Supplementary Table 2 1

Total Page:16

File Type:pdf, Size:1020Kb

Supplementary Table 2 1 J. Qian: Supplementary Table 2 1 Supplementary Table 2. Up-regulated genes in H6c7eR-Kr cells with signal log ratio >=2 Signal Unigene Log Ratio Gene Symbol Title Hs.104636 2 TULP2 tubby like protein 2 Hs.108080 2 CSRP1 cysteine and glycine-rich protein 1 solute carrier family 1 (glutamate/neutral amino Hs.323878 2 SLC1A4 acid transporter), member 4 Hs.172816 2 NRG1 neuregulin 1 Hs.376206 2 KLF4 Kruppel-like factor 4 (gut) serine (or cysteine) proteinase inhibitor, clade G Hs.384598 2 SERPING1 (C1 inhibitor), member 1, (angioedema, hereditary) Hs.123159 2 SPAG4 sperm associated antigen 4 Hs.132380 2 FAXDC1 fatty acid hydroxylase domain containing 1 Hs.9003 2 FLJ13868 hypothetical protein FLJ13868 Hs.80409 2 GADD45A growth arrest and DNA-damage-inducible, alpha Hs.284217 2 SDCCAG33 serologically defined colon cancer antigen 33 Hs.337774 2 ARHGEF2 rho/rac guanine nucleotide exchange factor (GEF) 2 Hs.51133 2 PTK6 PTK6 protein tyrosine kinase 6 Homo sapiens transcribed sequence with strong similarity to protein sp:P07478 (H.sapiens) TRY2_HUMAN Trypsin II precursor (Anionic Hs.447753 2 --- trypsinogen) v-maf musculoaponeurotic fibrosarcoma oncogene Hs.460889 2 MAFF homolog F (avian) Hs.47313 2 KIAA0258 KIAA0258 gene product Hs.31210 2 BCL3 B-cell CLL/lymphoma 3 Hs.94392 2.1 LOC51157 LDL induced EC protein Hs.146233 2.1 NEURL neuralized-like (Drosophila) Hs.376792 2.1 CDH4 cadherin 4, type 1, R-cadherin (retinal) Hs.296638 2.1 PLAB prostate differentiation factor Hs.370771 2.1 CDKN1A cyclin-dependent kinase inhibitor 1A (p21, Cip1) Hs.348802 2.1 NMA putative transmembrane protein Hs.100194 2.1 ALOX5AP arachidonate 5-lipoxygenase-activating protein Hs.301664 2.1 RPS6KA2 ribosomal protein S6 kinase, 90kDa, polypeptide 2 Hs.438862 2.1 EPS8L1 EPS8-like 1 Hs.83169 2.2 MMP1 matrix metalloproteinase 1 (interstitial collagenase) cytochrome P450, family 1, subfamily B, Hs.154654 2.2 CYP1B1 polypeptide 1 Hs.86947 2.2 ADAM8 a disintegrin and metalloproteinase domain 8 matrix metalloproteinase 3 (stromelysin 1, Hs.375129 2.2 MMP3 progelatinase) J. Qian: Supplementary Table 2 2 Hs.2030 2.2 THBD thrombomodulin Hs.512648 2.2 C6orf59 chromosome 6 open reading frame 59 Homo sapiens transcribed sequence with strong similarity to protein ref:NP_073729.1 (H.sapiens) microtubule-associated proteins 1A/1B light chain Hs.506947 2.2 --- 3 [Homo sapiens] Hs.73793 2.2 VEGF vascular endothelial growth factor Hs.435699 2.2 PRSS3 protease, serine, 3 (mesotrypsin) Hs.437647 2.2 FLJ10415 hypothetical protein FLJ10415 prostaglandin-endoperoxide synthase 2 Hs.196384 2.3 PTGS2 (prostaglandin G/H synthase and cyclooxygenase) Homo sapiens cDNA clone IMAGE:3880075, Hs.400876 2.3 --- partial cds Hs.81008 2.3 FLNB filamin B, beta (actin binding protein 