Supplementary Table 1: Genes Affected by Anoikis. A, Ratio of Signal
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Legends for Supplemental Figures and Tables Figure S1. Expression of Tlx during retinogenesis. (A) Staged embryos were stained for β- galactosidase knocked into the Tlx locus to indicate Tlx expression. Tlx was expressed in the neural blast layer in the early phase of neural retina development (blue signal). (B) Expression of Tlx in neural retina was quantified using Q-PCR at multiple developmental stages. Figure S2. Expression of p27kip1 and cyclin D1 (Ccnd1) at various developmental stages in wild-type or Tlx-/- retinas. (A) Q-PCR analysis of p27kip1 mRNA expression. (B) Western blotting analysis of p27kip1 protein expression. (C) Q-PCR analysis of cyclin D1 mRNA expression. Figure S3. Q-PCR analysis of mRNA expression of Sf1 (A), Lrh1 (B), and Atn1 (C) in wild-type mouse retinas. RNAs from testis and liver were used as controls. Table S1. List of genes dysregulated both at E15.5 and P0 Tlx-/- retinas. Gene E15.5 P0 Cluste Gene Title Fold Fold r Name p-value p-value Change Change nuclear receptor subfamily 0, group B, Nr0b1 1.65 0.0024 2.99 0.0035 member 1 1 Pou4f3 1.91 0.0162 2.39 0.0031 POU domain, class 4, transcription factor 3 1 Tcfap2d 2.18 0.0000 2.37 0.0001 transcription factor AP-2, delta 1 Zic5 1.66 0.0002 2.02 0.0218 zinc finger protein of the cerebellum 5 1 Zfpm1 1.85 0.0030 1.88 0.0025 zinc finger protein, multitype 1 1 Pten 1.60 0.0155 1.82 0.0131 phospatase and tensin homolog 2 Itgb5 -1.85 0.0063 -1.85 0.0007 integrin beta 5 2 Gpr49 6.86 0.0001 15.16 0.0001 G protein-coupled receptor 49 3 Cmkor1 2.60 0.0007 2.72 0.0013 -
Endothelial Cells and the IGF System
L A Bach Endothelial cells as IGF targets 54:1 R1–R13 Review Endothelial cells and the IGF system Correspondence 1,2 Leon A Bach should be addressed to L A Bach 1Department of Medicine (Alfred), Monash University, Prahran 3181, Australia Email 2Department of Endocrinology and Diabetes, Alfred Hospital, Commercial Road, Melbourne 3004, Australia [email protected] Abstract Endothelial cells line blood vessels and modulate vascular tone, thrombosis, inflammatory Key Words responses and new vessel formation. They are implicated in many disease processes including " insulin-like growth factor atherosclerosis and cancer. IGFs play a significant role in the physiology of endothelial cells " binding protein by promoting migration, tube formation and production of the vasodilator nitric oxide. " receptor These actions are mediated by the IGF1 and IGF2/mannose 6-phosphate receptors and are " endothelial cell modulated by a family of high-affinity IGF binding proteins. IGFs also increase the number " angiogenesis and function of endothelial progenitor cells, which may contribute to protection from atherosclerosis. IGFs promote angiogenesis, and dysregulation of the IGF system may contribute to this process in cancer and eye diseases including retinopathy of prematurity and diabetic retinopathy. In some situations, IGF deficiency appears to contribute to endothelial dysfunction, whereas IGF may be deleterious in others. These differences may be due to tissue-specific endothelial cell phenotypes or IGFs having distinct roles in different phases of vascular disease. Further studies are therefore required to delineate the Journal of Molecular therapeutic potential of IGF system modulation in pathogenic processes. Endocrinology (2015) 54, R1–R13 Journal of Molecular Endocrinology Introduction Insulin-like growth factor 1 (IGF1) and IGF2 are essential metabolically active and regulate vascular tone, thrombosis, for normal pre- and postnatal growth and development inflammatory responses and new vessel formation. -
Genetic and Epigenetic Variation in the Human Genome
