Circulating Intercellular Adhesion Molecule 1 (ICAM-1), E-Selectin
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Bioinformatics Approach for Pattern of Myelin-Specific Proteins And
CORE Metadata, citation and similar papers at core.ac.uk Provided by Qazvin University of Medical Sciences Repository Biotech Health Sci. 2016 November; 3(4):e38278. doi: 10.17795/bhs-38278. Published online 2016 August 16. Research Article Bioinformatics Approach for Pattern of Myelin-Specific Proteins and Related Human Disorders Samiie Pouragahi,1,2,3 Mohammad Hossein Sanati,4 Mehdi Sadeghi,2 and Marjan Nassiri-Asl3,* 1Department of Molecular Medicine, School of Medicine, Qazvin university of Medical Sciences, Qazvin, IR Iran 2Department of Bioinformatics, National Institute of Genetic Engineering and Biotechnology (NIGEB), Tehran, IR Iran 3Department of Pharmacology, Cellular and Molecular Research Center, School of Medicine, Qazvin university of Medical Sciences, Qazvin, IR Iran 4Department of Molecular Genetics, National Institute of Genetic Engineering and Biotechnology (NIGEB), Tehran, IR Iran *Corresponding author: Marjan Nassiri-Asl, School of Medicine, Qazvin University of Medical Sciences, Qazvin, IR Iran. Tel: +98-2833336001, Fax: +98-2833324971, E-mail: [email protected] Received 2016 April 06; Revised 2016 May 30; Accepted 2016 June 22. Abstract Background: Recent neuroinformatic studies, on the structure-function interaction of proteins, causative agents basis of human disease have implied that dysfunction or defect of different protein classes could be associated with several related diseases. Objectives: The aim of this study was the use of bioinformatics approaches for understanding the structure, function and relation- ship of myelin protein 2 (PMP2), a myelin-basic protein in the basis of neuronal disorders. Methods: A collection of databases for exploiting classification information systematically, including, protein structure, protein family and classification of human disease, based on a new approach was used. -
Targeting E-Selectin to Tackle Cancer Using Uproleselan
cancers Review Targeting E-selectin to Tackle Cancer Using Uproleselan Barbara Muz 1 , Anas Abdelghafer 1,2, Matea Markovic 1,2 , Jessica Yavner 1 , Anupama Melam 1 , Noha Nabil Salama 2,3 and Abdel Kareem Azab 1,* 1 Department of Radiation Oncology, Cancer Biology Division, Washington University in St. Louis School of Medicine, St. Louis, MO 63108, USA; [email protected] (B.M.); [email protected] (A.A.); [email protected] (M.M.); [email protected] (J.Y.); [email protected] (A.M.) 2 Department of Pharmaceutical and Administrative Sciences, St. Louis College of Pharmacy, University of Health Sciences and Pharmacy in St. Louis, St. Louis, MO 63110, USA; [email protected] 3 Department of Pharmaceutics and Industrial Pharmacy, Faculty of Pharmacy, Cairo University, Cairo 11562, Egypt * Correspondence: [email protected]; Tel.: +1-(314)-362-9254; Fax: +1-(314)-362-9790 Simple Summary: This review focuses on eradicating cancer by targeting a surface protein expressed on the endothelium—E-selectin—with a novel drug, uproleselan (GMI-1271). Blocking E-selectin in the tumor microenvironment acts on multiple levels; uproleselan was shown (i) to inhibit cancer cell tethering, rolling and extravasating, i.e., cancer dissemination, (ii) to reduce adhesion and lose stem cell-like properties, (iii) to mobilize cancer cells to circulation where they are more susceptible to chemotherapy, which altogether contributes (iv) to overcome drug resistance. Uproleselan has been tested effective in leukemia, myeloma, pancreatic, colon and breast cancer cells, all of which can be found in the bone marrow as a primary or as a metastatic tumor site. -
Luminex Performance Assay Human Adhesion Molecule Multiplex