278) Hs.103915 2.3 KIAA0346 KIAA0346 protein solute carrier family 1 (glutamate/neutral amino Hs.323878 2.3 SLC1A4 acid transporter), member 4 Hs.212892 2.3 PRLR prolactin receptor Hs.46679 2.3 C14orf34 chromosome 14 open reading frame 34 Hs.250632 2.3 FLJ11078 hypothetical protein FLJ11078 diphtheria toxin receptor (heparin-binding Hs.799 2.3 DTR epidermal growth factor-like growth factor) Hs.127826 2.3 EPOR erythropoietin receptor Hs.356061 2.3 MAP1LC3B microtubule-associated protein 1 light chain 3 beta Hs.65135 2.3 KIAA0913 KIAA0913 protein serine (or cysteine) proteinase inhibitor, clade B Hs.75716 2.3 SERPINB2 (ovalbumin), member 2 Hs.276916 2.3 NR1D1 nuclear receptor subfamily 1, group D, member 1 Hs.217754 2.3 FLJ22202 hypothetical protein FLJ22202 Hs.79432 2.4 FBN2 fibrillin 2 (congenital contractural arachnodactyly) Hs.73853 2.4 BMP2 bone morphogenetic protein 2 potassium voltage-gated channel, subfamily G, Hs.118695 2.4 KCNG1 member 1 Hs.155651 2.4 FOXA2 forkhead box A2 Hs.172851 2.4 ARG2 arginase, type II Hs.135183 2.4 CENTA1 centaurin, alpha 1 Hs.41502 2.4 C14orf139 chromosome 14 open reading frame 139 Hs.77768 2.4 DNAJB2 DnaJ (Hsp40) homolog, subfamily B, member 2 Hs.103527 2.4 SH2D2A SH2 domain protein 2A diphtheria toxin receptor (heparin-binding Hs.799 2.5 DTR epidermal growth factor-like growth factor) Hs.6846 2.5 LPPR2 lipid phosphate phosphatase-related protein type 2 J. Qian: Supplementary Table 2 3 Hs.126256 2.5 IL1B interleukin 1, beta Hs.246381 2.5 CD68 CD68 antigen Hs.73793 2.5 VEGF vascular endothelial growth factor chromobox homolog 4 (Pc class homolog, Hs.5637 2.5 CBX4 Drosophila) Hs.110571 2.5 GADD45B growth arrest and DNA-damage-inducible, beta wingless-type MMTV integration site family, Hs.512714 2.5 WNT7B member 7B Hs.126256 2.5 IL1B interleukin 1, beta Hs.232770 2.5 ALOXE3 arachidonate lipoxygenase 3 dolichyl-p-mannose:Man7GlcNAc2-PP-dolichyl Hs.77575 2.5 ALG12 mannosyltransferase Hs.128071 2.6 FLJ21302 hypothetical protein FLJ21302 Hs.446644 2.6 PSG1 pregnancy specific beta-1-glycoprotein 1 fucosyltransferase 3 (galactoside 3(4)-L- Hs.169238 2.7 FUT3 fucosyltransferase, Lewis blood group included) Hs.436943 2.7 SOCS3 suppressor of cytokine signaling 3 Hs.13011 2.7 GTPBP2 GTP binding protein 2 Hs.171003 2.8 CBS cystathionine-beta-synthase Hs.155109 2.9 HSD17B2 hydroxysteroid (17-beta) dehydrogenase 2 Hs.282209 3 PON1 paraoxonase 1 Hs.73853 3 BMP2 bone morphogenetic protein 2 Hs.73793 3.1 VEGF vascular endothelial growth factor Hs.110571 3.2 GADD45B growth arrest and DNA-damage-inducible, beta Hs.106070 3.2 CDKN1C cyclin-dependent kinase inhibitor 1C (p57, Kip2) Hs.171695 3.3 DUSP1 dual specificity phosphatase 1 Hs.321164 3.3 NPAS2 neuronal PAS domain protein 2 Hs.411311 3.4 IL24 interleukin 24 Hs.318567 3.5 NDRG1 N-myc downstream regulated gene 1 Hs.2258 3.5 MMP10 matrix