Maternal Folic Acid Impacts DNA Methylation Profile in Male Rat Offspring Implicated in Neurodevelopment and Learning/Memory
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Original Article Upregulation of HOXA13 As a Potential Tumorigenesis and Progression Promoter of LUSC Based on Qrt-PCR and Bioinformatics
Int J Clin Exp Pathol 2017;10(10):10650-10665 www.ijcep.com /ISSN:1936-2625/IJCEP0065149 Original Article Upregulation of HOXA13 as a potential tumorigenesis and progression promoter of LUSC based on qRT-PCR and bioinformatics Rui Zhang1*, Yun Deng1*, Yu Zhang1, Gao-Qiang Zhai1, Rong-Quan He2, Xiao-Hua Hu2, Dan-Ming Wei1, Zhen-Bo Feng1, Gang Chen1 Departments of 1Pathology, 2Medical Oncology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, China. *Equal contributors. Received September 7, 2017; Accepted September 29, 2017; Epub October 1, 2017; Published October 15, 2017 Abstract: In this study, we investigated the levels of homeobox A13 (HOXA13) and the mechanisms underlying the co-expressed genes of HOXA13 in lung squamous cancer (LUSC), the signaling pathways in which the co-ex- pressed genes of HOXA13 are involved and their functional roles in LUSC. The clinical significance of 23 paired LUSC tissues and adjacent non-tumor tissues were gathered. HOXA13 levels in LUSC were detected by quantita- tive real-time polymerase chain reaction (qRT-PCR). HOXA13 levels in LUSC from The Cancer Genome Atlas (TCGA) and Oncomine were analyzed. We performed receiver operator characteristic (ROC) curves of various clinicopath- ological features of LUSC. Co-expressed of HOXA13 were collected from MEM, cBioPortal and GEPIA. The func- tions and pathways of the most reliable overlapped genes were achieved from the Gene Otology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases, respectively. The protein-protein interaction (PPI) net- works were mapped using STRING. HOXA13 in LUSC were markedly upregulated compared with those in the non- cancerous controls as demonstrated by qRT-PCR (LUSC: 0.330±0.360; CONTROLS: 0.155±0.142; P=0.021). -
Dynamin Functions and Ligands: Classical Mechanisms Behind
1521-0111/91/2/123–134$25.00 http://dx.doi.org/10.1124/mol.116.105064 MOLECULAR PHARMACOLOGY Mol Pharmacol 91:123–134, February 2017 Copyright ª 2017 by The American Society for Pharmacology and Experimental Therapeutics MINIREVIEW Dynamin Functions and Ligands: Classical Mechanisms Behind Mahaveer Singh, Hemant R. Jadhav, and Tanya Bhatt Department of Pharmacy, Birla Institute of Technology and Sciences Pilani, Pilani Campus, Rajasthan, India Received May 5, 2016; accepted November 17, 2016 Downloaded from ABSTRACT Dynamin is a GTPase that plays a vital role in clathrin-dependent pathophysiology of various disorders, such as Alzheimer’s disease, endocytosis and other vesicular trafficking processes by acting Parkinson’s disease, Huntington’s disease, Charcot-Marie-Tooth as a pair of molecular scissors for newly formed vesicles originating disease, heart failure, schizophrenia, epilepsy, cancer, dominant ’ from the plasma membrane. Dynamins and related proteins are optic atrophy, osteoporosis, and Down s syndrome. This review is molpharm.aspetjournals.org important components for the cleavage of clathrin-coated vesicles, an attempt to illustrate the dynamin-related mechanisms involved phagosomes, and mitochondria. These proteins help in organelle in the above-mentioned disorders and to help medicinal chemists division, viral resistance, and mitochondrial fusion/fission. Dys- to design novel dynamin ligands, which could be useful in the function and mutations in dynamin have been implicated in the treatment of dynamin-related disorders. Introduction GTP hydrolysis–dependent conformational change of GTPase dynamin assists in membrane fission, leading to the generation Dynamins were originally discovered in the brain and identi- of endocytic vesicles (Praefcke and McMahon, 2004; Ferguson at ASPET Journals on September 23, 2021 fied as microtubule binding partners. -
