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CHL1 and Nrcam Are Primarily Expressed in Low Grade Pediatric
Open Med. 2019; 14: 920-927 Research Article Robin Wachowiak, Steffi Mayer, Anne Suttkus, Illya Martynov, Martin Lacher, Nathaniel Melling, Jakob R. Izbicki, Michael Tachezy CHL1 and NrCAM are primarily expressed in low grade pediatric neuroblastoma https://doi.org/10.1515/med-2019-0109 Keywords: CHL1; NrCAM; Neuroblastoma; Immunohisto- received November 7, 2018; accepted October 19, 2019 chemistry; Tumor markers; Neuropathology Abstract: Background. Neural cell adhesion molecules like close homolog of L1 protein (CHL1) and neuronal glia related cell adhesion molecule (NrCAM) play an impor- tant role in development and regeneration of the central 1 Introduction nervous system. However, they are also associated with Neuroblastoma is an embryonic malignancy deriving cancerogenesis and progression in adult malignancies, from neural crest cells that undergo rapid differentia- thus gain increasing importance in cancer research. We tion during fetal development. As the transition from therefore studied the expression of CHL1 and NrCAM normal to malignant tissue can occur in multiple steps, according to the course of disease in children with neu- its phenotype is highly heterogeneous [1]. Although pro- roblastoma. gress has been made in the treatment of neuroblastoma, Methods. CHL1 and NrCAM expression levels were histo- the outcome of children at high risk remains poor with a logically assessed by tissue microarrays from surgically long-term survival as low as 50 % [2]. Different parameters resected neuroblastoma specimens of 56 children. Expres- such as age, stage and chromosomal aberrations have an sion of both markers was correlated to demographics as impact on prognosis. Still, there is an ongoing need for well as clinical data including metastatic dissemination tumor markers, which allow a better determination of the and survival. -
Upregulation of NETO2 Gene in Colorectal Cancer Maria S
Fedorova et al. BMC Genetics 2017, 18(Suppl 1):117 DOI 10.1186/s12863-017-0581-8 RESEARCH Open Access Upregulation of NETO2 gene in colorectal cancer Maria S. Fedorova1†, Anastasiya V. Snezhkina1†, Elena A. Pudova1, Ivan S. Abramov1, Anastasiya V. Lipatova1, Sergey L. Kharitonov1, Asiya F. Sadritdinova1, Kirill M. Nyushko2, Kseniya M. Klimina3, Mikhail M. Belyakov2, Elena N. Slavnova2, Nataliya V. Melnikova1, Maria A. Chernichenko2, Dmitry V. Sidorov2, Marina V. Kiseleva2, Andrey D. Kaprin2, Boris Y. Alekseev2, Alexey A. Dmitriev1 and Anna V. Kudryavtseva1,2* From Belyaev Conference Novosibirsk, Russia. 07-10 August 2017 Abstract Background: Neuropilin and tolloid-like 2 (NETO2) is a single-pass transmembrane protein that has been shown primarily implicated in neuron-specific processes. Upregulation of NETO2 gene was also detected in several cancer types. In colorectal cancer (CRC), it was associated with tumor progression, invasion, and metastasis, and seems to be involved in epithelial-mesenchymal transition (EMT). However, the mechanism of NETO2 action is still poorly understood. Results: We have revealed significant increase in the expression of NETO2 gene and deregulation of eight EMT-related genes in CRC. Four of them were upregulated (TWIST1, SNAIL1, LEF1,andFOXA2); the mRNA levels of other genes (FOXA1, BMP2, BMP5,andSMAD7) were decreased. Expression of NETO2 gene was weakly correlated with that of genes involved in the EMT process. Conclusions: We found considerable NETO2 upregulation, but no significant correlation between the expression of NETO2 and EMT-related genes in CRC. Thus, NETO2 may be involved in CRC progression, but is not directly associated with EMT. Keywords: Colorectal cancer, NETO2, Epithelial-mesenchymal transition, Gene expression, QPCR Background and signaling pathways [3–6]. -
