a geographical area politically controlled by a distant country (同)dependency
a body of people who settle far from home but maintain ties with their homeland; inhabitants remain nationals of their home state but are not literally under the home states system of government; "the American colony in Paris" (同)settlement
(microbiology) a group of organisms grown from a single parent cell
a group of organisms of the same type living or growing together
a place where a group of people with the same interest or occupation are concentrated; "a nudist colony"; "an artists colony"
be a contributing factor; "make things factor into a companys profitability"
any of the numbers (or symbols) that form a product when multiplied together
an independent variable in statistics
anything that contributes causally to a result; "a number of factors determined the outcome"
consider as relevant when making a decision; "You must factor in the recent developments" (同)factor in, factor out
resolve into factors; "a quantum computer can factor the number 15" (同)factor in, factor out
an event known to have happened or something known to have existed; "your fears have no basis in fact"; "how much of the story is fact and how much fiction is hard to tell"
a concept whose truth can be proved; "scientific hypotheses are not facts"
a piece of information about circumstances that exist or events that have occurred; "first you must collect all the facts of the case"
a statement or assertion of verified information about something that is the case or has happened; "he supported his argument with an impressive array of facts"
the basic unit of money in Costa Rica; equal to 100 centimos (同)Costa Rican colon
the basic unit of money in El Salvador; equal to 100 centavos (同)El Salvadoran colon
a punctuation mark (:) used after a word introducing a series or an example or an explanation (or after the salutation of a business letter)
the part of the large intestine between the cecum and the rectum; it extracts moisture from food residues before they are excreted
a cellular structure that is postulated to exist in order to mediate between a chemical agent that acts on nervous tissue and the physiological response
PrepTutorEJDIC
『植民地』 / 植民団,居留民;(外国人の)集団居留地 / (同ど人種・宗教・職業などの人たちが住む)『集団』,部落 / (動物・鳥・虫などの)集団;(生物の)群体,群落《+『of』+『名』》 / 《the Colonies》アメリカ合衆国を形成した13州のイギリス植民地
• integral component of membrane • membrane • plasma membrane • integral component of plasma membrane • extracellular region • intracellular • external side of plasma membrane • receptor complex
Biological process
• cellular protein metabolic process • MAPK cascade • peptidyl-tyrosine phosphorylation • cytokine-mediated signaling pathway
The granulocyte-macrophage colony-stimulating factor receptor also known as CD116 (Cluster of Differentiation 116), is a receptor for granulocyte-macrophage colony-stimulating factor, which stimulates the production of white blood cells. The receptor is normally located on myeloblast, mature neutrophil, but not on any erythroid or megakaryocytic lineage cells.[5]
It is associated with Surfactant metabolism dysfunction type 4.
Contents
1Structure
2Signal transduction
3References
4Further reading
5External links
Structure
The granulocyte-macrophage colony-stimulating factor receptor is a heterodimer composed of at least two different subunits; an α chain, and a β chain which is also present in the receptors for IL-3 and IL-5. The α subunit contains a binding site for granulocyte macrophage colony-stimulating factor.[6] The β chain is involved in signal transduction. Association of the α and β subunits results in receptor activation.[7]
Signal transduction
Upon dimerisation of the α and β subunits the β subunit becomes phosphorylated on tyrosine residues by members of the Janus kinase (JAK) family.[7] This leads to association with a Shc adaptor protein. Then Shc interacts with GRB2/SoS complex which results in activation of more downstream molecules in the pathway.[8]
References
^ abcGRCh38: Ensembl release 89: ENSG00000198223 - Ensembl, May 2017
^ abcGRCm38: Ensembl release 89: ENSMUSG00000059326 - Ensembl, May 2017
^"Human PubMed Reference:".
^"Mouse PubMed Reference:".
^Nicola NA, Metcalf D (Aug 1985). "Binding of 125I-labeled granulocyte colony-stimulating factor to normal murine hemopoietic cells". Journal of Cellular Physiology. 124 (2): 313–21. doi:10.1002/jcp.1041240222. PMID 3876343.
^ abGeijsen N, Koenderman L, Coffer PJ (Mar 2001). "Specificity in cytokine signal transduction: lessons learned from the IL-3/IL-5/GM-CSF receptor family". Cytokine & Growth Factor Reviews. 12 (1): 19–25. doi:10.1016/S1359-6101(00)00019-8. PMID 11312115.