PERK Antibody / EIF2AK3 (RQ4206)
PERK Antibody / EIF2AK3 (RQ4206) Catalog No. Formulation Size RQ4206 0.5mg/ml if reconstituted with 0.2ml sterile DI water 100 ug Bulk quote request Availability 1-3 business days Species Reactivity Human, Mouse, Rat Format Antigen affinity purified Clonality Polyclonal (rabbit origin) Isotype Rabbit IgG Purity Antigen affinity purified Buffer Lyophilized from 1X PBS with 2% Trehalose and 0.025% sodium azide UniProt Q9NZJ5 Applications Western Blot : 0.5-1ug/ml Flow cytometry : 1-3ug/10^6 cells Direct ELISA : 0.1-0.5ug/ml Limitations This PERK antibody is available for research use only. Western blot testing of human 1) HeLa, 2) COLO320, 3) A549, 4) SK-OV-3, 5) A431, 6) rat brain and 7) mouse brain lysate with PERK antibody at 0.5ug/ml. Predicted molecular weight ~125 kDa, observed here at ~140 kDa. Flow cytometry testing of human HepG2 cells with PERK antibody at 1ug/10^6 cells (blocked with goat sera); Red=cells alone, Green=isotype control, Blue= PERK antibody. Description Eukaryotic translation initiation factor 2-alpha kinase 3, also known as protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK), is an enzyme that in humans is encoded by the EIF2AK3 gene. The protein encoded by this gene phosphorylates the alpha subunit of eukaryotic translation-initiation factor 2, leading to its inactivation, and thus to a rapid reduction of translational initiation and repression of global protein synthesis. This protein is thought to modulate mitochondrial function. It is a type I membrane protein located in the endoplasmic reticulum (ER), where it is induced by ER stress caused by malfolded proteins. -
The Rise and Fall of the Bovine Corpus Luteum
University of Nebraska Medical Center DigitalCommons@UNMC Theses & Dissertations Graduate Studies Spring 5-6-2017 The Rise and Fall of the Bovine Corpus Luteum Heather Talbott University of Nebraska Medical Center Follow this and additional works at: https://digitalcommons.unmc.edu/etd Part of the Biochemistry Commons, Molecular Biology Commons, and the Obstetrics and Gynecology Commons Recommended Citation Talbott, Heather, "The Rise and Fall of the Bovine Corpus Luteum" (2017). Theses & Dissertations. 207. https://digitalcommons.unmc.edu/etd/207 This Dissertation is brought to you for free and open access by the Graduate Studies at DigitalCommons@UNMC. It has been accepted for inclusion in Theses & Dissertations by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. THE RISE AND FALL OF THE BOVINE CORPUS LUTEUM by Heather Talbott A DISSERTATION Presented to the Faculty of the University of Nebraska Graduate College in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy Biochemistry and Molecular Biology Graduate Program Under the Supervision of Professor John S. Davis University of Nebraska Medical Center Omaha, Nebraska May, 2017 Supervisory Committee: Carol A. Casey, Ph.D. Andrea S. Cupp, Ph.D. Parmender P. Mehta, Ph.D. Justin L. Mott, Ph.D. i ACKNOWLEDGEMENTS This dissertation was supported by the Agriculture and Food Research Initiative from the USDA National Institute of Food and Agriculture (NIFA) Pre-doctoral award; University of Nebraska Medical Center Graduate Student Assistantship; University of Nebraska Medical Center Exceptional Incoming Graduate Student Award; the VA Nebraska-Western Iowa Health Care System Department of Veterans Affairs; and The Olson Center for Women’s Health, Department of Obstetrics and Gynecology, Nebraska Medical Center. -
