Anti-UNC5C (Aa 88-117) Polyclonal Antibody (DPABH-05511) This Product Is for Research Use Only and Is Not Intended for Diagnostic Use

Total Page：16

File Type：pdf, Size：1020Kb

Anti-UNC5C (aa 88-117) polyclonal antibody (DPABH-05511) This product is for research use only and is not intended for diagnostic use. PRODUCT INFORMATION Antigen Description Receptor for netrin required for axon guidance. Mediates axon repulsion of neuronal growth cones in the developing nervous system upon ligand binding. Axon repulsion in growth cones may be caused by its association with DCC that may trigger signaling for repulsion. Also involved in corticospinal tract axon guidances independently of DCC. It also acts as a dependence receptor required for apoptosis induction when not associated with netrin ligand. Immunogen Synthetic peptide conjugated to KLH, corresponding to a region within N terminal amino acids 88-117 of Human UNC5C (NP_003719.2). Isotype IgG Source/Host Rabbit Species Reactivity Human Purification Immunogen affinity purified Conjugate Unconjugated Applications WB Format Liquid Size 400 μl Buffer Constituent: 99% PBS Preservative 0.09% Sodium Azide Storage Store at 4°C. Aliquot and store at -20°C long-term. GENE INFORMATION Gene Name UNC5C unc-5 homolog C (C. elegans) [ Homo sapiens ] Official Symbol UNC5C Synonyms UNC5C; unc-5 homolog C (C. elegans); unc5 (C.elegans homolog) c; netrin receptor UNC5C; 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 1 © Creative Diagnostics All Rights Reserved unc-5 homolog 3; protein unc-5 homolog 3; protein unc-5 homolog C; UNC5H3; Entrez Gene ID 8633 Protein Refseq NP_003719 UniProt ID A8K385 Chromosome Location 4q21-q23 Pathway Axon guidance; Developmental Biology; Netrin mediated repulsion signals; Netrin-1 signaling; Function netrin receptor activity; receptor activity; 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 2 © Creative Diagnostics All Rights Reserved.

Copy Link

Recommended publications

The Identification of Chromosomal Translocation, T(4;6)(Q22;Q15), In
The identification of chromosomal translocation, t(4;6)(q22;q15), in prostate cancer Yong-Jie Lu, Ling Shan, Laurence Ambroisine, Jeremy Clark, Rafael Yáñez-Muñoz, Gabrielle Fisher, Sakunthala Kudahetti, Jin-Shu Yang, Sanam Kia, Xueying Mao, et al. To cite this version: Yong-Jie Lu, Ling Shan, Laurence Ambroisine, Jeremy Clark, Rafael Yáñez-Muñoz, et al.. The identification of chromosomal translocation, t(4;6)(q22;q15), in prostate cancer. Prostate Cancer and Prostatic Diseases, Nature Publishing Group, 2010, n/a (n/a), pp.n/a-n/a. 10.1038/pcan.2010.2. hal-00510976 HAL Id: hal-00510976 https://hal.archives-ouvertes.fr/hal-00510976 Submitted on 23 Aug 2010 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. The identification of chromosomal translocation, t(4;6)(q22;q15), in prostate cancer L Shan1, L Ambroisine2, J Clark3, RJ Yáñez-Muñoz1, G Fisher2, SC Kudahetti1, J Yang1, S Kia1, X Mao1, A Fletcher3, P Flohr3, S Edwards3, G Attard3, J De- Bono3, BD Young1, CS Foster4, V Reuter5, H Moller6, TD Oliver1, DM Berney1, P Scardino7, J Cuzick2, CS Cooper3,
[Show full text]
Novel Candidate Genes of Thyroid Tumourigenesis Identified in Trk-T1 Transgenic Mice
Endocrine-Related Cancer (2012) 19 409–421 Novel candidate genes of thyroid tumourigenesis identified in Trk-T1 transgenic mice Katrin-Janine Heiliger*, Julia Hess*, Donata Vitagliano1, Paolo Salerno1, Herbert Braselmann, Giuliana Salvatore 2, Clara Ugolini 3, Isolde Summerer 4, Tatjana Bogdanova5, Kristian Unger 6, Gerry Thomas6, Massimo Santoro1 and Horst Zitzelsberger Research Unit of Radiation Cytogenetics, Helmholtz Zentrum Mu¨nchen, Ingolsta¨dter Landstr. 