Luminex® Performance Assay Human Adhesion Molecule Multiplex Kit Catalog Number LKT007 For the simultaneous quantitative determination of multiple human cell adhesion molecules in cell culture supernates, serum, and plasma. This package insert must be read in its entirety before using this product. For research use only. Not for use in diagnostic procedures. TABLE OF CONTENTS SECTION PAGE INTRODUCTION .....................................................................................................................................................................1 PRINCIPLE OF THE ASSAY ...................................................................................................................................................1 LIMITATIONS OF THE PROCEDURE .................................................................................................................................2 TECHNICAL HINTS .................................................................................................................................................................2 PRECAUTIONS .........................................................................................................................................................................2 MATERIALS PROVIDED & STORAGE CONDITIONS ...................................................................................................3 OTHER SUPPLIES REQUIRED .............................................................................................................................................4 -
Increased Expression of Cell Adhesion Molecule P-Selectin in Active Inflammatory Bowel Disease Gut: First Published As 10.1136/Gut.36.3.411 on 1 March 1995
Gut 1995; 36: 411-418 411 Increased expression of cell adhesion molecule P-selectin in active inflammatory bowel disease Gut: first published as 10.1136/gut.36.3.411 on 1 March 1995. Downloaded from G M Schurmann, A E Bishop, P Facer, M Vecchio, J C W Lee, D S Rampton, J M Polak Abstract proposed, entailing margination from the The pathogenic changes of inflammatory centreline of blood flow towards the vascular bowel disease (IBD) depend on migration wall, rolling, tethering to the endothelia, stable of circulating leucocytes into intestinal adhesion, and finally, transendothelial migra- tissues. Although leucocyte rolling and tion.1 Each of these steps involves specific fam- tenuous adhesion are probably regulated ilies of adhesion molecules, which are by inducible selectins on vascular expressed on endothelial cells and on circulat- endothelia, little is known about the ing cells as their counterparts and ligands.2 3 expression of these molecules in Crohn's The selectin family of adhesion molecules, disease and ulcerative colitis. Using which comprises E-selectin, P-selectin, and L- immunohistochemistry on surgically selectin, predominantly mediates the first steps resected specimens, this study investi- of cellular adhesion4 5 and several studies have gated endothelial P-selectin (CD62, gran- shown upregulation of E-selectin on activated ular membrane protein-140) in frozen endothelial cells in a variety oftissues6-8 includ- sections of histologically uninvolved ing the gut in patients with IBD.9 10 Little tissues adjacent to inflammation (Crohn's investigation has been made, however, of P- disease= 10; ulcerative colitis= 10), from selectin in normal and diseased gut, although highly inflamed areas (Crohn's its DNA was cloned and sequenced in 1989.11 disease=20; ulcerative colitis=13), and P-selectin (also known as PADGEM, from normal bowel (n=20). -
B Lymphocyte Binding to E- and P-Selectins Is Mediated Through the De Novo Expression of Carbohydrates on in Vitro and in Vivo Activated Human B Cells
B lymphocyte binding to E- and P-selectins is mediated through the de novo expression of carbohydrates on in vitro and in vivo activated human B cells. A A Postigo, … , F Sánchez-Madrid, M O de Landázuri J Clin Invest. 1994;94(4):1585-1596. https://doi.org/10.1172/JCI117500. Research Article Cell adhesion to endothelium regulates the trafficking and recruitment of leukocytes towards lymphoid organs and sites of inflammation. This phenomenon is mediated by the expression of a number of adhesion molecules on both the endothelium and circulating cells. Activation of endothelial cells (EC) with different stimuli induces the expression of several adhesion molecules (E- and P-selectins, ICAM-1, VCAM-1), involved in their interaction with circulating cells. In this report, we have studied the binding of nonactivated and activated B cells to purified E- and P-selectins. Activated but not resting B cells were able to interact with both selectins. This binding capacity of activated B cells paralleled the induction of different carbohydrate epitopes (Lewisx, sialyl-Lewisx, CD57 and CDw65) as well as other molecules bearing these or related epitopes in myeloid cells (L-selectin, alpha L beta 2 and alpha X beta 2 integrins, and CD35) involved in the interaction of different cell types with selectins. B cells infiltrating inflamed tissues like in Hashimoto's thyroiditis, also expressed these selectin-binding carbohydrates in parallel with the expression of E-selectin by surrounding follicular dendritic cells. Moreover, the crosslinking of these selectin-binding epitopes resulted in an increased binding of B cells to different integrin ligands. -