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. -
Supplementary Table 1: Adhesion Genes Data Set
Supplementary Table 1: Adhesion genes data set PROBE Entrez Gene ID Celera Gene ID Gene_Symbol Gene_Name 160832 1 hCG201364.3 A1BG alpha-1-B glycoprotein 223658 1 hCG201364.3 A1BG alpha-1-B glycoprotein 212988 102 hCG40040.3 ADAM10 ADAM metallopeptidase domain 10 133411 4185 hCG28232.2 ADAM11 ADAM metallopeptidase domain 11 110695 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 195222 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 165344 8751 hCG20021.3 ADAM15 ADAM metallopeptidase domain 15 (metargidin) 189065 6868 null ADAM17 ADAM metallopeptidase domain 17 (tumor necrosis factor, alpha, converting enzyme) 108119 8728 hCG15398.4 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 117763 8748 hCG20675.3 ADAM20 ADAM metallopeptidase domain 20 126448 8747 hCG1785634.2 ADAM21 ADAM metallopeptidase domain 21 208981 8747 hCG1785634.2|hCG2042897 ADAM21 ADAM metallopeptidase domain 21 180903 53616 hCG17212.4 ADAM22 ADAM metallopeptidase domain 22 177272 8745 hCG1811623.1 ADAM23 ADAM metallopeptidase domain 23 102384 10863 hCG1818505.1 ADAM28 ADAM metallopeptidase domain 28 119968 11086 hCG1786734.2 ADAM29 ADAM metallopeptidase domain 29 205542 11085 hCG1997196.1 ADAM30 ADAM metallopeptidase domain 30 148417 80332 hCG39255.4 ADAM33 ADAM metallopeptidase domain 33 140492 8756 hCG1789002.2 ADAM7 ADAM metallopeptidase domain 7 122603 101 hCG1816947.1 ADAM8 ADAM metallopeptidase domain 8 183965 8754 hCG1996391 ADAM9 ADAM metallopeptidase domain 9 (meltrin gamma) 129974 27299 hCG15447.3 ADAMDEC1 ADAM-like, -
L1 Cell Adhesion Molecule in Cancer, a Systematic Review on Domain-Specific Functions
International Journal of Molecular Sciences Review L1 Cell Adhesion Molecule in Cancer, a Systematic Review on Domain-Specific Functions Miriam van der Maten 1,2, Casper Reijnen 1,3, Johanna M.A. Pijnenborg 1,* and Mirjam M. Zegers 2,* 1 Department of Obstetrics and Gynaecology, Radboud university medical center, 6525 GA Nijmegen, The Netherlands 2 Department of Cell Biology, Radboud Institute for Molecular Life Sciences, Radboud university medical center, 6525 GA Nijmegen, The Netherlands 3 Department of Obstetrics and Gynaecology, Canisius-Wilhelmina Hospital, 6532 SZ Nijmegen, The Netherlands * Correspondence: [email protected] (J.M.A.P); [email protected] (M.M.Z.) Received: 24 June 2019; Accepted: 23 August 2019; Published: 26 August 2019 Abstract: L1 cell adhesion molecule (L1CAM) is a glycoprotein involved in cancer development and is associated with metastases and poor prognosis. Cellular processing of L1CAM results in expression of either full-length or cleaved forms of the protein. The different forms of L1CAM may localize at the plasma membrane as a transmembrane protein, or in the intra- or extracellular environment as cleaved or exosomal forms. Here, we systematically analyze available literature that directly relates to L1CAM domains and associated signaling pathways