metalloproteinase 10 (stromelysin 2) Hs.2050 3.5 PTX3 pentaxin-related gene, rapidly induced by IL-1 beta Hs.105434 3.6 ISG20 interferon stimulated gene 20kDa Hs.7972 3.7 RIPX rap2 interacting protein x solute carrier family 7 (cationic amino acid Hs.14846 3.7 SLC7A1 transporter, y+ system), member 1 Hs.417050 4 CCNA1 cyclin A1 nuclear factor of kappa light polypeptide gene Hs.73090 4.1 NFKB2 enhancer in B-cells 2 (p49/p100) Hs.336046 4.1 IL13RA2 interleukin 13 receptor, alpha 2 Hs.155651 4.2 FOXA2 forkhead box A2 Hs.419 4.4 DLX2 distal-less homeo box 2 J. Qian: Supplementary Table 2 4 Hs.66 4.4 IL1RL1 interleukin 1 receptor-like 1 death effector filament-forming Ced-4-like Hs.511937 4.6 DEFCAP apoptosis protein Hs.171695 4.9 DUSP1 dual specificity phosphatase 1 .
Recommended publications
  • Multiplex Diagnosis of Oncogenic Fusion and MET Exon Skipping by Molecular Counting Using Formalin-Fixed Paraffin Embedded Lung
    ORIGINAL ARTICLE Multiplex Diagnosis of Oncogenic Fusion and MET Exon Skipping by Molecular Counting Using Formalin-Fixed Paraffin Embedded Lung Adenocarcinoma Tissues Kuniko Sunami, MD,a,g Koh Furuta, MD, PhD,b Koji Tsuta, MD, PhD,c Shinji Sasada, MD, PhD,d Takehiro Izumo, MD, PhD,d Takashi Nakaoku, MD,a Yoko Shimada, MFSc,a Motonobu Saito, MD, PhD,a Hiroshi Nokihara, MD, PhD,e Shun-ichi Watanabe, MD, PhD,f Yuichiro Ohe, MD, PhD,e,g Takashi Kohno, PhDa,* aDivision of Genome Biology, National Cancer Center Research Institute, Tokyo, Japan bDivision of Clinical Laboratory, National Cancer Center Hospital, Tokyo, Japan cDivision of Pathology, National Cancer Center Research Institute, Tokyo, Japan dDepartment of Endoscopy, Respiratory Endoscopy Division, National Cancer Center Research Institute, Tokyo, Japan eDepartment of Thoracic Oncology, National Cancer Center Research Institute, Tokyo, Japan fDepartment of Thoracic Surgery, National Cancer Center Hospital, Tokyo, Japan gCourse of Advanced Clinical Research of Cancer, Juntendo University Graduate School of Medicine, Tokyo, Japan Received 31 July 2015; revised 23 September 2015; accepted 13 October 2015 ABSTRACT detected oncogenic fusions in bronchial lavage fluid and transbronchial biopsy samples. Introduction: Fusions of the anaplastic lymphoma receptor tyrosine kinase gene (ALK), ret proto-oncogene (RET), ROS Conclusions: The MC assay allows multiplex detection of proto-oncogene 1, receptor tyrosine kinase gene (ROS1), B- oncogenic fusion and exon-skipped transcripts in tumor Raf proto-oncogene, serine/threonine kinase gene (BRAF), samples, including in formalin-fixed paraffin-embedded and neuregulin 1 gene (NRG1) and intronic MMNG HOS samples obtained in the clinic. Transforming gene (MET) mutations are druggable onco- Ó 2015 International Association for the Study of Lung gene alterations in lung adenocarcinoma that cause Cancer.