1, 85764 Neuherberg, Germany 1Istituto di Endocrinologia ed Oncologia Sperimentale del CNR, c/o Dipartimento di Biologia e Patologia Cellulare e Molecolare, Universita` Federico II, Naples 80131, Italy 2Dipartimento di Studi delle Istituzioni e dei Sistemi Territoriali, Universita` ‘Parthenope’, Naples 80133, Italy 3Division of Pathology, Department of Surgery, University of Pisa, 56100 Pisa, Italy 4Institute of Radiation Biology, Helmholtz Zentrum Mu¨nchen, 85764 Neuherberg, Germany 5Institute of Endocrinology and Metabolism, Academy of Medical Sciences of the Ukraine, 254114 Kiev, Ukraine 6Department of Surgery and Cancer, Imperial College London, Hammersmith Hospital, London W12 0HS, UK (Correspondence should be addressed to H Zitzelsberger; Email: [email protected]) *(K-J Heiliger and J Hess contributed equally to this work) Abstract For an identification of novel candidate genes in thyroid tumourigenesis, we have investigated gene copy number changes in a Trk-T1 transgenic mouse model of thyroid neoplasia. For this aim, 30 thyroid tumours from Trk-T1 transgenics were investigated by comparative genomic hybridisation. Recurrent gene copy number alterations were identified and genes located in the altered chromosomal regions were analysed by Gene Ontology term enrichment analysis in order to reveal gene functions potentially associated with thyroid tumourigenesis. In thyroid neoplasms from Trk-T1 mice, a recurrent gain on chromosomal bands 1C4–E2.3 (10.0% of cases), and losses on 3H1–H3 (13.3%), 4D2.3–E2 (43.3%) and 14E4–E5 (6.7%) were identified.
[Show full text]
Human Induced Pluripotent Stem Cell–Derived Podocytes Mature Into Vascularized Glomeruli Upon Experimental Transplantation
BASIC RESEARCH www.jasn.org Human Induced Pluripotent Stem Cell–Derived Podocytes Mature into Vascularized Glomeruli upon Experimental Transplantation † Sazia Sharmin,* Atsuhiro Taguchi,* Yusuke Kaku,* Yasuhiro Yoshimura,* Tomoko Ohmori,* ‡ † ‡ Tetsushi Sakuma, Masashi Mukoyama, Takashi Yamamoto, Hidetake Kurihara,§ and | Ryuichi Nishinakamura* *Department of Kidney Development, Institute of Molecular Embryology and Genetics, and †Department of Nephrology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan; ‡Department of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University, Hiroshima, Japan; §Division of Anatomy, Juntendo University School of Medicine, Tokyo, Japan; and |Japan Science and Technology Agency, CREST, Kumamoto, Japan ABSTRACT Glomerular podocytes express proteins, such as nephrin, that constitute the slit diaphragm, thereby contributing to the ﬁltration process in the kidney. Glomerular development has been analyzed mainly in mice, whereas analysis of human kidney development has been minimal because of limited access to embryonic kidneys. We previously reported the induction of three-dimensional primordial glomeruli from human induced pluripotent stem (iPS) cells. Here, using transcription activator–like effector nuclease-mediated homologous recombination, we generated human iPS cell lines that express green ﬂuorescent protein (GFP) in the NPHS1 locus, which encodes nephrin, and we show that GFP expression facilitated accurate visualization of nephrin-positive podocyte formation in
[Show full text]
Neurology Genetics
An Official Journal of the American Academy of Neurology Neurology.org/ng • Online ISSN: 2376-7839 Volume 3, Number 4, August 2017 Genetics Functionally pathogenic ExACtly zero or once: Clinical and experimental EARS2 variants in vitro A clinically helpful guide studies of a novel P525R may not manifest a to assessing genetic FUS mutation in amyotrophic phenotype in vivo variants in mild epilepsies lateral sclerosis Table of Contents Neurology.org/ng Online ISSN: 2376-7839 Volume 3, Number 4, August 2017 THE HELIX e171 Autopsy case of the C12orf65 mutation in a patient e175 What does phenotype have to do with it? with signs of mitochondrial dysfunction S.M. Pulst H. Nishihara, M. Omoto, M. Takao, Y. Higuchi, M. Koga, M. Kawai, H. Kawano, E. Ikeda, H. Takashima, and T. Kanda EDITORIAL e173 This variant alters protein function, but is it pathogenic? M. Pandolfo e174 Prevalence of spinocerebellar ataxia 36 in a US Companion article, e162 population J.M. Valera, T. Diaz, L.E. Petty, B. Quintáns, Z. Yáñez, ARTICLES E. Boerwinkle, D. Muzny, D. Akhmedov, R. Berdeaux, e162 Functionally pathogenic EARS2 variants in vitro may M.J. Sobrido, R. Gibbs, J.R. Lupski, D.H. Geschwind, not manifest a phenotype in vivo S. Perlman, J.E. Below, and B.L. Fogel N. McNeill, A. Nasca, A. Reyes, B. Lemoine, B. Cantarel, A. Vanderver, R. Schiffmann, and D. Ghezzi Editorial, e173 e170 Loss-of-function variants of SCN8A in intellectual disability without seizures e163 ExACtly zero or once: A clinically helpful guide to J.L. Wagnon, B.S. Barker, M.