Adenylate Cyclase 3: a New Target for Anti‐Obesity Drug Development
obesity reviews doi: 10.1111/obr.12430 Obesity Pharmacotherapy Adenylate cyclase 3: a new target for anti-obesity drug development L. Wu,1 C. Shen,2 M. Seed Ahmed,3 C.-G. Östenson4 and H. F. Gu5,6 1Jiangsu Key Laboratory of Drug Screening, Summary China Pharmaceutical University, Nanjing Obesity has become epidemic worldwide, and abdominal obesity has a negative im- 210009, China, 2Department of Epidemiology, pact on health. Current treatment options on obesity, however, still remain limited. School of Public Health, Nanjing Medical It is then of importance to find a new target for anti-obesity drug development University, Nanjing 211166, China, 3Unit for based upon recent molecular studies in obesity. Adenylate cyclase 3 (ADCY3) is Medical Education, Centre for Learning and the third member of adenylyl cyclase family and catalyses the synthesis of cAMP Knowledge, Department of Learning, from ATP. Genetic studies with candidate gene and genome-wide association study Informatics, Management and Ethics, approaches have demonstrated that ADCY3 genetic polymorphisms are associated Karolinska Institutet, Stockholm 17177, with obesity in European and Chinese populations. Epigenetic studies have indi- Sweden, 4Rolf Luft Center for Diabetes cated that increased DNA methylation levels in the ADCY3 gene are involved in Research and Endocrinology, Department of the pathogenesis of obesity. Furthermore, biological analyses with animal models Molecular Medicine and Surgery, Karolinska have implicated that ADCY3 dysfunction resulted in increased body weight and Institutet, Karolinska University Hospital, Solna, fat mass, while reduction of body weight is partially explained by ADCY3 activa- Stockholm 17176, Sweden, 5Department of tion. In this review, we describe genomic and biological features of ADCY3, sum- Clinical Science, Intervention and marize genetic and epigenetic association studies of the ADCY3 gene with obesity Technologies, Karolinska Institutet, Karolinska and discuss dysfunction and activation of ADCY3. -
Supplemental Table S1
Entrez Gene Symbol Gene Name Affymetrix EST Glomchip SAGE Stanford Literature HPA confirmed Gene ID Profiling profiling Profiling Profiling array profiling confirmed 1 2 A2M alpha-2-macroglobulin 0 0 0 1 0 2 10347 ABCA7 ATP-binding cassette, sub-family A (ABC1), member 7 1 0 0 0 0 3 10350 ABCA9 ATP-binding cassette, sub-family A (ABC1), member 9 1 0 0 0 0 4 10057 ABCC5 ATP-binding cassette, sub-family C (CFTR/MRP), member 5 1 0 0 0 0 5 10060 ABCC9 ATP-binding cassette, sub-family C (CFTR/MRP), member 9 1 0 0 0 0 6 79575 ABHD8 abhydrolase domain containing 8 1 0 0 0 0 7 51225 ABI3 ABI gene family, member 3 1 0 1 0 0 8 29 ABR active BCR-related gene 1 0 0 0 0 9 25841 ABTB2 ankyrin repeat and BTB (POZ) domain containing 2 1 0 1 0 0 10 30 ACAA1 acetyl-Coenzyme A acyltransferase 1 (peroxisomal 3-oxoacyl-Coenzyme A thiol 0 1 0 0 0 11 43 ACHE acetylcholinesterase (Yt blood group) 1 0 0 0 0 12 58 ACTA1 actin, alpha 1, skeletal muscle 0 1 0 0 0 13 60 ACTB actin, beta 01000 1 14 71 ACTG1 actin, gamma 1 0 1 0 0 0 15 81 ACTN4 actinin, alpha 4 0 0 1 1 1 10700177 16 10096 ACTR3 ARP3 actin-related protein 3 homolog (yeast) 0 1 0 0 0 17 94 ACVRL1 activin A receptor type II-like 1 1 0 1 0 0 18 8038 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 1 0 0 0 0 19 8751 ADAM15 ADAM metallopeptidase domain 15 (metargidin) 1 0 0 0 0 20 8728 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 1 0 0 0 0 21 81792 ADAMTS12 ADAM metallopeptidase with thrombospondin type 1 motif, 12 1 0 0 0 0 22 9507 ADAMTS4 ADAM metallopeptidase with thrombospondin type 1 -