in cancer. Specifically, we chart its domain-specific functions in relation to cancer progression, and outline pre-clinical assays used to assess L1CAM. It is found that full-length L1CAM has both intracellular and extracellular targets, including interactions with integrins, and linkage with ezrin. Cellular processing leading to proteolytic cleavage and/or exosome formation results in extracellular soluble forms of L1CAM that may act through similar mechanisms as compared to full-length L1CAM, such as integrin-dependent signals, but also through distinct mechanisms. -
Interaction of the Cell Adhesion Molecule CHL1 with Vitronectin
14606 • The Journal of Neuroscience, October 29, 2014 • 34(44):14606–14623 Cellular/Molecular Interaction of the Cell Adhesion Molecule CHL1 with Vitronectin, Integrins, and the Plasminogen Activator Inhibitor-2 Promotes CHL1-Induced Neurite Outgrowth and Neuronal Migration Jelena Katic,1* Gabriele Loers,1* Ralf Kleene,1* Nicole Karl,1* Carsten Schmidt,1 Friedrich Buck,2 Jaroslaw W. Zmijewski,6 Igor Jakovcevski,1 Klaus T. Preissner,3 and Melitta Schachner4,5 1Zentrum fu¨r Molekulare Neurobiologie, and 2Institut fu¨r Klinische Chemie, Universita¨tsklinikum Hamburg-Eppendorf, 20246 Hamburg, Germany, 3Department of Biochemistry, Medical School, Justus-Liebig-University, 35392 Giessen, Germany, 4Keck Center for Collaborative Neuroscience and Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, New Jersey 08854, 5Center for Neuroscience, Shantou University Medical College, Shantou 515041, People’s Republic of China, and 6Division of Pulmonary, Allergy & Critical Care Medicine, University of Alabama at Birmingham, BMRII-304, Birmingham, Alabama 35294 The cell adhesion molecule close homolog of L1 (CHL1) plays important functional roles in the developing and adult nervous system. In search of the binding partners that mediate the diverse and sometimes opposing functions of CHL1, the extracellular matrix-associated proteins vitronectin and plasminogen activator inhibitor-2 (PAI-2) were identified as novel CHL1 interaction partners and tested for involvement in CHL1-dependent functions during mouse cerebellar development. CHL1-induced cerebellar neurite outgrowth and cell migration at postnatal days 6–8 were inhibited by a CHL1-derived peptide comprising the integrin binding RGD motif, and by antibodies against vitronectin or several integrins, indicating a vitronectin-dependent integrin-mediated pathway. A PAI-2-derived peptide, or antibodies against PAI-2, urokinase type plasminogen activator (uPA), uPA receptor, and several integrins reduced cell migration. -
140503 IPF Signatures Supplement Withfigs Thorax
Supplementary material for Heterogeneous gene expression signatures correspond to distinct lung pathologies and biomarkers of disease severity in idiopathic pulmonary fibrosis Daryle J. DePianto1*, Sanjay Chandriani1⌘*, Alexander R. Abbas1, Guiquan Jia1, Elsa N. N’Diaye1, Patrick Caplazi1, Steven E. Kauder1, Sabyasachi Biswas1, Satyajit K. Karnik1#, Connie Ha1, Zora Modrusan1, Michael A. Matthay2, Jasleen Kukreja3, Harold R. Collard2, Jackson G. Egen1, Paul J. Wolters2§, and Joseph R. Arron1§ 1Genentech Research and Early Development, South San Francisco, CA 2Department of Medicine, University of California, San Francisco, CA 3Department of Surgery, University of California, San Francisco, CA ⌘Current address: Novartis Institutes for Biomedical