[Show full text]
Identifying Novel Unc5b Interacting Partners to Understand Its Function in Cns White Matter
IDENTIFYING NOVEL UNC5B INTERACTING PARTNERS TO UNDERSTAND ITS FUNCTION IN CNS WHITE MATTER SAMUEL CLÉMOT-DUPONT February 2020 Integrated Program in Neuroscience Department of Neurology and Neurosurgery Montreal Neurological Institute Montreal, Quebec A Thesis submitted to McGill University in partial fulfillment of the requirements for the degree of Master of Science © Samuel Clémot-DuPont 2020 Table of Contents ACKNOWLEDGEMENTS ........................................................................................................................... 3 ABSTRACT ................................................................................................................................................ 5 RÉSUMÉ ................................................................................................................................................... 6 AUTHOR CONTRIBUTIONS ...................................................................................................................... 7 INTRODUCTION ....................................................................................................................................... 8 GENERAL LITERATURE REVIEW ............................................................................................................. 10 The UNC5 family of proteins ............................................................................................................. 12 1.1. First Descriptions of the UNC5 family ..............................................................................
[Show full text]
Statistical and Bioinformatic Analysis of Hemimethylation Patterns in Non-Small Cell Lung Cancer Shuying Sun1* , Austin Zane2, Carolyn Fulton3 and Jasmine Philipoom4
Sun et al. BMC Cancer (2021) 21:268 https://doi.org/10.1186/s12885-021-07990-7 RESEARCH ARTICLE Open Access Statistical and bioinformatic analysis of hemimethylation patterns in non-small cell lung cancer Shuying Sun1* , Austin Zane2, Carolyn Fulton3 and Jasmine Philipoom4 Abstract Background: DNA methylation is an epigenetic event involving the addition of a methyl-group to a cytosine- guanine base pair (i.e., CpG site). It is associated with different cancers. Our research focuses on studying non-small cell lung cancer hemimethylation, which refers to methylation occurring on only one of the two DNA strands. Many studies often assume that methylation occurs on both DNA strands at a CpG site. However, recent publications show the existence of hemimethylation and its significant impact. Therefore, it is important to identify cancer hemimethylation patterns. Methods: In this paper, we use the Wilcoxon signed rank test to identify hemimethylated CpG sites based on publicly available non-small cell lung cancer methylation sequencing data. We then identify two types of hemimethylated CpG clusters, regular and polarity clusters, and genes with large numbers of hemimethylated sites. Highly hemimethylated genes are then studied for their biological interactions using available bioinformatics tools. Results: In this paper, we have conducted the first-ever investigation of hemimethylation in lung cancer. Our results show that hemimethylation does exist in lung cells either as singletons or clusters. Most clusters contain only two or three CpG sites. Polarity clusters are much shorter than regular clusters and appear less frequently. The majority of clusters found in tumor samples have no overlap with clusters found in normal samples, and vice versa.