Exosome-Mediated MIR211 Modulates Tumor Microenvironment Via the DUSP6-ERK5 Axis and Contributes to BRAFV600E Inhibitor Resistan
bioRxiv preprint doi: https://doi.org/10.1101/548818; this version posted February 13, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Exosome-mediated MIR211 modulates tumor microenvironment via the DUSP6-ERK5 axis and contributes to BRAFV600E inhibitor resistance in melanoma. Bongyong Lee1,3, Anupama Sahoo3, Junko Sawada1,3, John Marchica1,3, Sanjay Sahoo3, Fabiana I. A. L. Layng4, Darren Finlay4, Joseph Mazar5, Piyush Joshi1, Masanobu Komatsu1,3, Kristiina Vuori4, Garth Powis4, Petrus R. de Jong4, Animesh Ray6,7, and Ranjan J. Perera 1,2,3* 1 Department of Cancer and Blood Disorders Institute, Johns Hopkins All Children’s Hospital, St. Petersburg, FL 33701 USA 2 Department of Oncology, Sydney Kimmel Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD 21287 USA 3 Sanford Burnham Prebys Medical Discovery Institute, Orlando, FL 32827 USA 4 Sanford Burnham Prebys Medical Discovery Institute, NCI-Designated Cancer Center, La Jolla, CA 92037, USA 5 Nemours Children Hospital, Orlando, FL 32827 USA 6 Keck Graduate Institute, Claremont CA 91711 USA, 7 Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125 USA. *Correspondence: Ranjan Perera Tel: 1-727-767-3491 Email: [email protected] 1 bioRxiv preprint doi: https://doi.org/10.1101/548818; this version posted February 13, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. ABSTRACT The microRNA MIR211 is an important regulator of melanoma tumor cell behavior. -
Dual-Specificity Phosphatase 3 Deletion Protects Female, but Not
Published August 28, 2017, doi:10.4049/jimmunol.1602092 The Journal of Immunology Dual-Specificity Phosphatase 3 Deletion Protects Female, but Not Male, Mice from Endotoxemia-Induced and Polymicrobial-Induced Septic Shock Maud M. Vandereyken,*,1 Pratibha Singh,*,1 Caroline P. Wathieu,* Sophie Jacques,* Tinatin Zurashvilli,* Lien Dejager,†,‡ Mathieu Amand,* Lucia Musumeci,* Maneesh Singh,* Michel P. Moutschen,* Claude R. F. Libert,†,‡ and Souad Rahmouni* Dual-specificity phosphatase 3 (DUSP3) is a small phosphatase with poorly known physiological functions and for which only a few substrates are known. Using knockout mice, we recently reported that DUSP3 deficiency confers resistance to endotoxin- and polymicrobial-induced septic shock. We showed that this protection was macrophage dependent. In this study, we further investigated the role of DUSP3 in sepsis tolerance and showed that the resistance is sex dependent. Using adoptive-transfer experiments and ovariectomized mice, we highlighted the role of female sex hormones in the phenotype. Indeed, in ovariec- tomized females and in male mice, the dominance of M2-like macrophages observed in DUSP32/2 female mice was reduced, suggesting a role for this cell subset in sepsis tolerance. At the molecular level, DUSP3 deletion was associated with estrogen- dependent decreased phosphorylation of ERK1/2 and Akt in peritoneal macrophages stimulated ex vivo by LPS. Our results demonstrate that estrogens may modulate M2-like responses during endotoxemia in a DUSP3-dependent manner. The Journal of Immunology, 2017, 199: 000–000. epsis and septic shock are complex clinical syndromes that ally, death (4). Sepsis occurrence and outcome depend on arise when the local body response to pathogens becomes pathogen characteristics, as well as on risk factors, such as age S systemic and injures its own tissues and organs (1). -