Research, Emeryville, CA. #Current address: Gilead Sciences, Foster City, CA. *DJD and SC contributed equally to this manuscript §PJW and JRA co-directed this project Address correspondence to Paul J. Wolters, MD University of California, San Francisco Department of Medicine Box 0111 San Francisco, CA 94143-0111 [email protected] or Joseph R. Arron, MD, PhD Genentech, Inc. MS 231C 1 DNA Way South San Francisco, CA 94080 [email protected] 1 METHODS Human lung tissue samples Tissues were obtained at UCSF from clinical samples from IPF patients at the time of biopsy or lung transplantation. All patients were seen at UCSF and the diagnosis of IPF was established through multidisciplinary review of clinical, radiological, and pathological data according to criteria established by the consensus classification of the American Thoracic Society (ATS) and European Respiratory Society (ERS), Japanese Respiratory Society (JRS), and the Latin American Thoracic Association (ALAT) (ref. 5 in main text). Non-diseased normal lung tissues were procured from lungs not used by the Northern California Transplant Donor Network. -
1714 Gene Comprehensive Cancer Panel Enriched for Clinically Actionable Genes with Additional Biologically Relevant Genes 400-500X Average Coverage on Tumor
xO GENE PANEL 1714 gene comprehensive cancer panel enriched for clinically actionable genes with additional biologically relevant genes 400-500x average coverage on tumor Genes A-C Genes D-F Genes G-I Genes J-L AATK ATAD2B BTG1 CDH7 CREM DACH1 EPHA1 FES G6PC3 HGF IL18RAP JADE1 LMO1 ABCA1 ATF1 BTG2 CDK1 CRHR1 DACH2 EPHA2 FEV G6PD HIF1A IL1R1 JAK1 LMO2 ABCB1 ATM BTG3 CDK10 CRK DAXX EPHA3 FGF1 GAB1 HIF1AN IL1R2 JAK2 LMO7 ABCB11 ATR BTK CDK11A CRKL DBH EPHA4 FGF10 GAB2 HIST1H1E IL1RAP JAK3 LMTK2 ABCB4 ATRX BTRC CDK11B CRLF2 DCC EPHA5 FGF11 GABPA HIST1H3B IL20RA JARID2 LMTK3 ABCC1 AURKA BUB1 CDK12 CRTC1 DCUN1D1 EPHA6 FGF12 GALNT12 HIST1H4E IL20RB JAZF1 LPHN2 ABCC2 AURKB BUB1B CDK13 CRTC2 DCUN1D2 EPHA7 FGF13 GATA1 HLA-A IL21R JMJD1C LPHN3 ABCG1 AURKC BUB3 CDK14 CRTC3 DDB2 EPHA8 FGF14 GATA2 HLA-B IL22RA1 JMJD4 LPP ABCG2 AXIN1 C11orf30 CDK15 CSF1 DDIT3 EPHB1 FGF16 GATA3 HLF IL22RA2 JMJD6 LRP1B ABI1 AXIN2 CACNA1C CDK16 CSF1R DDR1 EPHB2 FGF17 GATA5 HLTF IL23R JMJD7 LRP5 ABL1 AXL CACNA1S CDK17 CSF2RA DDR2 EPHB3 FGF18 GATA6 HMGA1 IL2RA JMJD8 LRP6 ABL2 B2M CACNB2 CDK18 CSF2RB DDX3X EPHB4 FGF19 GDNF HMGA2 IL2RB JUN LRRK2 ACE BABAM1 CADM2 CDK19 CSF3R DDX5 EPHB6 FGF2 GFI1 HMGCR IL2RG JUNB LSM1 ACSL6 BACH1 CALR CDK2 CSK DDX6 EPOR FGF20 GFI1B HNF1A IL3 JUND LTK ACTA2 BACH2 CAMTA1 CDK20 CSNK1D DEK ERBB2 FGF21 GFRA4 HNF1B IL3RA JUP LYL1 ACTC1 BAG4 CAPRIN2 CDK3 CSNK1E DHFR ERBB3 FGF22 GGCX HNRNPA3 IL4R KAT2A LYN ACVR1 BAI3 CARD10 CDK4 CTCF DHH ERBB4 FGF23 GHR HOXA10 IL5RA KAT2B LZTR1 ACVR1B BAP1 CARD11 CDK5 CTCFL DIAPH1 ERCC1 FGF3 GID4 HOXA11 IL6R KAT5 ACVR2A -
Somatic Mutational Landscapes of Adherens Junctions and Their
1 Somatic mutational landscapes of adherens junctions and their 2 functional consequences in cutaneous melanoma development 3 4 Praveen Kumar Korla,1 Chih-Chieh Chen,2 Daniel Esguerra Gracilla,1 Ming-Tsung Lai,3 Chih- 5 Mei Chen,4 Huan Yuan Chen,5 Tritium Hwang,1 Shih-Yin Chen,4,6,* Jim Jinn-Chyuan Sheu1,4, 6-9,* 6 1Institute of Biomedical Sciences, National Sun Yat-sen University, Kaohsiung 80242, Taiwan; 7 2Institute of Medical Science and Technology, National Sun Yat-sen University, Kaohsiung 80424, 8 Taiwan; 3Department of Pathology, Taichung