[Show full text]
Peripheral Nerve Single-Cell Analysis Identifies Mesenchymal Ligands That Promote Axonal Growth
Research Article: New Research Development Peripheral Nerve Single-Cell Analysis Identifies Mesenchymal Ligands that Promote Axonal Growth Jeremy S. Toma,1 Konstantina Karamboulas,1,ª Matthew J. Carr,1,2,ª Adelaida Kolaj,1,3 Scott A. Yuzwa,1 Neemat Mahmud,1,3 Mekayla A. Storer,1 David R. Kaplan,1,2,4 and Freda D. Miller1,2,3,4 https://doi.org/10.1523/ENEURO.0066-20.2020 1Program in Neurosciences and Mental Health, Hospital for Sick Children, 555 University Avenue, Toronto, Ontario M5G 1X8, Canada, 2Institute of Medical Sciences University of Toronto, Toronto, Ontario M5G 1A8, Canada, 3Department of Physiology, University of Toronto, Toronto, Ontario M5G 1A8, Canada, and 4Department of Molecular Genetics, University of Toronto, Toronto, Ontario M5G 1A8, Canada Abstract Peripheral nerves provide a supportive growth environment for developing and regenerating axons and are es- sential for maintenance and repair of many non-neural tissues. This capacity has largely been ascribed to paracrine factors secreted by nerve-resident Schwann cells. Here, we used single-cell transcriptional profiling to identify ligands made by different injured rodent nerve cell types and have combined this with cell-surface mass spectrometry to computationally model potential paracrine interactions with peripheral neurons. These analyses show that peripheral nerves make many ligands predicted to act on peripheral and CNS neurons, in- cluding known and previously uncharacterized ligands. While Schwann cells are an important ligand source within injured nerves, more than half of the predicted ligands are made by nerve-resident mesenchymal cells, including the endoneurial cells most closely associated with peripheral axons. At least three of these mesen- chymal ligands, ANGPT1, CCL11, and VEGFC, promote growth when locally applied on sympathetic axons.
[Show full text]
Downloaded from the European Nucleotide Archive (ENA; 126
Preprints (www.preprints.org) | NOT PEER-REVIEWED | Posted: 5 September 2018 doi:10.20944/preprints201809.0082.v1 1 Article 2 Transcriptomics as precision medicine to classify in 3 vivo models of dietary-induced atherosclerosis at 4 cellular and molecular levels 5 Alexei Evsikov 1,2, Caralina Marín de Evsikova 1,2* 6 1 Epigenetics & Functional Genomics Laboratory, Department of Molecular Medicine, Morsani College of 7 Medicine, University of South Florida, Tampa, Florida, 33612, USA; 8 2 Department of Research and Development, Bay Pines Veteran Administration Healthcare System, Bay 9 Pines, FL 33744, USA 10 11 * Correspondence: [email protected]; Tel.: +1-813-974-2248 12 13 Abstract: The central promise of personalized medicine is individualized treatments that target 14 molecular mechanisms underlying the physiological changes and symptoms arising from disease. 15 We demonstrate a bioinformatics analysis pipeline as a proof-of-principle to test the feasibility and 16 practicality of comparative transcriptomics to classify two of the most popular in vivo diet-induced 17 models of coronary atherosclerosis, apolipoprotein E null mice and New Zealand White rabbits. 18 Transcriptomics analyses indicate the two models extensively share dysregulated genes albeit with 19 some unique pathways. For instance, while both models have alterations in the mitochondrion, the 20 biochemical pathway analysis revealed, Complex IV in the electron transfer chain is higher in mice, 21 whereas the rest of the electron transfer chain components are higher in the rabbits. Several fatty 22 acids anabolic pathways are expressed higher in mice, whereas fatty acids and lipids degradation 23 pathways are higher in rabbits.