De Novo EIF2AK1 and EIF2AK2 Variants Are Associated with Developmental Delay, Leukoencephalopathy, and Neurologic Decompensation
bioRxiv preprint doi: https://doi.org/10.1101/757039; this version posted September 16, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. De novo EIF2AK1 and EIF2AK2 variants are associated with developmental delay, leukoencephalopathy, and neurologic decompensation Dongxue Mao1,2, Chloe M. Reuter3,4, Maura R.Z. Ruzhnikov5,6, Anita E. Beck7, Emily G. Farrow8,9,10, Lisa T. Emrick1,11,12,13, Jill A. Rosenfeld12, Katherine M. Mackenzie5, Laurie Robak2,12,13, Matthew T. Wheeler3,14, Lindsay C. Burrage12,13, Mahim Jain15, Pengfei Liu12, Daniel Calame11,13, Sebastien Küry17,18, Martin Sillesen19, Klaus Schmitz-Abe20, Davide Tonduti21, Luigina Spaccini22, Maria Iascone23, Casie A. Genetti20, Madeline Graf16, Alyssa Tran12, Mercedes Alejandro12, Undiagnosed Diseases Network, Brendan H. Lee12,13, Isabelle Thiffault8,9,24, Pankaj B. Agrawal#,20, Jonathan A. Bernstein#,3,25, Hugo J. Bellen#,2,12,26,27,28, Hsiao- Tuan Chao#,1,2,11,12,13,28,27,29 #Correspondence should be addressed: [email protected] (P.A.), [email protected] (J.A.B.), [email protected] (H.J.B.), [email protected] (H.T.C.) 1Department of Pediatrics, Baylor College of Medicine (BCM), Houston, TX 2Jan and Dan Duncan Neurological Research Institute, Texas Children’s Hospital, Houston, TX 3Stanford Center for Undiagnosed Diseases, Stanford University, Stanford, CA 4Stanford Center for Inherited Cardiovascular Disease, Division of Cardiovascular Medicine, -
CXCR4 Pathway Retards Muscle Atrophy During Cancer Cachexia
Oncogene (2016) 35, 6212–6222 © 2016 Macmillan Publishers Limited, part of Springer Nature. All rights reserved 0950-9232/16 www.nature.com/onc ORIGINAL ARTICLE Activation of the SDF1/CXCR4 pathway retards muscle atrophy during cancer cachexia GB Martinelli1, D Olivari1, AD Re Cecconi1, L Talamini1, L Ottoboni2, SH Lecker3, C Stretch4, VE Baracos4, OF Bathe5, A Resovi6, R Giavazzi1, L Cervo7 and R Piccirillo1 Cancer cachexia is a life-threatening syndrome that affects most patients with advanced cancers and causes severe body weight loss, with rapid depletion of skeletal muscle. No treatment is available. We analyzed microarray data sets to identify a subset of genes whose expression is specifically altered in cachectic muscles of Yoshida hepatoma-bearing rodents but not in those with diabetes, disuse, uremia or fasting. Ingenuity Pathways Analysis indicated that three genes belonging to the C-X-C motif chemokine receptor 4 (CXCR4) pathway were downregulated only in muscles atrophying because of cancer: stromal cell-derived factor 1 (SDF1), adenylate cyclase 7 (ADCY7), and p21 protein-activated kinase 1 (PAK1). Notably, we found that, in the Rectus Abdominis muscle of cancer patients, the expression of SDF1 and CXCR4 was inversely correlated with that of two ubiquitin ligases induced in muscle wasting, atrogin-1 and MuRF1, suggesting a possible clinical relevance of this pathway. The expression of all main SDF1 isoforms (α, β, γ) also declined in Tibialis Anterior muscle from cachectic mice bearing murine colon adenocarcinoma or human renal cancer and drugs with anticachexia properties restored their expression. Overexpressing genes of this pathway (that is, SDF1 or CXCR4) in cachectic muscles increased the fiber area by 20%, protecting them from wasting. -
