly assigned to consume either the control (n=24) or the DASH eating pattern (n=24) for 8 weeks. The DASH diet consisted of 52% carbohydrates, 18% proteins, and 30% total fats. It was designed to be rich in fruits, vegetables, whole grains, and low-fat dairy products and low in saturated fats, cholesterol, refined grains, and sweets. Sodium content of the DASH diet was designed to be less than 2 400 mg/day. The control diet was also designed to contain 52% carbohydrates, 18% protein, and 30% total fat. Fasting blood samples were taken at baseline and after 8 weeks intervention to measure -insulin resistance and serum hs-CRP levels. -Adherence to the DASH eating pattern, compared to the -control diet, resulted in a significant reduction of serum insulin levels (-1.88 vs. 2.89 μIU/ml, p=0.03), HOMA-IR score (-0.45 vs. 0.80; p=0.01), and serum hs-CRP levels (-763.29 vs. 665.95 ng/ml, p=0.009). Additionally, a significant reduction in waist (-5.2 vs. -2.1 cm; p=0.003) and hip circumference (-5.9 vs. -1 cm; p&lt;0.0001) was also seen in the DASH group compared with the control group. In conclusion, consumption of the DASH eating pattern for 8 weeks in overweight and obese women with PCOS resulted in the improvement of insulin resistance, serum hs-CRP levels, and abdominal fat accumulation. Clinical trial registration number: www.irct.ir: IRCT201304235623N6. 

Retracted: No

PubPeer comments:
 There are many concerns about the integrity of 172 publications by this research group, including this one. Some of the concerns are published 1. Anaesthesia 2020;75:1683u201392, see Supplementary data. This paper is A26 2. Account Res 2020;28:149-61. 3. J Clin Epidemiol 2021;131:22-29. Journals and publishers were notified of these concerns in July 2019. 23 publications have an expression of concern. To our knowledge there has been no public response about any of the concerns. We think these publications are unreliable ,
Retraction statement: MicroRNA‐222 promotes tumorigenesis via targeting DKK2 and activating the Wnt/β‐catenin signaling pathway
Authors: Baocheng Wang
Ke Shen
Qifeng Li
Chenkai Ma
Yang Zhao
Jianwen Liu
Xiaoguang He
Lin Wang
Jie Ma
Journal: FEBS Letters (2021)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Retraction; Duplications; Figures; Raw data; Conclusions

Abstract:  https://doi.org/10.1016/j.febslet.2013.04.002 The above article from FEBS Letters by Qifeng Li, Ke Shen, Yang Zhao, Xiaoguang He, Chenkai Ma, Lin Wang, Baocheng Wang, Jianwen Liu, Jie Ma, published online on 12 April 2013, in Wiley Online Library (https://doi.org/10.1016/j.febslet.2013.04.002), has been retracted by agreement between the authors, the journal Managing Editor, Felix Wieland, and John Wiley &amp; Sons. The retraction has been agreed due to the identification of duplications in Figures 1D, 3B, and 4A-C. The authors were unable to provide the raw data underlying these figure panels. As a result, the journal cannot independently verify the conclusions of the article. All authors have agreed to the retraction of this paper and regret any inconvenience caused. 

Retracted: No

PubPeer comments:
 2021 retraction. https: febs.onlinelibrary.wiley.com doi 10.1002 1873-3468.14066 https: doi.org 10.1016 j.febslet.2013.04.002 The above article from FEBS Letters by Qifeng Li, Ke Shen, Yang Zhao, Xiaoguang He, Chenkai Ma, Lin Wang, Baocheng Wang, Jianwen Liu, Jie Ma, published online on 12 April 2013, in Wiley Online Library , has been retracted by agreement between the authors, the journal Managing Editor, Felix Wieland, and John Wiley Sons. The retraction has been agreed due to the identification of duplications in Figures 1D, 3B, and 4Au2013C. The authors were unable to provide the raw data underlying these figure panels. As a result, the journal cannot independently verify the conclusions of the article. All authors have agreed to the retraction of this paper and regret any inconvenience caused. ,
Baicalin protects human retinal pigment epithelial cell lines against high glucose-induced cell injury by up-regulation of microRNA-145
Authors: Cuiying Chu
Meng Xin
Bojun Zhao
Shanhao Jiang
Xiufen Song
Chunhua Dai
Journal: Experimental and Molecular Pathology (2019)
Discipline: CLINICAL MEDICINE
Keywords: Baicalin; Diabetic retinopathy; MicroRNA-145; NF-κB; p38MAPK.
Affiliations: Department of Ophthalmology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China; Department of Ophthalmology, Yantai Affiliated Hospital of Binzhou Medical University, Yantai 264100, China., Department of Ophthalmology, Yantai Affiliated Hospital of Binzhou Medical University, Yantai 264100, China., Department of Ophthalmology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China. Electronic address: .