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine 122 Genetic and Epigenetic Variation in the Human Genome Analysis of Phenotypically Normal Individuals and Patients Affected with Brain Tumors CECILIA DE BUSTOS ACTA UNIVERSITATIS UPSALIENSIS ISSN 1651-6206 UPPSALA ISBN 91-554-6490-4 2006 urn:nbn:se:uu:diva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
Gene Expression Profiles of Estrogen Receptor–Positive and Estrogen Receptor–Negative Breast Cancers Are Detectable in Histologically Normal Breast Epithelium
Published OnlineFirst November 8, 2010; DOI: 10.1158/1078-0432.CCR-10-1369 Clinical Cancer Human Cancer Biology Research Gene Expression Profiles of Estrogen Receptor–Positive and Estrogen Receptor–Negative Breast Cancers Are Detectable in Histologically Normal Breast Epithelium Kelly Graham1, Xijin Ge4, Antonio de las Morenas2, Anusri Tripathi3, and Carol L. Rosenberg1,2,3 Abstract Purpose: Previously, we found that gene expression in histologically normal breast epithelium (NlEpi) from women at high breast cancer risk can resemble gene expression in NlEpi from cancer-containing breasts. Therefore, we hypothesized that gene expression characteristic of a cancer subtype might be seen in NlEpi of breasts containing that subtype. Experimental Design: We examined gene expression in 46 cases of microdissected NlEpi from untreated women undergoing breast cancer surgery. From 30 age-matched cases [15 estrogen receptor (ER)þ,15ERÀ] we used Affymetryix U133A arrays. From 16 independent cases (9 ERþ,7ERÀ), we validated selected genes using quantitative real-time PCR (qPCR). We then compared gene expression between NlEpi and invasive breast cancer using four publicly available data sets. Results: We identified 198 genes that are differentially expressed between NlEpi from breasts with ERþ (NlEpiERþ) compared with ERÀ cancers (NlEpiERÀ). These include genes characteristic of ERþ and ERÀ cancers (e.g., ESR1, GATA3, and CX3CL1, FABP7). qPCR validated the microarray results in both the 30 original cases and the 16 independent cases. Gene expression in NlEpiERþ and NlEpiERÀ resembled gene expression in ERþ and ERÀ cancers, respectively: 25% to 53% of the genes or probes examined in four external data sets overlapped between NlEpi and the corresponding cancer subtype. -
Insulin-Like Growth Factor Axis in Pregnancies Affected by Fetal Growth Disorders Aamod R
Nawathe et al. Clinical Epigenetics (2016) 8:11 DOI 10.1186/s13148-016-0178-5 RESEARCH Open Access Insulin-like growth factor axis in pregnancies affected by fetal growth disorders Aamod R. Nawathe1,2, Mark Christian3, Sung Hye Kim2, Mark Johnson1,2, Makrina D. Savvidou1,2 and Vasso Terzidou1,2* Abstract Background: Insulin-like growth factors 1 and 2 (IGF1 and IGF2) and their binding proteins (IGFBPs) are expressed in the placenta and known to regulate fetal growth. DNA methylation is an epigenetic mechanism which involves addition of methyl group to a cytosine base in the DNA forming a methylated cytosine-phosphate-guanine (CpG) dinucleotide which is known to silence gene expression. This silences gene expression, potentially altering the expression of IGFs and their binding proteins. This study investigates the relationship between DNA methylation of components of the IGF axis in the placenta and disorders in fetal growth. Placental samples were obtained from cord insertions immediately after delivery from appropriate, small (defined as birthweight <10th percentile for the gestation [SGA]) and macrosomic (defined as birthweight > the 90th percentile for the gestation [LGA]) neonates. Placental DNA methylation, mRNA expression and protein levels of components of the IGF axis were determined by pyrosequencing, rtPCR and Western blotting. Results: In the placenta from small for gestational age (SGA) neonates (n = 16), mRNA and protein levels of IGF1 were lower and of IGFBPs (1, 2, 3, 4 and 7) were higher (p < 0.05) compared to appropriately grown neonates (n =37).In contrast, in the placenta from large for gestational age (LGA) neonates (n = 20), mRNA and protein levels of IGF1 was not different and those of IGFBPs (1, 2, 3 and 4) were lower (p < 0.05) compared to appropriately grown neonates. -
