C:\Users\Administrator\Desktop\Array Datasheet\Disease Gene Array
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Genes Retina/RPE Choroid Sclera
Supplementary Materials: Genes Retina/RPE Choroid Sclera Fold Change p-value Fold Change p-value Fold Change p-value PPFIA2 NS NS 2.35 1.3X10-3 1.5 1.6X10-3 PTPRF 1.24 2.65X10-5 6.42 7X10-4 1.11 1X10-4 1.19 2.65X10-5 NS NS 1.11 3.3X10-3 PTPRR 1.44 2.65X10-5 3.04 4.7X10-3 NS NS Supplementary Table S1. Genes Differentially Expressed Related to Candidate Genes from Association. Genes selected for follow up validation by real time quantitative PCR. Multiple values for each gene indicate multiple probes within the same gene. NS indicates the fold change was not statistically significant. Gene/SNP Assay ID rs4764971 C__30866249_10 rs7134216 C__30023434_10 rs17306116 C__33218892_10 rs3803036 C__25749934_20 rs824311 C___8342112_10 PPFIA2 Hs00170308_m1 PTPRF Hs00160858_m1 PTPRR Hs00373136_m1 18S Hs03003631_g1 GAPDH Hs02758991_g1 Supplementary Table S2. Taqman® Genotyping and Gene Expression Assay Identification Numbers. SNP Chimp Orangutan Rhesus Marmoset Mouse Rat Cow Pig Guinea Pig Dog Elephant Opossum Chicken rs3803036 X X X X X X X X X X X X X rs1520562 X X X X X X rs1358228 X X X X X X X X X X X rs17306116 X X X X X X rs790436 X X X X X X X rs1558726 X X X X X X X X rs741525 X X X X X X X X rs7134216 X X X X X X rs4764971 X X X X X X X Supplementary Table S3. Conservation of Top SNPs from Association. X indicates SNP is conserved. -
Structural Characterization of Polysaccharides from Cordyceps Militaris and Their Hypolipidemic Effects Cite This: RSC Adv.,2018,8,41012 in High Fat Diet Fed Mice†
RSC Advances View Article Online PAPER View Journal | View Issue Structural characterization of polysaccharides from Cordyceps militaris and their hypolipidemic effects Cite this: RSC Adv.,2018,8,41012 in high fat diet fed mice† Zhen-feng Huang, ‡ Ming-long Zhang,‡ Song Zhang,* Ya-hui Wang and Xue-wen Jiang Cordyceps militaris is a crude dietary therapeutic mushroom with high nutritional and medicinal values. Mushroom-derived polysaccharides have been found to possess antihyperglycemic and antihyperlipidemic activities. This study aimed to partially clarify the structural characterization and comparatively evaluate hypolipidemic potentials of intracellular- (IPCM) and extracellular polysaccharides of C. militaris (EPCM) in high fat diet fed mice. Results indicated that IPCM-2 is a-pyran polysaccharide with an average molecular weight of 32.5 kDa, was mainly composed of mannose, glucose and galactose with mass percentages of 51.94%, 10.54%, and 37.25%, respectively. EPCM-2 is an a-pyran Creative Commons Attribution 3.0 Unported Licence. polysaccharide with an average molecular weight of 20 kDa that is mainly composed of mannose, glucose and galactose with mass percentages of 44.51%, 18.33%, and 35.38%, respectively. In in vivo study, EPCM-1 treatment (100 mg kgÀ1 dÀ1) showed potential effects on improving serum lipid profiles of hyperlipidemic mice, reflected by decreasing serum total cholesterol (TC), triglyceride (TG) and low density lipoprotein-cholesterol (LDL-C) levels by 20.05%, 45.45% and 52.63%, respectively, while IPCM-1 treatment -
Table S1 the Four Gene Sets Derived from Gene Expression Profiles of Escs and Differentiated Cells
Table S1 The four gene sets derived from gene expression profiles of ESCs and differentiated cells Uniform High Uniform Low ES Up ES Down EntrezID GeneSymbol EntrezID GeneSymbol EntrezID GeneSymbol EntrezID GeneSymbol 269261 Rpl12 11354 Abpa 68239 Krt42 15132 Hbb-bh1 67891 Rpl4 11537 Cfd 26380 Esrrb 15126 Hba-x 55949 Eef1b2 11698 Ambn 73703 Dppa2 15111 Hand2 18148 Npm1 11730 Ang3 67374 Jam2 65255 Asb4 67427 Rps20 11731 Ang2 22702 Zfp42 17292 Mesp1 15481 Hspa8 11807 Apoa2 58865 Tdh 19737 Rgs5 100041686 LOC100041686 11814 Apoc3 26388 Ifi202b 225518 Prdm6 11983 Atpif1 11945 Atp4b 11614 Nr0b1 20378 Frzb 19241 Tmsb4x 