Abstract:  Background: Diabetic retinopathy (DR) is a common complication of diabetes mellitus, which is a major reason of blindness. Baicalin (BAI) is a flavonoid extracted from Scutellaria baicalensis, whose pharmacological characterizes have been widely reported in various diseases. However, it remains unclear the effect of BAI on DR. The study aimed to confirm the protective effect of BAI on DR. Methods: ARPE-19 cells and HRMECs were exposed to the high glucose (HG) environment to construct a cell injury model. After treatment with HG and BAI, cell viability, apoptosis, inflammatory cytokines and ROS generations were determined in ARPE-19 cells and HRMECs. Subsequently, microRNA-145 (miR-145) inhibitor and its negative control were transfected into ARPE-19 cells, and the regulatory effects on HG-and BAI-co-treated cells were detected. NF-κB and p38MAPK signaling pathways were finally examined to state the underling mechanisms. Results: HG treatment significantly induced ARPE-19 cells and HRMECs injury in vitro. BAI significantly promoted cell proliferation, reduced apoptosis, as well as inhibited the release of IL-1β, IL-6, IL-8 and ROS level in HG-injured ARPE-19 cells and HRMECs. Additionally, the expression level of miR-145 was up-regulated in HG-and BAI-co-treated cells. More importantly, miR-145 inhibition reversed the protective effect of BAI on HG-injured ARPE-19 cells. Besides, we observed that BAI inhibited the activations of NF-κB and p38MAPK pathways by up-regulating miR-145. Conclusions: Results demonstrated that BAI exhibited the protective effect against HG-induced cell injury by up-regulation of miR-145. 

Retracted: No

PubPeer comments:
null, 
 #1 The link in above showed as 404 Not Found , 
 See https: yulab-smu.top treedata-book instead. ,
Butein suppresses constitutive and inducible signal transducer and activator of transcription (STAT) 3 activation and STAT3-regulated gene products through the induction of a protein tyrosine phosphatase SHP-1
Authors: Bokyung Sung
Kwang Seok Ahn
Manoj K Pandey
Bharat B Aggarwal
Journal: Molecular pharmacology (2009)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: butein; antiproliferative effects; tumor cells; STAT3 activation pathway; tyrosine kinases
Affiliations: Department of Experimental Therapeutics, Cytokine Research Laboratory, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.

Abstract:  The aim of the current study is to determine whether butein (3,4,2',4'-tetrahydroxychalcone) exhibits antiproliferative effects against tumor cells through suppression of the signal transducer and activator of transcription 3 (STAT3) activation pathway. We investigated the effects of butein on constitutive and inducible STAT3 activation, role of tyrosine kinases and phosphatases in STAT3 activation, STAT3-regulated gene products, and growth modulation of tumor cells. We found that this chalcone inhibited both constitutive and interleukin-6-inducible STAT3 activation in multiple myeloma (MM) cells. The suppression was mediated through the inhibition of activation of the upstream kinases c-Src, Janus-like kinase (JAK) 1, and JAK2. Vanadate treatment reversed the butein-induced down-regulation of STAT3 activation, suggesting the involvement of a tyrosine phosphatase. Indeed, we found that butein induced the expression of the tyrosine phosphatase SHP-1 and deletion of SHP-1 gene by small interfering RNA abolished the ability of butein to inhibit STAT3 activation, suggesting the critical role of SHP-1 in the action of this chalcone. Butein down-regulated the expression of STAT3-regulated gene products such as Bcl-xL, Bcl-2, cyclin D1, and Mcl-1, and this led to the suppression of proliferation and induction of apoptosis. Consistent with these results, overexpression of constitutive active STAT3 significantly reduced the butein-induced apoptosis. Moreover, we found that butein significantly potentiated the apoptotic effects of thalidomide and Velcade in MM cells. Overall, these results suggest that butein is a novel blocker of STAT3 activation and thus may have potential in suppression of tumor cell proliferation and reversal of chemoresistance in MM cells. 