Hospital, Ministry of Health and Welfare, Taichung 9 40343, Taiwan; 4Genetics Center, China Medical University Hospital, Taichung 40447, Taiwan; 10 5Institute of Biomedical Sciences, Academia Sinica, Taipei 11574, Taiwan; 6School of Chinese 11 Medicine, China Medical University, Taichung 40402, Taiwan; 7Department of Health and 12 Nutrition Biotechnology, Asia University, Taichung 41354, Taiwan; 8Department of 13 Biotechnology, Kaohsiung Medical University, Kaohsiung 80708, Taiwan; 9Institute of 14 Biopharmaceutical Sciences, National Sun Yat-sen University, Kaohsiung 80242, Taiwan 15 16 PKK, CCC and DEG contributed equally to this study. 17 *Correspondence to: Dr. Shih-Yin Chen ([email protected]) at Genetics Center, China 18 Medical University Hospital, Taichung, 40447, TAIWAN; or Dr. Jim Jinn-Chyuan Sheu 19 ([email protected]) at Institute of Biomedical Sciences, National Sun Yat-sen 20 University, Kaohsiung City 80424, TAIWAN. 21 22 Running title: mutational landscape of cadherins in melanoma 1 23 Abstract 24 Cell-cell interaction in skin homeostasis is tightly controlled by adherens junctions (AJs). 25 Alterations in such regulation lead to melanoma development. -
Sterculic Acid Alters Adhesion Molecules Expression and Extracellular Matrix Compounds to Regulate Migration of Lung Cancer Cells
cancers Article Sterculic Acid Alters Adhesion Molecules Expression and Extracellular Matrix Compounds to Regulate Migration of Lung Cancer Cells Rafael Peláez * , Rodrigo Ochoa, Ana Pariente, Ángela Villanueva-Martínez, Álvaro Pérez-Sala and Ignacio M. Larráyoz * Biomarkers and Molecular Signaling Group, Neurodegeneration Area, Center for Biomedical Research of La Rioja (CIBIR), Piqueras 98, 26006 Logroño, Spain; [email protected] (R.O.); [email protected] (A.P.); [email protected] (Á.V.-M.); [email protected] (Á.P.-S.) * Correspondence: [email protected] (R.P.); [email protected] (I.M.L.); Tel.: +34-941-278-770 ((ext. 84866) (R.P.) & (ext. 89878) (I.M.L.)) Simple Summary: Sterculic acid (SA) is a naturally occurring lipid with SCD1 inhibitory activity, but it also modifies many other pathways and underlying gene expression. SCD upregulation has been associated with tumor aggressiveness and progression. Effects of SA treatment over extracellular matrix compounds and adhesion molecule expression have not been described in cancer cells up to now. Our results show that SA induces cell death at high dose, but we also observed that lower concentrations of SA treatments also reduce cell adhesion-migration and modify integrins and extracellular matrix compounds expression. Citation: Peláez, R.; Ochoa, R.; Abstract: Sterculic acid (SA) is a cyclopropenoid fatty acid isolated from Sterculia foetida seeds. Pariente, A.; Villanueva-Martínez, Á.; This molecule is a well-known inhibitor of SCD1 enzyme, also known as D9-desaturase, which Pérez-Sala, Á.; Larráyoz, I.M. main function is related to lipid metabolism. However, recent studies have demonstrated that Sterculic Acid Alters Adhesion it also modifies many other pathways and the underlying gene expression. -
MALE Protein Name Accession Number Molecular Weight CP1 CP2 H1 H2 PDAC1 PDAC2 CP Mean H Mean PDAC Mean T-Test PDAC Vs. H T-Test