    [Show full text]
  • Promoting Myelin Repair and Return of Function in Multiple Sclerosis
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector FEBS Letters 585 (2011) 3813–3820 journal homepage: www.FEBSLetters.org Review Promoting myelin repair and return of function in multiple sclerosis Jingya Zhang a,b,c, Elisabeth G. Kramer a,b,c, Linnea Asp a,b,c, Dipankar J. Dutta a,b,c, Kristina Navrazhina a,b,c, Trinh Pham a,b,c, John N. Mariani a,b,c, Azeb Tadesse Argaw a,b,c, Carmen V. Melendez-Vasquez d, ⇑ Gareth R. John a,b,c, a Corinne Goldsmith Dickinson Center for MS, Mount Sinai School of Medicine, 1 Gustave L. Levy Place, New York, NY 10029, USA b Department of Neurology, Mount Sinai School of Medicine, 1 Gustave L. Levy Place, New York, NY 10029, USA c Friedman Brain Institute, Mount Sinai School of Medicine, 1 Gustave L. Levy Place, New York, NY 10029, USA d Department of Biological Sciences, Hunter College, 695 Park Avenue, New York, NY 10065, USA article info abstract Article history: Multiple sclerosis (MS) is an inflammatory demyelinating disease of the CNS. Conduction block in Received 7 July 2011 demyelinated axons underlies early neurological symptoms, but axonal transection and neuronal Revised 8 August 2011 loss are believed to be responsible for more permanent chronic deficits. Several therapies are Accepted 9 August 2011 approved for treatment of relapsing-remitting MS, all of which are immunoregulatory and clinically Available online 18 August 2011 proven to reduce the rate of lesion formation and exacerbation. However, existing approaches are Edited by Richard Williams, Alexander only partially effective in preventing the onset of disability in MS patients, and novel treatments Flügel and Wilhelm Just to protect myelin-producing oligodendrocytes and enhance myelin repair may improve long-term outcomes.
    [Show full text]
  • Biomarker Testing in Non- Small Cell Lung Cancer (NSCLC)
    The biopharma business of Merck KGaA, Darmstadt, Germany operates as EMD Serono in the U.S. and Canada. Biomarker testing in non- small cell lung cancer (NSCLC) Copyright © 2020 EMD Serono, Inc. All rights reserved. US/TEP/1119/0018(1) Lung cancer in the US: Incidence, mortality, and survival Lung cancer is the second most common cancer diagnosed annually and the leading cause of mortality in the US.2 228,820 20.5% 57% Estimated newly 5-year Advanced or 1 survival rate1 metastatic at diagnosed cases in 2020 diagnosis1 5.8% 5-year relative 80-85% 2 135,720 survival with NSCLC distant disease1 Estimated deaths in 20201 2 NSCLC, non-small cell lung cancer; US, United States. 1. National Institutes of Health (NIH), National Cancer Institute. Cancer Stat Facts: Lung and Bronchus Cancer website. www.seer.cancer.gov/statfacts/html/lungb.html. Accessed May 20, 2020. 2. American Cancer Society. What is Lung Cancer? website. https://www.cancer.org/cancer/non-small-cell-lung-cancer/about/what-is-non-small-cell-lung-cancer.html. Accessed May 20, 2020. NSCLC is both histologically and genetically diverse 1-3 NSCLC distribution by histology Prevalence of genetic alterations in NSCLC4 PTEN 10% DDR2 3% OTHER 25% PIK3CA 12% LARGE CELL CARCINOMA 10% FGFR1 20% SQUAMOUS CELL CARCINOMA 25% Oncogenic drivers in adenocarcinoma Other or ADENOCARCINOMA HER2 1.9% 40% KRAS 25.5% wild type RET 0.7% 55% NTRK1 1.7% ROS1 1.7% Oncogenic drivers in 0% 20% 40% 60% RIT1 2.2% squamous cell carcinoma Adenocarcinoma DDR2 2.9% Squamous cell carcinoma NRG1 3.2% Large cell carcinoma
    [Show full text]
  • Angiocrine Endothelium: from Physiology to Cancer Jennifer Pasquier1,2*, Pegah Ghiabi2, Lotf Chouchane3,4,5, Kais Razzouk1, Shahin Rafi3 and Arash Rafi1,2,3