[Show full text]
UNC5C Antibody (N-Term) Affinity Purified Rabbit Polyclonal Antibody (Pab) Catalog # Ap19910a
10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 UNC5C Antibody (N-term) Affinity Purified Rabbit Polyclonal Antibody (Pab) Catalog # AP19910a Specification UNC5C Antibody (N-term) - Product Information Application WB,E Primary Accession O95185 Other Accession NP_003719.2 Reactivity Human Host Rabbit Clonality Polyclonal Isotype Rabbit Ig Calculated MW 103146 Antigen Region 88-117 UNC5C Antibody (N-term) - Additional Information UNC5C Antibody (N-term) (Cat. #AP19910a) Gene ID 8633 western blot analysis in CEM cell line lysates (35ug/lane).This demonstrates the UNC5C Other Names Netrin receptor UNC5C, Protein unc-5 antibody detected the UNC5C protein homolog 3, Protein unc-5 homolog C, (arrow). UNC5C, UNC5H3 Target/Specificity This UNC5C antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 88-117 amino acids from the N-terminal region of human UNC5C. Dilution WB~~1:1000 Format Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. Anti-UNC5C Antibody (N-term) at 1:1000 Storage dilution + Jurkat whole cell lysate Maintain refrigerated at 2-8°C for up to 2 Lysates/proteins at 20 µg per lane. weeks. For long term storage store at -20°C Secondary Goat Anti-Rabbit IgG, (H+L), in small aliquots to prevent freeze-thaw Peroxidase conjugated at 1/10000 dilution. cycles. Predicted band size : 103 kDa Blocking/Dilution buffer: 5% NFDM/TBST. Precautions UNC5C Antibody (N-term) is for research Page 1/3 10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 use only and not for use in diagnostic or UNC5C Antibody (N-term) - Background therapeutic procedures.
[Show full text]
An Extracellular Biochemical Screen Reveals That Flrts and Unc5s Mediate
1 An extracellular biochemical screen reveals that FLRTs and Unc5s mediate 2 neuronal subtype recognition in the retina 3 4 5 Jasper J. Visser1, Yolanda Cheng1, Steven C. Perry1, Andrew B. Chastain1, Bayan Parsa1, Shatha S. Masri1, 6 Thomas A. Ray2, Jeremy N. Kay2, Woj M. Wojtowicz1* 7 8 1University of California Berkeley, Department of Molecular and Cell Biology, Berkeley, CA 94720 USA. 9 2Duke University School of Medicine, Departments of Neurobiology and Opthalmology, Durham, NC 10 27710 USA. 11 12 *Correspondence: [email protected] 13 The authors declare no competing interest. 14 15 16 17 1 18 Abstract 19 In the inner plexiform layer (IPL) of the mouse retina, ~70 neuronal subtypes organize their neurites into 20 an intricate laminar structure that underlies visual processing. To find recognition proteins involved in 21 lamination, we utilized microarray data from 13 subtypes to identify differentially-expressed 22 extracellular proteins and performed a high-throughput biochemical screen. We identified ~50 23 previously-unknown receptor-ligand pairs, including new interactions among members of the FLRT and 24 Unc5 families. These proteins show laminar-restricted IPL localization and induce attraction and/or 25 repulsion of retinal neurites in culture, placing them in ideal position to mediate laminar targeting. 26 Consistent with a repulsive role in arbor lamination, we observed complementary expression patterns 27 for one interaction pair, FLRT2-Unc5C, in vivo. Starburst amacrine cells and their synaptic partners, ON- 28 OFF direction-selective ganglion cells, express FLRT2 and are repelled by Unc5C. These data suggest that 29 a single molecular mechanism may have been co-opted by synaptic partners to ensure joint laminar 30 restriction.