Rabbit Anti-FAM19A1/FITC Conjugated Antibody-SL14779R
SunLong Biotech Co.,LTD Tel: 0086-571- 56623320 Fax:0086-571- 56623318 E-mail:[email protected] www.sunlongbiotech.com Rabbit Anti-FAM19A1/FITC Conjugated antibody SL14779R-FITC Product Name: Anti-FAM19A1/FITC Chinese Name: FITC标记的FAM19A1蛋白抗体 C630007B19Rik,; Chemokine-like protein TAFA-1; F19A1_HUMAN; Fam19a1; Alias: Family with sequence similarity 19 (chemokine (C-C motif) like), member A1; Protein FAM19A1; RGD1563030; TAFA 1; TAFA1. Organism Species: Rabbit Clonality: Polyclonal React Species: Human,Mouse,Rat,Chicken,Dog,Pig,Cow, ICC=1:50-200IF=1:50-200 Applications: not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. Molecular weight: 13kDa Form: Lyophilized or Liquid Concentration: 1mg/ml immunogen: KLH conjugated synthetic peptide derived from human FAM19A1 Lsotype: IgG Purification: affinity purified by Protein A Storage Buffer: 0.01Mwww.sunlongbiotech.com TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year Storage: when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. background: A group of small secreted proteins known as the TAFA family consists of five highly homologous genes: TAFA1, TAFA2, TAFA3, TAFA4 and TAFA5. Members of the TAFA family contain conserved cysteine residues at fixed positions and are highly Product Detail: expressed in brain. The TAFA family may be distantly related to a member of the CC- chemokine family known as MIP-1A, and have been postulated to regulate nervous and immune cells of the brain as neurokines or chemokines. -
Development and Validation of a Protein-Based Risk Score for Cardiovascular Outcomes Among Patients with Stable Coronary Heart Disease
Supplementary Online Content Ganz P, Heidecker B, Hveem K, et al. Development and validation of a protein-based risk score for cardiovascular outcomes among patients with stable coronary heart disease. JAMA. doi: 10.1001/jama.2016.5951 eTable 1. List of 1130 Proteins Measured by Somalogic’s Modified Aptamer-Based Proteomic Assay eTable 2. Coefficients for Weibull Recalibration Model Applied to 9-Protein Model eFigure 1. Median Protein Levels in Derivation and Validation Cohort eTable 3. Coefficients for the Recalibration Model Applied to Refit Framingham eFigure 2. Calibration Plots for the Refit Framingham Model eTable 4. List of 200 Proteins Associated With the Risk of MI, Stroke, Heart Failure, and Death eFigure 3. Hazard Ratios of Lasso Selected Proteins for Primary End Point of MI, Stroke, Heart Failure, and Death eFigure 4. 9-Protein Prognostic Model Hazard Ratios Adjusted for Framingham Variables eFigure 5. 9-Protein Risk Scores by Event Type This supplementary material has been provided by the authors to give readers additional information about their work. Downloaded From: https://jamanetwork.com/ on 10/02/2021 Supplemental Material Table of Contents 1 Study Design and Data Processing ......................................................................................................... 3 2 Table of 1130 Proteins Measured .......................................................................................................... 4 3 Variable Selection and Statistical Modeling ........................................................................................ -
Ssecks/Gravin/AKAP12 Attenuates Expression of Proliferative And