12007 Azgp1 76815 Calcoco2 12767 Cxcr4 20116 Rps8 12044 Bcl2a1a 219132 D14Ertd668e 103889 Hoxb2 20103 Rps5 12047 Bcl2a1d 381411 Gm1967 17701 Msx1 14694 Gnb2l1 12049 Bcl2l10 20899 Stra8 23796 Aplnr 19941 Rpl26 12096 Bglap1 78625 1700061G19Rik 12627 Cfc1 12070 Ngfrap1 12097 Bglap2 21816 Tgm1 12622 Cer1 19989 Rpl7 12267 C3ar1 67405 Nts 21385 Tbx2 19896 Rpl10a 12279 C9 435337 EG435337 56720 Tdo2 20044 Rps14 12391 Cav3 545913 Zscan4d 16869 Lhx1 19175 Psmb6 12409 Cbr2 244448 Triml1 22253 Unc5c 22627 Ywhae 12477 Ctla4 69134 2200001I15Rik 14174 Fgf3 19951 Rpl32 12523 Cd84 66065 Hsd17b14 16542 Kdr 66152 1110020P15Rik 12524 Cd86 81879 Tcfcp2l1 15122 Hba-a1 66489 Rpl35 12640 Cga 17907 Mylpf 15414 Hoxb6 15519 Hsp90aa1 12642 Ch25h 26424 Nr5a2 210530 Leprel1 66483 Rpl36al 12655 Chi3l3 83560 Tex14 12338 Capn6 27370 Rps26 12796 Camp 17450 Morc1 20671 Sox17 66576 Uqcrh 12869 Cox8b 79455 Pdcl2 20613 Snai1 22154 Tubb5 12959 Cryba4 231821 Centa1 17897 -
A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated. -
TNAP As a New Player in Chronic Inflammatory Conditions And
International Journal of Molecular Sciences Review TNAP as a New Player in Chronic Inflammatory Conditions and Metabolism Stephanie Graser 1,*, Daniel Liedtke 2,† and Franz Jakob 1,† 1 Bernhard-Heine-Center for Locomotion Research, Department of Orthopedics, Julius-Maximilians-University Würzburg, 97076 Würzburg, Germany; [email protected] 2 Institute for Human Genetics, Biocenter, Julius-Maximilians-University Würzburg, 97074 Würzburg, Germany; [email protected] * Correspondence: [email protected] † These authors contributed equally to this work. Abstract: This review summarizes important information on the ectoenzyme tissue-nonspecific alkaline phosphatase (TNAP) and gives a brief insight into the symptoms, diagnostics, and treatment of the rare disease Hypophosphatasia (HPP), which is resulting from mutations in the TNAP encoding ALPL gene. We emphasize the role of TNAP beyond its well-known contribution to mineralization processes. Therefore, above all, the impact of the enzyme on central molecular processes in the nervous system and on inflammation is presented here. Keywords: TNAP; Hypophosphatasia; HPP; mineralization; nervous system; inflammation 1. Structure, Function, and Substrates of TNAP Tissue-nonspecific alkaline phosphatase (TNAP) or liver/bone/kidney alkaline phos- phatase is an ectoenzyme that is anchored to the outer cell membrane (e.g. in osteoblasts) Citation: Graser, S.; Liedtke, D.; and to extracellular vesicles via its glycosyl-inositol-phosphate (GPI)-anchor [1,2]. TNAP Jakob, F. TNAP as a New Player in belongs to the family of alkaline phosphatases (AP) that comprises in humans three addi- Chronic Inflammatory Conditions tional tissue-specific isoforms: placental (PLAP, ALPP National Center for Biotechnology and Metabolism. Int. -
Circhipk3 Facilitates the G2/M Transition in Prostate Cancer Cells by Sponging Mir-338-3P
OncoTargets and Therapy Dovepress open access to scientific and medical research Open Access Full Text Article ORIGINAL RESEARCH CircHIPK3 Facilitates the G2/M Transition in Prostate Cancer Cells by Sponging miR-338-3p This article was published in the following Dove Press journal: OncoTargets and Therapy Fengchun Liu1 Background: Circular RNAs (circRNAs) play a crucial role in gene expression regulation. Yanru Fan 1 CircHIPK3 is a circRNA derived from Exon 2 of HIPK3 gene and its role in prostate cancer Liping Ou1 (PCa) is still unclear. fl Ting Li1 Methods: CCK8 assays, ow cytometry and colony formation assays were performed to assess Jiaxin Fan1 the effects of circHIPK3 in PCa cells. Bioinformatics analysis, RNA pull-down assay, RNA immunoprecipitation assay (RIP), and luciferase activity assay were performed to dissect the Limei Duan1 mechanism underlying circHIPK3-mediated G2/M transition in PCa cells. Jinxiao Yang1 1 Results: CircHIPK3 expression was upregulated in PCa cells and prostate cancer tissues. Chunli Luo Overexpression of circHIPK3 or circHIPK3 silencing altered PCa viability, proliferation and 2 Xiaohou Wu apoptosis in vitro. CircHIPK3 could sponge miR-338-3p and inhibit its activity, resulting in 1Department of Laboratory Diagnosis, increased expression of Cdc25B and Cdc2 in vitro. Chongqing Medical University, Yuzhong, Conclusion: CircHIPK3 promotes G2/M transition and induces PCa cell proliferation by Chongqing 408000, People’s Republic of China; 2Department of Urology, The First sponging miR-338-3p and increasing the -