^Doyle SE, Gasson JC (Aug 1998). "Characterization of the role of the human granulocyte-macrophage colony-stimulating factor receptor alpha subunit in the activation of JAK2 and STAT5" (– Scholar search). Blood. 92 (3): 867–76. PMID 9680354.[dead link]
Further reading
Rappold G, Willson TA, Henke A, Gough NM (Oct 1992). "Arrangement and localization of the human GM-CSF receptor alpha chain gene CSF2RA within the X-Y pseudoautosomal region". Genomics. 14 (2): 455–61. doi:10.1016/S0888-7543(05)80241-1. PMID 1358805.
Hayashida K, Kitamura T, Gorman DM, Arai K, Yokota T, Miyajima A (Dec 1990). "Molecular cloning of a second subunit of the receptor for human granulocyte-macrophage colony-stimulating factor (GM-CSF): reconstitution of a high-affinity GM-CSF receptor". Proceedings of the National Academy of Sciences of the United States of America. 87 (24): 9655–9. doi:10.1073/pnas.87.24.9655. PMC 55231. PMID 1702217.
Crosier KE, Wong GG, Mathey-Prevot B, Nathan DG, Sieff CA (Sep 1991). "A functional isoform of the human granulocyte/macrophage colony-stimulating factor receptor has an unusual cytoplasmic domain". Proceedings of the National Academy of Sciences of the United States of America. 88 (17): 7744–8. doi:10.1073/pnas.88.17.7744. PMC 52379. PMID 1715577.
Raines MA, Liu L, Quan SG, Joe V, DiPersio JF, Golde DW (Sep 1991). "Identification and molecular cloning of a soluble human granulocyte-macrophage colony-stimulating factor receptor". Proceedings of the National Academy of Sciences of the United States of America. 88 (18): 8203–7. doi:10.1073/pnas.88.18.8203. PMC 52475. PMID 1832774.
Gough NM, Gearing DP, Nicola NA, Baker E, Pritchard M, Callen DF, Sutherland GR (Jun 1990). "Localization of the human GM-CSF receptor gene to the X-Y pseudoautosomal region". Nature. 345 (6277): 734–6. doi:10.1038/345734a0. PMID 1972780.
Ashworth A, Kraft A (Dec 1990). "Cloning of a potentially soluble receptor for human GM-CSF". Nucleic Acids Research. 18 (23): 7178. doi:10.1093/nar/18.23.7178. PMC 332824. PMID 2148207.
Gearing DP, King JA, Gough NM, Nicola NA (Dec 1989). "Expression cloning of a receptor for human granulocyte-macrophage colony-stimulating factor". The EMBO Journal. 8 (12): 3667–76. PMC 402049. PMID 2555171.
DiPersio J, Billing P, Kaufman S, Eghtesady P, Williams RE, Gasson JC (Feb 1988). "Characterization of the human granulocyte-macrophage colony-stimulating factor receptor". The Journal of Biological Chemistry. 263 (4): 1834–41. PMID 2828352.
Williams WV, VonFeldt JM, Rosenbaum H, Ugen KE, Weiner DB (Oct 1994). "Molecular cloning of a soluble form of the granulocyte-macrophage colony-stimulating factor receptor alpha chain from a myelomonocytic cell line. Expression, biologic activity, and preliminary analysis of transcript distribution". Arthritis and Rheumatism. 37 (10): 1468–78. doi:10.1002/art.1780371010. PMID 7945472.
Jubinsky PT, Laurie AS, Nathan DG, Yetz-Aldepe J, Sieff CA (Dec 1994). "Expression and function of the human granulocyte-macrophage colony-stimulating factor receptor alpha subunit". Blood. 84 (12): 4174–85. PMID 7994031.
Hu X, Emanuel PD, Zuckerman KS (Sep 1994). "Cloning and sequencing of the cDNAs encoding two alternative splicing-derived variants of the alpha subunit of the granulocyte-macrophage colony-stimulating factor receptor". Biochimica et Biophysica Acta. 1223 (2): 306–8. doi:10.1016/0167-4889(94)90241-0. PMID 8086503.