BMC Cancer BioMed Central Research article Open Access SSeCKS/Gravin/AKAP12 attenuates expression of proliferative and angiogenic genes during suppression of v-Src-induced oncogenesis Yongzhong Liu1, Lingqiu Gao2 and Irwin H Gelman*2 Address: 1Mucosal Immunology Unit, National Institutes of Health, Bethesda, MD 20892, USA and 2Department of Cancer Genetics, Roswell Park Cancer Institute, Buffalo, NY 14263, USA Email: Yongzhong Liu - [email protected]; Lingqiu Gao - [email protected]; Irwin H Gelman* - [email protected] * Corresponding author Published: 25 April 2006 Received: 24 January 2006 Accepted: 25 April 2006 BMC Cancer2006, 6:105 doi:10.1186/1471-2407-6-105 This article is available from: http://www.biomedcentral.com/1471-2407/6/105 © 2006Liu et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background: SSeCKS is a major protein kinase C substrate with kinase scaffolding and metastasis- suppressor activity whose expression is severely downregulated in Src- and Ras-transformed fibroblast and epithelial cells and in human prostate, breast, and gastric cancers. We previously used NIH3T3 cells with tetracycline-regulated SSeCKS expression plus a temperature-sensitive v-Src allele to show that SSeCKS re-expression inhibited parameters of v-Src-induced oncogenic growth without attenuating in vivo Src kinase activity. Methods: We use cDNA microarrays and semi-quantitative RT-PCR analysis to identify changes in gene expression correlating with i) SSeCKS expression in the absence of v-Src activity, ii) activation of v-Src activity alone, and iii) SSeCKS re-expression in the presence of active v-Src. -
Supplementary Table 2
Supplementary Table 2. Differentially Expressed Genes following Sham treatment relative to Untreated Controls Fold Change Accession Name Symbol 3 h 12 h NM_013121 CD28 antigen Cd28 12.82 BG665360 FMS-like tyrosine kinase 1 Flt1 9.63 NM_012701 Adrenergic receptor, beta 1 Adrb1 8.24 0.46 U20796 Nuclear receptor subfamily 1, group D, member 2 Nr1d2 7.22 NM_017116 Calpain 2 Capn2 6.41 BE097282 Guanine nucleotide binding protein, alpha 12 Gna12 6.21 NM_053328 Basic helix-loop-helix domain containing, class B2 Bhlhb2 5.79 NM_053831 Guanylate cyclase 2f Gucy2f 5.71 AW251703 Tumor necrosis factor receptor superfamily, member 12a Tnfrsf12a 5.57 NM_021691 Twist homolog 2 (Drosophila) Twist2 5.42 NM_133550 Fc receptor, IgE, low affinity II, alpha polypeptide Fcer2a 4.93 NM_031120 Signal sequence receptor, gamma Ssr3 4.84 NM_053544 Secreted frizzled-related protein 4 Sfrp4 4.73 NM_053910 Pleckstrin homology, Sec7 and coiled/coil domains 1 Pscd1 4.69 BE113233 Suppressor of cytokine signaling 2 Socs2 4.68 NM_053949 Potassium voltage-gated channel, subfamily H (eag- Kcnh2 4.60 related), member 2 NM_017305 Glutamate cysteine ligase, modifier subunit Gclm 4.59 NM_017309 Protein phospatase 3, regulatory subunit B, alpha Ppp3r1 4.54 isoform,type 1 NM_012765 5-hydroxytryptamine (serotonin) receptor 2C Htr2c 4.46 NM_017218 V-erb-b2 erythroblastic leukemia viral oncogene homolog Erbb3 4.42 3 (avian) AW918369 Zinc finger protein 191 Zfp191 4.38 NM_031034 Guanine nucleotide binding protein, alpha 12 Gna12 4.38 NM_017020 Interleukin 6 receptor Il6r 4.37 AJ002942 -
Trim24-Regulated Estrogen Response Is Dependent on Specific Histone Modifications in Breast Cancer Cells
The Texas Medical Center Library DigitalCommons@TMC The University of Texas MD Anderson Cancer Center UTHealth Graduate School of The University of Texas MD Anderson Cancer Biomedical Sciences Dissertations and Theses Center UTHealth Graduate School of (Open Access) Biomedical Sciences 12-2012 TRIM24-REGULATED ESTROGEN RESPONSE IS DEPENDENT ON SPECIFIC HISTONE MODIFICATIONS IN BREAST CANCER CELLS Teresa T. Yiu Follow this and additional works at: https://digitalcommons.library.tmc.edu/utgsbs_dissertations Part of the Biochemistry Commons, Cancer Biology Commons, Medicine and Health Sciences Commons, and the Molecular Biology Commons Recommended Citation Yiu, Teresa T., "TRIM24-REGULATED ESTROGEN RESPONSE IS DEPENDENT ON SPECIFIC HISTONE MODIFICATIONS IN BREAST CANCER CELLS" (2012). The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences Dissertations and Theses (Open Access). 313. https://digitalcommons.library.tmc.edu/utgsbs_dissertations/313 This Dissertation (PhD) is brought to you for free and open access by the The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences at DigitalCommons@TMC. It has been accepted for inclusion in The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences Dissertations and Theses (Open Access) by an authorized administrator of DigitalCommons@TMC. For more information, please contact [email protected]. TRIM24-REGULATED ESTROGEN RESPONSE IS DEPENDENT ON SPECIFIC HISTONE -