Datasheet Blank Template
SAN TA C RUZ BI OTEC HNOL OG Y, INC . MTMR3 (N-20): sc-47187 BACKGROUND RECOMMENDED SECONDARY REAGENTS Myotubularin and the myotubularin-related proteins (MTMR1-9) belong to a To ensure optimal results, the following support (secondary) reagents are highly conserved family of eukaryotic phosphatases. They are protein tyrosine recommended: 1) Western Blotting: use donkey anti-goat IgG-HRP: sc-2020 phosphatases that utilize inositol phospholipids, rather than phosphoproteins, (dilution range: 1:2000-1:100,000) or Cruz Marker™ compatible donkey as substrates. MTMR family members hydrolyze both Phosphatidylinositol anti- goat IgG-HRP: sc-2033 (dilution range: 1:2000-1:5000), Cruz Marker™ 3-phosphate (PtdIns3P) and PtdIns P2. MTMR2 interacts with MTMR5, an Molecular Weight Standards: sc-2035, TBS Blotto A Blocking Reagent: inactive family member that increases the enzymatic activity of MTMR2 and sc-2333 and Western Blotting Luminol Reagent: sc-2048. 2) Immunoprecip- dictates its subcellular localization. Mutations in MTMR2 cause autosomal itation: use Protein A/G PLUS-Agarose: sc-2003 (0.5 ml agarose/2.0 ml). recessive Charcot-Marie-Tooth type 4B1 (CMT4B1), which is characterized 3) Immunofluorescence: use donkey anti-goat IgG-FITC: sc-2024 (dilution by reduced nerve conduction velocities, focally folded myelin sheaths and range: 1:100-1:400) or donkey anti-goat IgG-TR: sc-2783 (dilution range: demyelination. MTMR3 and MTMR4 can either interact with each other or self 1:100-1:400) with UltraCruz™ Mounting Medium: sc-24941. associate. MTMR6 regulates the activity of the calcium-activated potassium channel 3.1. MTMR9 regulates the activity of MTMR7 and MTMR8. -
A Rapid Transcriptome Response Is Associated with Desiccation Resistance in Aerially-Exposed Killifish Embryos
A Rapid Transcriptome Response Is Associated with Desiccation Resistance in Aerially-Exposed Killifish Embryos Ange`le Tingaud-Sequeira1¤a, Juan-Jose´ Lozano2, Cinta Zapater1, David Otero1, Michael Kube3¤b, Richard Reinhardt3¤c, Joan Cerda` 1* 1 Institut de Recerca i Tecnologia Agroalimenta`ries (IRTA)-Institut de Cie`ncies del Mar, CSIC, Barcelona, Spain, 2 Bioinformatics Platform, CIBERHED, Barcelona, Spain, 3 Max Planck Institute for Molecular Genetics, Berlin-Dahlem, Germany Abstract Delayed hatching is a form of dormancy evolved in some amphibian and fish embryos to cope with environmental conditions transiently hostile to the survival of hatchlings or larvae. While diapause and cryptobiosis have been extensively studied in several animals, very little is known concerning the molecular mechanisms involved in the sensing and response of fish embryos to environmental cues. Embryos of the euryhaline killifish Fundulus heteroclitus advance dvelopment when exposed to air but hatching is suspended until flooding with seawater. Here, we investigated how transcriptome regulation underpins this adaptive response by examining changes in gene expression profiles of aerially incubated killifish embryos at ,100% relative humidity, compared to embryos continuously flooded in water. The results confirm that mid-gastrula embryos are able to stimulate development in response to aerial incubation, which is accompanied by the differential expression of at least 806 distinct genes during a 24 h period. Most of these genes (,70%) appear to be differentially expressed within 3 h of aerial exposure, suggesting a broad and rapid transcriptomic response. This response seems to include an early sensing phase, which overlaps with a tissue remodeling and activation of embryonic development phase involving many regulatory and metabolic pathways. -