[Show full text]
Rare Copy Number Variants and Congenital Heart Defects in the 22Q11.2 Deletion Syndrome
UC Davis UC Davis Previously Published Works Title Rare copy number variants and congenital heart defects in the 22q11.2 deletion syndrome. Permalink https://escholarship.org/uc/item/49g9k7pj Journal Human genetics, 135(3) ISSN 0340-6717 Authors Mlynarski, Elisabeth E Xie, Michael Taylor, Deanne et al. Publication Date 2016-03-01 DOI 10.1007/s00439-015-1623-9 Peer reviewed eScholarship.org Powered by the California Digital Library University of California Hum Genet DOI 10.1007/s00439-015-1623-9 ORIGINAL INVESTIGATION Rare copy number variants and congenital heart defects in the 22q11.2 deletion syndrome Elisabeth E. Mlynarski1 · Michael Xie2 · Deanne Taylor2 · Molly B. Sheridan1 · Tingwei Guo3 · Silvia E. Racedo3 · Donna M. McDonald‑McGinn1,4 · Eva W. C. Chow5 · Jacob Vorstman6 · Ann Swillen7 · Koen Devriendt7 · Jeroen Breckpot7 · Maria Cristina Digilio8 · Bruno Marino9 · Bruno Dallapiccola8 · Nicole Philip10 · Tony J. Simon11 · Amy E. Roberts12 · Małgorzata Piotrowicz13 · Carrie E. Bearden14 · Stephan Eliez15 · Doron Gothelf16,17 · Karlene Coleman18 · Wendy R. Kates19 · Marcella Devoto1,4,20,21 · Elaine Zackai1,4 · Damian Heine‑ Suñer22 · Elizabeth Goldmuntz4,23 · Anne S. Bassett5 · Bernice E. Morrow3 · Beverly S. Emanuel1,4 · The International Chromosome 22q11.2 Consortium Received: 16 October 2015 / Accepted: 8 December 2015 © Springer-Verlag Berlin Heidelberg 2016 Abstract The 22q11.2 deletion syndrome (22q11DS; defect (CHD), mostly of the conotruncal type, and/or velocardiofacial/DiGeorge syndrome; VCFS/DGS; MIM aortic arch defect. The etiology of the cardiac pheno- #192430; 188400) is the most common microdeletion typic variability is not currently known for the major- syndrome. The phenotypic presentation of 22q11DS is ity of patients. We hypothesized that rare copy number highly variable; approximately 60–75 % of 22q11DS variants (CNVs) outside the 22q11.2 deleted region may patients have been reported to have a congenital heart modify the risk of being born with a CHD in this sen- sitized population.
[Show full text]
The Netrin-1 Receptors UNC5H Are Putative Tumor Suppressors Controlling Cell Death Commitment
The netrin-1 receptors UNC5H are putative tumor suppressors controlling cell death commitment Karine Thie´ bault*, Laetitia Mazelin*, Laurent Pays*, Fabien Llambi*, Marie-Odile Joly†, Jean-Yves Scoazec†, Jean-Christophe Saurin†, Giovanni Romeo‡§, and Patrick Mehlen*‡¶ *Apoptosis͞Differentiation Laboratory, Equipe Labelliseé la Ligue, Molecular and Cellular Genetic Center, Centre National de la Recherche Scientifique, Unite´Mixte de Recherche 5534, University of Lyon, 69622 Villeurbanne, France; †Edouard Herriot Hospital, 69437 Lyon, France; ‡International Agency for Research in Cancer, 69008 Lyon, France; and §Laboratorio di Genetica Medica dell’Universita`di Bologna, Policlinico S. Orsola-Malpighi, 40138 Bologna, Italy Edited by Michael H. Wigler, Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, and approved January 24, 2003 (received for review December 30, 2002) The three mammalian receptors UNC5H1, UNC5H2, and UNC5H3 11, L.M., C. Bidaud-Bonot, J.-Y.S., and P.M., unpublished work). (also named UNC5A, UNC5B, and UNC5C in human) that belong to Interestingly, netrin-1 is a ligand for other receptors that belong to the family of the netrin-1 receptors, UNC5H, were initially pro- the dependence receptor family (17). Thus, the netrin-1 receptors posed as mediators of the chemorepulsive effect of netrin-1 on UNC5H1, UNC5H2, and UNC5H3 that are type 1 transmembrane specific axons. However, they were also recently shown to act as receptors probably mediate the chemorepulsive activity of netrin-1 dependence receptors. Such receptors induce apoptosis when (18, 19) but also drive cell death induction in the absence of netrin-1, unbound to their ligand. We show here that the expression of the the latter proapoptotic activity depending on the caspase cleavage human UNC5A, UNC5B, or UNC5C is down-regulated in multiple of these receptors and the conserved ‘‘death domain’’ located in the cancers including colorectal, breast, ovary, uterus, stomach, lung, C terminus of their intracellular domains (17, 20).
[Show full text]