MALE t-test t-test Accession Molecular H PDAC PDAC vs. PDAC vs. Protein Name Number Weight CP1 CP2 H1 H2 PDAC1 PDAC2 CP Mean Mean Mean H CP PDAC/H PDAC/CP - 22 kDa protein IPI00219910 22 kDa 7 5 4 8 1 0 6 6 1 0.1126 0.0456 0.1 0.1 - Cold agglutinin FS-1 L-chain (Fragment) IPI00827773 12 kDa 32 39 34 26 53 57 36 30 55 0.0309 0.0388 1.8 1.5 - HRV Fab 027-VL (Fragment) IPI00827643 12 kDa 4 6 0 0 0 0 5 0 0 - 0.0574 - 0.0 - REV25-2 (Fragment) IPI00816794 15 kDa 8 12 5 7 8 9 10 6 8 0.2225 0.3844 1.3 0.8 A1BG Alpha-1B-glycoprotein precursor IPI00022895 54 kDa 115 109 106 112 111 100 112 109 105 0.6497 0.4138 1.0 0.9 A2M Alpha-2-macroglobulin precursor IPI00478003 163 kDa 62 63 86 72 14 18 63 79 16 0.0120 0.0019 0.2 0.3 ABCB1 Multidrug resistance protein 1 IPI00027481 141 kDa 41 46 23 26 52 64 43 25 58 0.0355 0.1660 2.4 1.3 ABHD14B Isoform 1 of Abhydrolase domain-containing proteinIPI00063827 14B 22 kDa 19 15 19 17 15 9 17 18 12 0.2502 0.3306 0.7 0.7 ABP1 Isoform 1 of Amiloride-sensitive amine oxidase [copper-containing]IPI00020982 precursor85 kDa 1 5 8 8 0 0 3 8 0 0.0001 0.2445 0.0 0.0 ACAN aggrecan isoform 2 precursor IPI00027377 250 kDa 38 30 17 28 34 24 34 22 29 0.4877 0.5109 1.3 0.8 ACE Isoform Somatic-1 of Angiotensin-converting enzyme, somaticIPI00437751 isoform precursor150 kDa 48 34 67 56 28 38 41 61 33 0.0600 0.4301 0.5 0.8 ACE2 Isoform 1 of Angiotensin-converting enzyme 2 precursorIPI00465187 92 kDa 11 16 20 30 4 5 13 25 5 0.0557 0.0847 0.2 0.4 ACO1 Cytoplasmic aconitate hydratase IPI00008485 98 kDa 2 2 0 0 0 0 2 0 0 - 0.0081 - 0.0 -
New Insights from Cell Adhesion Molecules In
New insights from cell adhesion molecules in antidepressant action: role of ITGB3 and GAP43 genes Chiara Fabbri1, Rosalba Martines1,5, Concetta Crisafulli4, David Gurwitz2, Julia Stingl3, Raffaella Calati1, Diego Albani5, Armando Chierchia5, Edoardo Spina6, Marco Calabrò4,6, Siegfried Kasper7, Marie Spies7, Joseph Zohar8, Alzbeta Juven-Wetzler8, Daniel Souery9, Stuart Montgomery10, Julien Mendlewicz11, Alessandro Serretti1 1: Department of Biomedical and NeuroMotor Sciences, University of Bologna, Italy 7: Department of Psychiatry and Psychotherapy, Medical University Vienna, Austria 2: Department of Human Molecular Genetics and Biochemistry, Sackler Faculty of Medicine, Tel-Aviv University 8: Department of Psychiatry, Sheba Medical Center, Tel Hashomer, and Sackler School of Medicine, 3: Bundesinstitut für Arzneimittel und Medizinprodukte, Translationale Pharmakologie, Universität Bonn Tel Aviv University, Israel 4: Department of Biomedical Science and morphological and functional images, University of Messina, Italy 9: Laboratoire de Psychologie Medicale, Universitè Libre de Bruxelles and Psy Pluriel, Centre 5: Unit of Genetics of Neurodegenerative DisordersNeuroscience Department, IRCCS Istituto di Ricerche Farmacologiche "Mario Européen de Psychologie Medicale, Brussels Negri", Milan, Italy 10: lmperial College School of Medicine, London, UK 6: Department of Clinical and Experimental Medicine, University of Messina, Italy 11: Universite´ Libre de Bruxelles Adhesion proteins implicated in TO INVESTIGATE ITGB3 AND neuronal plasticity and axonal Regulation of serotonergic GAP43 GENETIC VARIANTS AND guidance neurotransmission MOLECULAR PATHWAYS IN ANTIDEPRESSANT EFFICACY IN AIMS HUMANS Altered expression in LCLs exposed to paroxetine [2] Correlation with CHL1, previously implicated in antidepressant efficacy [1] METHODS: 10 tag SNPs in GAP43 and ITGB3 were genotyped in two independent samples (European n=373 and Italian n=96) of patients with major depression who were treated with antidepressants in a naturalistic setting.