    Pasquier et al. J Transl Med (2020) 18:52 https://doi.org/10.1186/s12967-020-02244-9 Journal of Translational Medicine REVIEW Open Access Angiocrine endothelium: from physiology to cancer Jennifer Pasquier1,2*, Pegah Ghiabi2, Lotf Chouchane3,4,5, Kais Razzouk1, Shahin Rafi3 and Arash Rafi1,2,3 Abstract The concept of cancer as a cell-autonomous disease has been challenged by the wealth of knowledge gathered in the past decades on the importance of tumor microenvironment (TM) in cancer progression and metastasis. The sig- nifcance of endothelial cells (ECs) in this scenario was initially attributed to their role in vasculogenesis and angiogen- esis that is critical for tumor initiation and growth. Nevertheless, the identifcation of endothelial-derived angiocrine factors illustrated an alternative non-angiogenic function of ECs contributing to both physiological and pathological tissue development. Gene expression profling studies have demonstrated distinctive expression patterns in tumor- associated endothelial cells that imply a bilateral crosstalk between tumor and its endothelium. Recently, some of the molecular determinants of this reciprocal interaction have been identifed which are considered as potential targets for developing novel anti-angiocrine therapeutic strategies. Keywords: Angiocrine, Endothelium, Cancer, Cancer microenvironment, Angiogenesis Introduction of blood vessels in initiation of tumor growth and stated Metastatic disease accounts for about 90% of patient that in the absence of such angiogenesis, tumors can- mortality. Te difculty in controlling and eradicating not expand their mass or display a metastatic phenotype metastasis might be related to the heterotypic interaction [7]. Based on this theory, many investigators assumed of tumor and its microenvironment [1].
    [Show full text]
  • Differential Expression of Neuregulin-1 Isoforms and Downregulation of Erbin Are Associated with Erb B2 Receptor Activation in Diabetic Peripheral Neuropathy
    Differential expression of neuregulin-1 isoforms and downregulation of erbin are associated with Erb B2 receptor activation in diabetic peripheral neuropathy By Pan Pan Submitted to the graduate degree program in Pharmacology and Toxicology and the Graduate Faculty of the University of Kansas in partial fulfillment of the requirements for the degree of Doctor of Philosophy. ______________________________ Rick T. Dobrowsky, Ph.D., Chairperson _______________________________ Jeff Staudinger, Ph.D. _______________________________ Alexander Moise, Ph.D. _______________________________ Honglian Shi. Ph.D. ________________________________ Brian Ackley, Ph.D. Date Defended: April 18th The Dissertation Committee for Pan Pan certifies that this is the approved version of the following dissertation: Differential expression of neuregulin-1 isoforms and downregulation of erbin are associated with Erb B2 receptor activation in diabetic peripheral neuropathy By Pan Pan _______________________________ Rick T. Dobrowsky, Ph.D., Chairperson th Date approved: April 18 ii Table of Contents Table of Contents ......................................................................................................................... iii Abstract ......................................................................................................................................... vi Acknowledgements ..................................................................................................................... vii List of Tables and Figures ..........................................................................................................