Alpha 1,3 Fucosyltransferases Are Master Regulators of Prostate Cancer Cell Trafficking
Alpha 1,3 fucosyltransferases are master regulators of prostate cancer cell trafficking Steven R. Barthela,b, Georg K. Wiesea, Jaehyung Chob,c, Matthew J. Oppermana, Danielle L. Haysa, Javed Siddiquid, Kenneth J. Pientad, Bruce Furieb,c, and Charles J. Dimitroffa,b,1 aHarvard Skin Disease Research Center, Department of Dermatology, Brigham and Women’s Hospital, Boston, MA 02115; bHarvard Medical School, Boston, MA 02115; cDivision of Hemostasis and Thrombosis, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02115; and dDepartment of Urology, University of Michigan Comprehensive Cancer Center, Ann Arbor, MI 48109 Edited by Carolyn R. Bertozzi, University of California, Berkeley, CA, and approved September 24, 2009 (received for review June 2, 2009) How cancer cells bind to vascular surfaces and extravasate into target sistent with several observations, including the association of sLeX organs is an underappreciated, yet essential step in metastasis. We with PCa grade and progression (2, 16, 17), cancer cell E-selectin postulate that the metastatic process involves discrete adhesive ligand activity is a direct correlate with metastatic potential (18, 19) interactions between circulating cancer cells and microvascular en- and cancer cells can trigger E-selectin expression on liver sinusoidal dothelial cells. Sialyl Lewis X (sLeX) on prostate cancer (PCa) cells is microvasculature to steer circulating cancer cells to the liver (20, thought to promote metastasis by mediating PCa cell binding to 21). Thus, mapping glyco-metabolic pathways regulating E-selectin microvascular endothelial (E)-selectin. Yet, regulation of sLeX and ligand synthesis may be vital for understanding PCa metastasis. related E-selectin ligand expression in PCa cells is a poorly understood In this report, we identify E-selectin ligand formation through factor in PCa metastasis. -
Cell Adhesion Molecules in Normal Skin and Melanoma
biomolecules Review Cell Adhesion Molecules in Normal Skin and Melanoma Cian D’Arcy and Christina Kiel * Systems Biology Ireland & UCD Charles Institute of Dermatology, School of Medicine, University College Dublin, D04 V1W8 Dublin, Ireland; [email protected] * Correspondence: [email protected]; Tel.: +353-1-716-6344 Abstract: Cell adhesion molecules (CAMs) of the cadherin, integrin, immunoglobulin, and selectin protein families are indispensable for the formation and maintenance of multicellular tissues, espe- cially epithelia. In the epidermis, they are involved in cell–cell contacts and in cellular interactions with the extracellular matrix (ECM), thereby contributing to the structural integrity and barrier for- mation of the skin. Bulk and single cell RNA sequencing data show that >170 CAMs are expressed in the healthy human skin, with high expression levels in melanocytes, keratinocytes, endothelial, and smooth muscle cells. Alterations in expression levels of CAMs are involved in melanoma propagation, interaction with the microenvironment, and metastasis. Recent mechanistic analyses together with protein and gene expression data provide a better picture of the role of CAMs in the context of skin physiology and melanoma. Here, we review progress in the field and discuss molecular mechanisms in light of gene expression profiles, including recent single cell RNA expression information. We highlight key adhesion molecules in melanoma, which can guide the identification of pathways and Citation: D’Arcy, C.; Kiel, C. Cell strategies for novel anti-melanoma therapies. Adhesion Molecules in Normal Skin and Melanoma. Biomolecules 2021, 11, Keywords: cadherins; GTEx consortium; Human Protein Atlas; integrins; melanocytes; single cell 1213. https://doi.org/10.3390/ RNA sequencing; selectins; tumour microenvironment biom11081213 Academic Editor: Sang-Han Lee 1. -
Review Selectin Ligands