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. -
9. Atypical Dusps: 19 Phosphatases in Search of a Role
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Digital.CSIC Transworld Research Network 37/661 (2), Fort P.O. Trivandrum-695 023 Kerala, India Emerging Signaling Pathways in Tumor Biology, 2010: 185-208 ISBN: 978-81-7895-477-6 Editor: Pedro A. Lazo 9. Atypical DUSPs: 19 phosphatases in search of a role Yolanda Bayón and Andrés Alonso Instituto de Biología y Genética Molecular, CSIC-Universidad de Valladolid c/ Sanz y Forés s/n, 47003 Valladolid, Spain Abstract. Atypical Dual Specificity Phosphatases (A-DUSPs) are a group of 19 phosphatases poorly characterized. They are included among the Class I Cys-based PTPs and contain the active site motif HCXXGXXR conserved in the Class I PTPs. These enzymes present a phosphatase domain similar to MKPs, but lack any substrate targeting domain similar to the CH2 present in this group. Although most of these phosphatases have no more than 250 amino acids, their size ranges from the 150 residues of the smallest A-DUSP, VHZ/DUSP23, to the 1158 residues of the putative PTP DUSP27. The substrates of this family include MAPK, but, in general terms, it does not look that MAPK are the general substrates for the whole group. In fact, other substrates have been described for some of these phosphatases, like the 5’CAP structure of mRNA, glycogen, or STATs and still the substrates of many A-DUSPs have not been identified. In addition to the PTP domain, most of these enzymes present no additional recognizable domains in their sequence, with the exception of CBM-20 in laforin, GTase in HCE1 and a Zn binding domain in DUSP12. -
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). -
Review Article PTEN Gene: a Model for Genetic Diseases in Dermatology
The Scientific World Journal Volume 2012, Article ID 252457, 8 pages The cientificWorldJOURNAL doi:10.1100/2012/252457 Review Article PTEN Gene: A Model for Genetic Diseases in Dermatology Corrado Romano1 and Carmelo Schepis2 1 Unit of Pediatrics and Medical Genetics, I.R.C.C.S. Associazione Oasi Maria Santissima, 94018 Troina, Italy 2 Unit of Dermatology, I.R.C.C.S. Associazione Oasi Maria Santissima, 94018 Troina, Italy Correspondence should be addressed to Carmelo Schepis, [email protected] Received 19 October 2011; Accepted 4 January 2012 Academic Editors: G. Vecchio and H. Zitzelsberger Copyright © 2012 C. Romano and C. Schepis. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. PTEN gene is considered one of the most mutated tumor suppressor genes in human cancer, and it’s likely to become the first one in the near future. Since 1997, its involvement in tumor suppression has smoothly increased, up to the current importance. Germline mutations of PTEN cause the PTEN hamartoma tumor syndrome (PHTS), which include the past-called Cowden, Bannayan- Riley-Ruvalcaba, Proteus, Proteus-like, and Lhermitte-Duclos syndromes. Somatic mutations of PTEN have been observed in glioblastoma, prostate cancer, and brest cancer cell lines, quoting only the first tissues where the involvement has been proven. The negative regulation of cell interactions with the extracellular matrix could be the way PTEN phosphatase acts as a tumor suppressor. PTEN gene plays an essential role in human development. A recent model sees PTEN function as a stepwise gradation, which can be impaired not only by heterozygous mutations and homozygous losses, but also by other molecular mechanisms, such as transcriptional regression, epigenetic silencing, regulation by microRNAs, posttranslational modification, and aberrant localization.