    [Show full text]
  • Tumorigenic Proteins Upregulated in the MYCN-Amplified IMR-32 Human Neuroblastoma Cells Promote Proliferation and Migration
    INTERNATIONAL JOURNAL OF ONCOLOGY 52: 787-803, 2018 Tumorigenic proteins upregulated in the MYCN-amplified IMR-32 human neuroblastoma cells promote proliferation and migration HAYAT ZAATITI1*, JAD ABDALLAH2*, ZEINA NASR1, GEORGE KHAZEN3, ANTHONY SANDLER4 and TAMARA J. ABOU-ANTOUN2 1Department of Biology, Faculty of Sciences, University of Balamand, El-Koura; 2Department of Pharmaceutical Sciences, School of Pharmacy, and 3School of Arts and Sciences, Lebanese American University, Byblos 1102-2801, Lebanon; 4Sheikh Zayed Institute for Pediatric Surgical Innovation, Joseph E. Robert Jr. Center for Surgical Care, Children's National Medical Center, Washington, DC 20010, USA Received September 20, 2017; Accepted December 5, 2017 DOI: 10.3892/ijo.2018.4236 Abstract. Childhood neuroblastoma is one of the most and non-MYCN-amplified SK-N-SH human neuroblastoma common types of extra-cranial cancer affecting children with cells. Tumorigenic proteins, including fatty-acid binding a clinical spectrum ranging from spontaneous regression to protein 5 (FABP5), L1-cell adhesion molecule (L1-CAM), bacu- malignant and fatal progression. In order to improve the clin- loviral IAP repeat containing 5 [BIRC5 (survivin)] and high ical outcomes of children with high-risk neuroblastoma, it is mobility group protein A1 (HMGA1) were found to be signifi- crucial to understand the tumorigenic mechanisms that govern cantly upregulated in the IMR-32 compared to the SK-N-SH its malignant behaviors. MYCN proto-oncogene, bHLH tran- cells and mapped to highly tumorigenic pathways including, scription factor (MYCN) amplification has been implicated in MYC, MYCN, microtubule associated protein Tau (MAPT), the malignant, treatment-evasive nature of aggressive, high- E2F transcription factor 1 (E2F1), sterol regulatory element risk neuroblastoma.
    [Show full text]
  • General Summary
    Molecular Psychiatry (2004) 9,2–4 & 2004 Nature Publishing Group All rights reserved 1359-4184/04 $25.00 www.nature.com/mp General Summary A Midei and J Licinio UCLA, Los Angeles, CA, USA Molecular Psychiatry (2004) 9, 2–4. doi:10.1038/sj.mp.4001454 SCIENTIFIC CORRESPONDENCE phenotype has made the task of identifying suscept- ibility genes difficult. Fortunately, there are now signs Polymorphisms within 50 end of the Neuregulin 1 of real progress. Studies of genetic linkage and gene are genetically associated with schizophrenia in chromosomal abnormalities in schizophrenia have the Chinese population implicated a number of chromosomal regions. Re- JX Tang, WY Chen, G He, J Zhou, NF Gu, GY Feng, cently, evidence implicating individual genes within LHe some of the linked regions has been reported and more importantly replicated. These findings and their The 8p gene Neuregulin 1, which is one of the glial implications are reviewed. growth factors expressed during neurodevelopment and in the adult CNS, has recently been identified as a IMMEDIATE COMMUNICATION susceptibility gene for schizophrenia by linkage and LD mapping studies in the Icelandic and Scottish Association of estrogen receptor b gene polymorph- population. In the present work, the authors provide isms with bulimic disease in women independent statistical support for the previous ´ 0 M Nilsson, S Naessen, I Dahlman, AL Hirschberg, findings that schizophrenia is associated with the 5 J-A˚ Gustafsson, K Dahlman-Wright end of the Neuregulin 1 gene. The potential association between estrogen receptor b (ERb) and disease was explored in a group of bulimic HERV-W-related RNA detected in plasma from women.