A Role for Glial Cell–Derived Neurotrophic Factor–Induced Expression by Inflammatory Cytokines and RET/GFRA1 Receptor Up-Regulation in Breast Cancer
Research Article A Role for Glial Cell–Derived Neurotrophic Factor–Induced Expression by Inflammatory Cytokines and RET/GFRA1 Receptor Up-regulation in Breast Cancer Selma Esseghir,1 S. Katrina Todd,1 Toby Hunt,2 Richard Poulsom,2 Ivan Plaza-Menacho,1 Jorge S. Reis-Filho,1 and Clare M. Isacke1 1Breakthrough Breast Cancer Research Centre, The Institute of Cancer Research and 2In Situ Hybridisation Service and Histopathology Unit, Cancer Research UK-London Research Institute, London, United Kingdom Abstract system homeostasis and the inflammatory response (3, 4) and in By screening a tissue microarray of invasive breast tumors, we tumor progression (5). The neurotrophic factor glial cell–derived have shown that the receptor tyrosine kinase RET (REar- neurotrophic factor (GDNF) was first identified for its trophic ranged during Transfection) and its coreceptor GFRA1(GDNF activity on midbrain dopaminergic neurons; however, GDNF has receptor family A-1) are overexpressed in a subset of estrogen subsequently been shown to have broader effects in regulating receptor–positive tumors. Germ line–activating oncogenic growth, survival, and migration of neurons in the brain, spinal cord, mutations in RET allow this receptor to signal independently and periphery as well as having an essential role in the growth and A branching of the ureteric buds of the developing kidney (6, 7). Mice of GFR 1and its ligand glial cell–derived neurotrophic factor Gdnf (GDNF) to promote a spectrum of endocrine neoplasias. with a homozygous deletion of die shortly after birth due to However, it is not known whether tumor progression can also severe defects in renal differentiation and the absence of an enteric nervous system (8, 9). -
Identification of Putative Causal Loci in Whole-Genome
ARTICLE https://doi.org/10.1038/s41467-021-22889-4 OPEN Identification of putative causal loci in whole- genome sequencing data via knockoff statistics ✉ Zihuai He 1,2 , Linxi Liu 3, Chen Wang 4, Yann Le Guen 1, Justin Lee2, Stephanie Gogarten 5, Fred Lu6, Stephen Montgomery 7,8, Hua Tang 6,7, Edwin K. Silverman9, Michael H. Cho 9, Michael Greicius1 & ✉ Iuliana Ionita-Laza4 The analysis of whole-genome sequencing studies is challenging due to the large number of 1234567890():,; rare variants in noncoding regions and the lack of natural units for testing. We propose a statistical method to detect and localize rare and common risk variants in whole-genome sequencing studies based on a recently developed knockoff framework. It can (1) prioritize causal variants over associations due to linkage disequilibrium thereby improving interpret- ability; (2) help distinguish the signal due to rare variants from shadow effects of significant common variants nearby; (3) integrate multiple knockoffs for improved power, stability, and reproducibility; and (4) flexibly incorporate state-of-the-art and future association tests to achieve the benefits proposed here. In applications to whole-genome sequencing data from the Alzheimer’s Disease Sequencing Project (ADSP) and COPDGene samples from NHLBI Trans-Omics for Precision Medicine (TOPMed) Program we show that our method com- pared with conventional association tests can lead to substantially more discoveries. 1 Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA, USA. 2 Quantitative Sciences Unit, Department of Medicine, Stanford University, Stanford, CA, USA. 3 Department of Statistics, Columbia University, New York, NY, USA. 4 Department of Biostatistics, Columbia University, New York, NY, USA.