Genome-Wide Association and Transcriptome Studies Identify Candidate Genes and Pathways for Feed Conversion Ratio in Pigs
Miao et al. BMC Genomics (2021) 22:294 https://doi.org/10.1186/s12864-021-07570-w RESEARCH ARTICLE Open Access Genome-wide association and transcriptome studies identify candidate genes and pathways for feed conversion ratio in pigs Yuanxin Miao1,2,3, Quanshun Mei1,2, Chuanke Fu1,2, Mingxing Liao1,2,4, Yan Liu1,2, Xuewen Xu1,2, Xinyun Li1,2, Shuhong Zhao1,2 and Tao Xiang1,2* Abstract Background: The feed conversion ratio (FCR) is an important productive trait that greatly affects profits in the pig industry. Elucidating the genetic mechanisms underpinning FCR may promote more efficient improvement of FCR through artificial selection. In this study, we integrated a genome-wide association study (GWAS) with transcriptome analyses of different tissues in Yorkshire pigs (YY) with the aim of identifying key genes and signalling pathways associated with FCR. Results: A total of 61 significant single nucleotide polymorphisms (SNPs) were detected by GWAS in YY. All of these SNPs were located on porcine chromosome (SSC) 5, and the covered region was considered a quantitative trait locus (QTL) region for FCR. Some genes distributed around these significant SNPs were considered as candidates for regulating FCR, including TPH2, FAR2, IRAK3, YARS2, GRIP1, FRS2, CNOT2 and TRHDE. According to transcriptome analyses in the hypothalamus, TPH2 exhibits the potential to regulate intestinal motility through serotonergic synapse and oxytocin signalling pathways. In addition, GRIP1 may be involved in glutamatergic and GABAergic signalling pathways, which regulate FCR by affecting appetite in pigs. Moreover, GRIP1, FRS2, CNOT2,andTRHDE may regulate metabolism in various tissues through a thyroid hormone signalling pathway. -
Gene and Pathway-Based Second-Wave Analysis of Genome-Wide Association Studies
European Journal of Human Genetics (2010) 18, 111–117 & 2010 Macmillan Publishers Limited All rights reserved 1018-4813/10 $32.00 www.nature.com/ejhg ARTICLE Gene and pathway-based second-wave analysis of genome-wide association studies Gang Peng1, Li Luo2, Hoicheong Siu1, Yun Zhu1, Pengfei Hu1, Shengjun Hong1, Jinying Zhao3, Xiaodong Zhou4, John D Reveille4, Li Jin1, Christopher I Amos5 and Momiao Xiong*,2 Despite the great success of genome-wide association studies (GWAS) in identification of the common genetic variants associated with complex diseases, the current GWAS have focused on single-SNP analysis. However, single-SNP analysis often identifies only a few of the most significant SNPs that account for a small proportion of the genetic variants and offers only a limited understanding of complex diseases. To overcome these limitations, we propose gene and pathway-based association analysis as a new paradigm for GWAS. As a proof of concept, we performed a comprehensive gene and pathway-based association analysis of 13 published GWAS. Our results showed that the proposed new paradigm for GWAS not only identified the genes that include significant SNPs found by single-SNP analysis, but also detected new genes in which each single SNP conferred a small disease risk; however, their joint actions were implicated in the development of diseases. The results also showed that the new paradigm for GWAS was able to identify biologically meaningful pathways associated with the diseases, which were confirmed by a gene-set-rich analysis using gene expression