    [Show full text]
  • Hirschsprung's Disease and Variants in Genes That Regulate Enteric Neural Crest Cell Proliferation, Migration and Differentiation
    Journal of Human Genetics (2012) 57, 485–493 & 2012 The Japan Society of Human Genetics All rights reserved 1434-5161/12 $32.00 www.nature.com/jhg ORIGINAL ARTICLE Hirschsprung’s disease and variants in genes that regulate enteric neural crest cell proliferation, migration and differentiation Tonia C Carter1, Denise M Kay2, Marilyn L Browne3,4, Aiyi Liu1, Paul A Romitti5, Devon Kuehn1, Mary R Conley1, Michele Caggana2, Charlotte M Druschel3,4, Lawrence C Brody6 and James L Mills1 Hirschsprung’s disease (HSCR) results from failed colonization of the embryonic gut by enteric neural crest cells (ENCCs); colonization requires RET proto-oncogene (RET) signaling. We sequenced RET to identify coding and splice-site variants in a population-based case group and we tested for associations between HSCR and common variants in RET and candidate genes (ASCL1, homeobox B5 (HOXB5), L1 cell adhesion molecule (L1CAM), paired-like homeobox 2b (PHOX2B), PROK1 and PROKR1) chosen because they are involved in ENCC proliferation, migration and differentiation in animal models. We conducted a nested case–control study of 304 HSCR cases and 1215 controls. Among 38 (12.5%) cases with 34 RET coding and splice-site variants, 18 variants were previously unreported. We confirmed associations with common variants in HOXB5 and PHOX2B but the associations with variants in ASCL1, L1CAM and PROK1 were not significant after multiple comparisons adjustment. RET variants were strongly associated with HSCR (P-values between 10 À3 and 10 À31) but this differed by race/ethnicity: associations were absent in African-Americans. Our population-based study not only identified novel RET variants in HSCR cases, it showed that common RET variants may not contribute to HSCR in all race/ethnic groups.
    [Show full text]
  • Activated K Channels in Parasympathetic Neurons
    ␤-Neuregulin-1 is required for the in vivo development of functional Ca2؉-activated K؉ channels in parasympathetic neurons Jill S. Cameron, Laurence Dryer, and Stuart E. Dryer* Department of Biology and Biochemistry, University of Houston, Houston, TX 77204-5513 Edited by Eric M. Shooter, Stanford University School of Medicine, Stanford, CA, and approved December 21, 2000 (received for review August 17, 2000) 2؉ ؉ The development of functional Ca -activated K channels (KCa)in are expressed in the chick Edinger–Westphal nucleus, the source chick ciliary ganglion (CG) neurons requires interactions with of midbrain preganglionic neurons that innervate the CG (20). afferent preganglionic nerve terminals. Here we show that the Second, functional erbB receptors are expressed in chick CG essential preganglionic differentiation factor is an isoform of neurons (20). Finally, application of recombinant ␤-NEU1 can ␤ ␤ -neuregulin-1. -Neuregulin-1 transcripts are expressed in the increase the density of functional KCa in cultured CG neurons, midbrain preganglionic Edinger–Westphal nucleus at developmen- at least at high concentrations (21). However, this effect also can tal stages that coincide with or precede the normal onset of be evoked by high concentrations of other erbB ligands such as ␤ macroscopic KCa in CG neurons. Injection of -neuregulin-1 peptide EGF and transforming growth factor ␣ (TGF␣), but not by into the brains of developing embryos evoked a robust stimulation ␣-neuregulin (21). In addition, it is not known whether ␤-Neu1 of functional KCa channels at stages before the normal appearance transcripts are expressed in the Edinger–Westphal nucleus at of these channels in CG neurons developing in vivo.
    [Show full text]
  • Revisiting the Role of Neurotrophic Factors in Inflammation
    cells Review Revisiting the Role of Neurotrophic Factors in Inflammation Lucas Morel, Olivia Domingues, Jacques Zimmer and Tatiana Michel * Department of Infection and Immunity, Luxembourg Institute of Health, 29 rue Henri Koch, L-4354 Esch-sur Alzette, Luxembourg; [email protected] (L.M.); [email protected] (O.D.); [email protected] (J.Z.) * Correspondence: [email protected]; Tel.: +352-26970-264 Received: 6 March 2020; Accepted: 31 March 2020; Published: 2 April 2020 Abstract: The neurotrophic factors are well known for their implication in the growth and the survival of the central, sensory, enteric and parasympathetic nervous systems. Due to these properties, neurturin (NRTN) and Glial cell-derived neurotrophic factor (GDNF), which belong to the GDNF family ligands (GFLs), have been assessed in clinical trials as a treatment for neurodegenerative diseases like Parkinson’s disease. In addition, studies in favor of a functional role for GFLs outside the nervous system are accumulating. Thus, GFLs are present in several peripheral tissues, including digestive, respiratory, hematopoietic and urogenital systems, heart, blood, muscles and skin. More precisely, recent data have highlighted that different types of immune and epithelial cells (macrophages, T cells, such as, for example, mucosal-associated invariant T (MAIT) cells, innate lymphoid cells (ILC) 3, dendritic cells, mast cells, monocytes, bronchial epithelial cells, keratinocytes) have the capacity to release GFLs and express their receptors, leading to the participation in the repair of epithelial barrier damage after inflammation. Some of these mechanisms pass on to ILCs to produce cytokines (such as IL-22) that can impact gut microbiota.