Nakagawa Y, Kosugi H, Miyajima A, Arai K, Yokota T (Apr 1994). "Structure of the gene encoding the alpha subunit of the human granulocyte-macrophage colony stimulating factor receptor. Implications for the evolution of the cytokine receptor superfamily". The Journal of Biological Chemistry. 269 (14): 10905–12. PMID 8144676.
Zhao Y, Rong H, Chegini N (Oct 1995). "Expression and selective cellular localization of granulocyte-macrophage colony-stimulating factor (GM-CSF) and GM-CSF alpha and beta receptor messenger ribonucleic acid and protein in human ovarian tissue". Biology of Reproduction. 53 (4): 923–30. doi:10.1095/biolreprod53.4.923. PMID 8547489.
Lia F, Rajotte D, Clark SC, Hoang T (Nov 1996). "A dominant negative granulocyte-macrophage colony-stimulating factor receptor alpha chain reveals the multimeric structure of the receptor complex". The Journal of Biological Chemistry. 271 (45): 28287–93. doi:10.1074/jbc.271.45.28287. PMID 8910448.
Wei S, Liu JH, Epling-Burnette PK, Gamero AM, Ussery D, Pearson EW, Elkabani ME, Diaz JI, Djeu JY (Dec 1996). "Critical role of Lyn kinase in inhibition of neutrophil apoptosis by granulocyte-macrophage colony-stimulating factor". Journal of Immunology. 157 (11): 5155–62. PMID 8943427.
Soldi R, Primo L, Brizzi MF, Sanavio F, Aglietta M, Polentarutti N, Pegoraro L, Mantovani A, Bussolino F (Feb 1997). "Activation of JAK2 in human vascular endothelial cells by granulocyte-macrophage colony-stimulating factor". Blood. 89 (3): 863–72. PMID 9028317.
Matsuguchi T, Zhao Y, Lilly MB, Kraft AS (Jul 1997). "The cytoplasmic domain of granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor alpha subunit is essential for both GM-CSF-mediated growth and differentiation". The Journal of Biological Chemistry. 272 (28): 17450–9. doi:10.1074/jbc.272.28.17450. PMID 9211889.
Rivas CI, Vera JC, Delgado-López F, Heaney ML, Guaiquil VH, Zhang RH, Scher HI, Concha II, Nualart F, Cordon-Cardo C, Golde DW (Feb 1998). "Expression of granulocyte-macrophage colony-stimulating factor receptors in human prostate cancer". Blood. 91 (3): 1037–43. PMID 9446667.
Hu X, Zuckerman KS (Jun 1998). "Cloning and sequencing of an alternative splicing-derived cDNA variant of the GM-CSF receptor alpha subunit, which encodes a truncated protein". American Journal of Hematology. 58 (2): 145–7. doi:10.1002/(SICI)1096-8652(199806)58:2<145::AID-AJH11>3.0.CO;2-A. PMID 9625584.
Taha RA, Leung DY, Ghaffar O, Boguniewicz M, Hamid Q (Aug 1998). "In vivo expression of cytokine receptor mRNA in atopic dermatitis". The Journal of Allergy and Clinical Immunology. 102 (2): 245–50. doi:10.1016/S0091-6749(98)70093-4. PMID 9723668.
External links
GM-CSF+Receptor at the US National Library of Medicine Medical Subject Headings (MeSH)
v
t
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Proteins: clusters of differentiation (see also list of human clusters of differentiation)
Efficacy and safety of mavrilimumab in Japanese subjects with rheumatoid arthritis: Findings from a Phase IIa study.
Takeuchi T1, Tanaka Y, Close D, Godwood A, Wu CY, Saurigny D.Author information 1Keio University School of Medicine , Tokyo , Japan.AbstractObjective. A phase IIa study investigated efficacy and safety/tolerability of ascending doses of mavrilimumab (anti-granulocyte-macrophage colony-stimulating factor receptor [GM-CSFR]α monoclonal antibody) in adult subjects with moderate to severe rheumatoid arthritis from Japan and Europe. Findings from the Japanese population are presented. Methods. Fifty-one subjects received mavrilimumab (10-100 mg) or placebo subcutaneously every other week for 12 weeks, followed by a 12-week follow-up period. The primary endpoint was the proportion of subjects achieving a Disease Activity Score using 28 joints (DAS28)-C-reactive protein (CRP) response (decrease > 1.2 from baseline). Secondary endpoints included DAS28-CRP remission, Health Assessment Questionnaire Disability Index (HAQ-DI) and American College of Rheumatology (ACR) response. Results. By Week 12, more mavrilimumab- versus placebo-treated subjects achieved a DAS28-CRP response (50.0% vs. 23.5%, p = 0.081); a significant response was seen in the 30 mg and 100 mg dose groups (both 75.0% vs. 23.5%, p = 0.028). The 100 mg group also demonstrated statistically significant HAQ-DI and ACR20 responses at Week 12. Results were generally consistent between Japanese and European populations. Overall, adverse events (AEs) were mild to moderate in intensity with one serious AE of pneumonia, considered possibly treatment-related. Conclusions. A rapid and clinically meaningful response was seen in subjects treated with GM-CSFRα blockade with mavrilimumab, supporting further investigation of mavrilimumab for the treatment of RA in Japanese subjects.