Retracted: No

PubPeer comments:
 Identified by another reader. *** ![file] ,
WITHDRWAN: Purified palmitoleic acid for the reduction of high-sensitivity C-reactive protein and serum lipids: a double-blinded, randomized, placebo controlled study
Authors: Michael F Roizen
Adam M Bernstein
Luis Martinez
Journal: Journal of Clinical Lipidology (2014)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: C-reactive protein; Cholesterol; Hyperlipidemia; Inflammation; Lipids
Affiliations: Wellness Institute, Cleveland Clinic, Lyndhurst, OH, USA. Electronic address: ., Wellness Institute, Cleveland Clinic, Lyndhurst, OH, USA., Xyrion Medical Institute, Ponce, PR, USA.

Abstract:  Background: Purified palmitoleic acid (16-1; omega-7) has shown lipid-lowering and anti-inflammatory benefits in open label, epidemiologic, and animal studies. Objective: Our objective was to perform the first randomized controlled trial of purified palmitoleic acid supplementation in humans. Methods: Adults with dyslipidemia and evidence of mild systemic inflammation (high-sensitivity C-reactive protein [hs-CRP] between 2 and 5 mg/L) were randomly allocated to receive either 220.5 mg of cis-palmitoleic acid (n = 30) or an identical capsule with placebo (1000 mg of medium chain triglycerides, n = 30) once per day for 30 days. Participants were asked to maintain their current diet. Serum lipids and hs-CRP were drawn at baseline and study completion. Results: At 30 days, there were significant mean (95% confidence interval [CI]) reductions in CRP (-1.9 [-2.3 to -1.4] mg/L), triglyceride (-30.2 [-40.2 to -25.3] mg/dL), and low-density lipoprotein (LDL) (-8.9 [-12.0 to -5.8] mg/dL), and a significant increase in high-density lipoprotein (HDL) (2.4 [1.5, 3.3] mg/dL) in the intervention group compared with control. These changes equated to 44%, 15%, and 8% reductions in CRP, triglyceride, and LDL respectively, and a 5% increase in HDL compared with control. Conclusions: Purified palmitoleic acid may be useful in the treatment of hypertriglyceridemia with the beneficial added effects of decreasing LDL and hs-CRP and raising HDL. Further study is needed to elucidate mechanisms and establish appropriate human doses. 

Retracted: Yes

PubPeer comments:
 u201cThis article has been retracted: please see Elsevier Policy on Article Withdrawal . This article has been retracted at the request of the Editor in Chief. It has come to our attention that this article presents serious concerns about Food and Drug Administration guidance and about data or statistical interpretation. The statistical accuracy claimed in the published article is not consistent with known variability of lipoprotein cholesterol and triglyceride levels. For these reasons the article is hereby retracted.u201d Via: https: retractionwatch.com 2021 04 16 palmitoleic-acid-paper-pulled-for-data-concerns ,
An N-terminal region of translationally controlled tumor protein is required for its antiapoptotic activity
Authors: Xinmen Wang
Hong Wang
Xiao-Feng Yang
Fan Yang
Zeyu Xiong
Yu Yang
Justin Nguyen
Michiya Nishino
Dragan Mirkovic
Yan Yan
Journal: Oncogene (2005)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Bcl-xL; TCTP; antiapoptotic; cytosolic proteins; cell survival
Affiliations: Department of Medicine, Laboratory of Immunopathology, Biology of Inflammation Center, Baylor College of Medicine, Houston, TX 77030, USA.

Abstract:  Bcl-xL plays a critical role in maintaining cell survival. However, the relationship between the potential interaction of Bcl-xL with other cytosolic proteins and the regulation of cell survival remains incompletely defined. We have identified translationally controlled tumor protein (TCTP), a multifunctional protein, as a novel antiapoptotic Bcl-xL-interacting protein. TCTP interacted in vivo and in vitro with Bcl-xL, and their sites have been mapped to an N-terminal region of TCTP and the Bcl-2 homology domain 3 of Bcl-xL. Consistent with a role in maintaining T-cell survival during activation, TCTP was significantly upregulated in murine T cells activated by T-cell antigen receptor (TCR) ligation and CD28 costimulation, which was correlated with the upregulation of Bcl-xL in activated T cells. Moreover, downregulation of TCTP expression by antisense technology in T cells results in the increase of T-cell apoptosis. Furthermore, the N-terminal region of TCTP was required for its ability to inhibit apoptosis. In conclusion, this study has demonstrated that an N-terminal region of a cytosolic protein, TCTP, is required for its binding to Bcl-xL and for its antiapoptotic activity. 

Retracted: No

PubPeer comments:
 Note: This article has been corrected. Please see the following link: https: www.oncotarget.com article 27986 ,