    [Show full text]
  • Related Erbb4 Receptor in Obesity-Induced Hippocampal Abnormalities
    bioRxiv preprint doi: https://doi.org/10.1101/2021.06.30.450398; this version posted July 1, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. ORIGINAL RESEARCH ARTICLE Title: Early neuroadaptations to an obesogenic diet identify the schizophrenia- related ErbB4 receptor in obesity-induced hippocampal abnormalities Authors: Julio David Vega-Torres*1, Perla Ontiveros-Angel*1, Esmeralda Terrones1, Erwin C. Stuffle1, Sara Solak2, Emma Tyner2, Marie Oropeza2, Ike Dela Peña2, Andre Obenaus3, Byron D. Ford4, and Johnny D. Figueroa1 *Both authors contributed equally to this work Affiliations: 1Center for Health Disparities and Molecular Medicine and Department of Basic Sciences, Physiology Division, Department of Basic Sciences, Loma Linda University Health School of Medicine, Loma Linda, California, USA; 2Department of Pharmaceutical and Administrative Sciences, Loma Linda University Health School of Pharmacy, Loma Linda, California, USA; 3Department of Pediatrics, University of California-Irvine, Irvine, California, USA; 4Division of Biomedical Sciences, University of California-Riverside School of Medicine, Riverside, California, USA. Contributions: JDV: wrote manuscript, performed Western blot experiments and analyses; designed and performed behavioral experiments; POA: performed and analyzed ELISA and histological experiments, prepared illustrations, wrote manuscript; ET, ES: performed behavior analyses; SS, ET, MO: performed Western blot experiments; IDL: performed behavioral experiments; JDV, JDF: analyzed behavioral data; AO: performed MRI experiments and analyses; BF: contributed to experimental design and data interpretation, facilitated drugs used in the study; JDF: planned experiments, analyzed and interpreted data, wrote manuscript.
    [Show full text]
  • Neuregulin-1 Is Increased in Schizophrenia Patients with Chronic
    Schizophrenia Research 208 (2019) 473–474 Contents lists available at ScienceDirect Schizophrenia Research journal homepage: www.elsevier.com/locate/schres Letter to the Editor Neuregulin-1 is increased in schizophrenia As the distribution of continuous variables was not normal, Mann- patients with chronic cannabis abuse: Whitney U test was used to compare the group of chronically cannabis- Preliminary results abusing schizophrenia patients and the group of non-abusing patients. Neuregulin-1 was higher in the group of cannabis abusing schizophrenia patients (U = 462.5; p = 0.026) and members of this group were signif- Keywords: icantly younger (U = 482.0; p = 0.001), with a shorter duration of illness Neuregulin Neurotrophins (U = 534.0; p = 0.003). The two groups did not differ in PANSS total and Schizophrenia the three main subscales. The levels of BDNF, NGF and NRG-1 were not Cannabis correlated with PANSS, age or duration of illness. Cannabis consummation was more frequent in males (chi = 15.584; df = 1; p = 0.001). To the Editor, Logistic regression with cannabis consummation/non-consummation as the dependent variable and neurotrophicfactors,age,genderanddura- tion of illness were included in the model. Male gender, younger age and Plenty of studies have shown that cannabis increases the risk of de- higher values of NRG-1 were significant predictors of the model pre- veloping schizophrenia and that chronic cannabis abuse leads to prob- sented in Table 1. lems in learning, attention and a decrease in brain volume (Van Gastel Our results suggest that NRG-1 was increased in the group of chronic et al., 2014).
    [Show full text]