Proc. Nati. Acad. Sci. USA Vol. 91, pp. 7390-7397, August 1994 Review Selectin ligands Ajit Varki Gfro bg Program, Cancer Cente, and Division of Cellular and Molecular Medicine, Univert of California, San Diego, La Jolla, CA 92093 ABSTRACT The selectins initiate many critical interactions among blood cells. The volume of information and di- versity of opinions on the nature of the biologically relevant ligands for selectins is remarkable. This review analyzes the mat- ter and suggests the hypothesis that at least some of the specificity may involve recog- nition of "clustered saccharide patches." Five years ago, the cloning of three vas- cular proteins resulted in identification of the selectin family of cell adhesion mol- ecules (1-9). A shared N-terminal carbo- hydrate-recognition domain homologous | L-SELECTIN yE-SELECTIN P-SELECTIN to other Ca2+-dependent (C-type) mam- malian lectins (10) strengthened predic- FIG. 1. Location and topology of the selectin family of cell adhesion molecules and their tions from functional studies (for review, carbohydrate ligands. Expression of the selectins and their ligands may be constitutive or see ref. 1) that the cognate ligands for induced, depending upon the cell type, the tissue, and the biological circumstance. The selectins these receptors would be cell-surface can also be shed from cell surfaces by proteolysis. carbohydrates (Fig. 1). Several groups then reported that previously known lectin came from the inhibitory effects of (15, 18, 55-57). Taken together, these mammalian oligosaccharides bearing Fuc phosphorylated monosaccharides and a data indicated that specific carbohydrate and sialic acid (Sia) are recognized in a phosphorylated yeast mannan on the in- ligands are recognized by selecting. -
Human P-Selectin/CD62P Parameter
Human P-Selectin/CD62P Immunoassay Catalog Number BBE6 Catalog Number SBBE6 Catalog Number PBBE6 For the quantitative determination of human P-Selectin (P-Selectin) in cell culture supernates, serum, and plasma. This package insert must be read in its entirety before using this product. For research use only. Not for use in diagnostic procedures. TABLE OF CONTENTS SECTION PAGE INTRODUCTION ....................................................................................................................................................................1 PRINCIPLE OF THE ASSAY ..................................................................................................................................................2 LIMITATIONS OF THE PROCEDURE ................................................................................................................................2 TECHNICAL HINTS ................................................................................................................................................................2 MATERIALS PROVIDED & STORAGE CONDITIONS ..................................................................................................3 OTHER SUPPLIES REQUIRED ............................................................................................................................................4 PRECAUTIONS ........................................................................................................................................................................4 SAMPLE -
Serum Se?Selectin Levels and Carcinoembryonic Antigen Mrna?
Original Article Serum sE-Selectin Levels and Carcinoembryonic Antigen mRNA-Expressing Cells in Peripheral Blood as Prognostic Factors in Colorectal Cancer Patients Patrizia Ferroni, MD, PhD1; Mario Roselli, MD2,3; Antonella Spila, PhD1; Roberta D’Alessandro, PhD1; Ilaria Portarena, MD3; Sabrina Mariotti, MD3; Raffaele Palmirotta, MD, PhD1; Oreste Buonomo, MD4; Giuseppe Petrella, MD4; and Fiorella Guadagni, MD, PhD1 BACKGROUND: This study analyzed the possible prognostic value of presurgical serum soluble (s)E-selectin levels and/or carcinoembryonic antigen (CEA) mRNA positivity in predicting the disease-free survival of colorectal cancer (CRC) patients. METHODS: CEA mRNA (obtained from blood-borne cells by reverse transcriptase-polymerase chain reaction [RT-PCR]), tumor necrosis factor-a (TNF-a), and sE-selectin levels were analyzed in blood samples obtained from 78 patients with primary (n ¼ 62) or recurrent (n ¼ 16) CRC, 40 patients with benign colorectal (CR) diseases, and 78 controls. RESULTS: CEA mRNA positivity by RT-PCR was significantly associated with