Modern rheumatology / the Japan Rheumatism Association.Mod Rheumatol.2014 Apr 11. [Epub ahead of print]
Objective. A phase IIa study investigated efficacy and safety/tolerability of ascending doses of mavrilimumab (anti-granulocyte-macrophage colony-stimulating factor receptor [GM-CSFR]α monoclonal antibody) in adult subjects with moderate to severe rheumatoid arthritis from Japan and Europe. Finding
Initially Lymphocytic Sweet's Syndrome in Male Patients with Myelodysplasia: A Distinguished Clinicopathological Entity? Case Report and Systematic Review of the Literature.
Acta haematologica.Acta Haematol.2014 Apr 4;132(2):220-225. [Epub ahead of print]
Background: Sweet's syndrome (SS) is an acute febrile neutrophilic dermatosis. It can occur as an idiopathic, drug-induced or malignancy-associated entity. SS is also seen in patients with myelodysplastic syndrome (MDS) where it may present atypically, both clinically and histologically. In a few ra
Bhlhe40 controls cytokine production by T cells and is essential for pathogenicity in autoimmune neuroinflammation.
Lin CC1, Bradstreet TR1, Schwarzkopf EA1, Sim J2, Carrero JA1, Chou C1, Cook LE1, Egawa T1, Taneja R3, Murphy TL1, Russell JH2, Edelson BT1.Author information 1Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA.2Department of Developmental Biology, Washington University School of Medicine, St Louis, Missouri 63110, USA.3Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597, Singapore.AbstractTH1 and TH17 cells mediate neuroinflammation in experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis. Pathogenic TH cells in EAE must produce the pro-inflammatory cytokine granulocyte-macrophage colony stimulating factor (GM-CSF). TH cell pathogenicity in EAE is also regulated by cell-intrinsic production of the immunosuppressive cytokine interleukin 10 (IL-10). Here we demonstrate that mice deficient for the basic helix-loop-helix (bHLH) transcription factor Bhlhe40 (Bhlhe40(-/-)) are resistant to the induction of EAE. Bhlhe40 is required in vivo in a T cell-intrinsic manner, where it positively regulates the production of GM-CSF and negatively regulates the production of IL-10. In vitro, GM-CSF secretion is selectively abrogated in polarized Bhlhe40(-/-) TH1 and TH17 cells, and these cells show increased production of IL-10. Blockade of IL-10 receptor in Bhlhe40(-/-) mice renders them susceptible to EAE. These findings identify Bhlhe40 as a critical regulator of autoreactive T-cell pathogenicity.
TH1 and TH17 cells mediate neuroinflammation in experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis. Pathogenic TH cells in EAE must produce the pro-inflammatory cytokine granulocyte-macrophage colony stimulating factor (GM-CSF). TH cell pathogenicity in EAE is also
High Expression Levels of Trigger Receptor Expressed on Myeloid Cells-1 on Neutrophils Associated with Increased Severity of Acute Pancreatitis in Mice
Biological and Pharmaceutical Bulletin 38(10), 1450-1457, 2015
Abstract Already 20 years have passed since the cloning of the granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor α-chain, the first member of the GM-CSF/interleukin (IL)–3/IL-5 family of hemopoietic cytokine ...
1. Blood. 2009 Aug 13;114(7):1289-98. doi: 10.1182/blood-2008-12-164004. Epub 2009 May 12. The granulocyte-macrophage colony-stimulating factor receptor: linking its structure to cell signaling and its role in disease.