advanced stage (P < .05). Median baseline sE-selectin levels were higher in patients with CRC (43 ng/mL) compared with controls (36 ng/mL) or patients with benign CR diseases (31 ng/mL, P < .001). These were significantly associated with CEA mRNA positivity by RT-PCR (P < .05). Multivariate analysis by forward stepping showed that elevated TNF-a (P ¼ .001) and CEA mRNA positivity by RT-PCR (P ¼ .0001) were independent predictors of elevated baseline sE-selectin levels. Positive presurgical sE-selectin levels were associated with an increased recurrence rate compared with patients with low levels of this molecule (P < .001). Positivity for both CEA mRNA and sE-selectin had a negative prognostic impact, with a 5-year recurrence-free survival rate of 51% compared with 95% of patients with negative parameters (P < .05). -
E-Cadherin and Gastric Cancer: Cause, Consequence, and Applications
Hindawi Publishing Corporation BioMed Research International Volume 2014, Article ID 637308, 9 pages http://dx.doi.org/10.1155/2014/637308 Review Article E-Cadherin and Gastric Cancer: Cause, Consequence, and Applications Xin Liu and Kent-Man Chu Department of Surgery, The University of Hong Kong, Queen Mary Hospital, Pokfulam, Hong Kong Correspondence should be addressed to Kent-Man Chu; [email protected] Received 13 March 2014; Revised 31 July 2014; Accepted 31 July 2014; Published 12 August 2014 Academic Editor: Valli De Re Copyright © 2014 X. Liu and K.-M. Chu. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. E-cadherin (epithelial-cadherin), encoded by the CDH1 gene, is a transmembrane glycoprotein playing a crucial role in maintaining cell-cell adhesion. E-cadherin has been reported to be a tumor suppressor and to be down regulated in gastric cancer. Besides genetic mutations in CDH1 gene to induce hereditary diffuse gastric cancer (HDGC), epigenetic factors such as DNA hypermethylation also contribute to the reduction of E-cadherin in gastric carcinogenesis. In addition, expression of E-cadherin could be mediated by infectious agents such as H. pylori (Helicobacter pylori). As E-cadherin is vitally involved in signaling pathways modulating cell proliferation, survival, invasion, and migration, dysregulation of E-cadherin leads to dysfunction of gastric epithelial cells and contributes to gastric cancer development. Moreover, changes in its expression could reflect pathological conditions of gastric mucosa, making its role in gastric cancer complicated. -
Small Cell Lung Cancer Young Kwang Chae1,2, Wooyoung M
www.nature.com/scientificreports OPEN Overexpression of adhesion molecules and barrier molecules is associated with diferential Received: 21 September 2017 Accepted: 12 December 2017 infltration of immune cells in non- Published: xx xx xxxx small cell lung cancer Young Kwang Chae1,2, Wooyoung M. Choi2, William H. Bae2, Jonathan Anker2, Andrew A. Davis2, Sarita Agte1, Wade T. Iams2, Marcelo Cruz2, Maria Matsangou1,2 & Francis J. Giles1,2 Immunotherapy is emerging as a promising option for lung cancer treatment. Various endothelial adhesion molecules, such as integrin and selectin, as well as various cellular barrier molecules such as desmosome and tight junctions, regulate T-cell infltration in the tumor microenvironment. However, little is known regarding how these molecules afect immune cells in patients with lung cancer. We demonstrated for the frst time that overexpression of endothelial adhesion molecules and cellular barrier molecule genes was linked to diferential infltration of particular immune cells in non-small cell lung cancer. Overexpression of endothelial adhesion molecule genes is associated with signifcantly lower infltration of activated CD4 and CD8 T-cells, but higher infltration of activated B-cells and regulatory T-cells. In contrast, overexpression of desmosome genes was correlated with signifcantly higher infltration of activated CD4 and CD8 T-cells, but lower infltration of activated B-cells and regulatory T-cells in lung adenocarcinoma. This inverse relation of immune cells aligns with previous studies of tumor-infltrating B-cells inhibiting T-cell activation. Although overexpression of endothelial adhesion molecule or cellular barrier molecule genes alone was not predictive of overall survival in our sample, these genetic signatures may serve as biomarkers of immune exclusion, or resistance to T-cell mediated immunotherapy.