syndecan-1

シンデカン1

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2012/11/05 01:38:58」(JST)

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Syndecan 1
Identifiers
Symbols	SDC1; CD138; SDC; SYND1; syndecan
External IDs	OMIM: 186355 MGI: 1349162 HomoloGene: 2252 GeneCards: SDC1 Gene
Gene Ontology Molecular function • protein binding • protein C-terminus binding • cytoskeletal protein binding Cellular component • extracellular region • cytoplasm • Golgi lumen • plasma membrane • integral to plasma membrane • focal adhesion • lysosomal lumen Biological process • carbohydrate metabolic process • glycosaminoglycan biosynthetic process • glycosaminoglycan catabolic process • lipid metabolic process • glycosaminoglycan metabolic process • chondroitin sulfate metabolic process • lipoprotein metabolic process • small molecule metabolic process • myoblast development • striated muscle cell development Sources: Amigo / QuickGO
RNA expression pattern
More reference expression data
Orthologs
Species	Human	Mouse
Entrez	6382	20969
Ensembl	ENSG00000115884	ENSMUSG00000020592
UniProt	P18827	P18828
RefSeq (mRNA)	NM_001006946.1	NM_011519.2
RefSeq (protein)	NP_001006947.1	NP_035649.1
Location (UCSC)	Chr 2: 20.4 – 20.43 Mb	Chr 12: 8.77 – 8.79 Mb
PubMed search	[1]	[2]

Syndecan 1 is a protein which in humans is encoded by the SDC1 gene.

Function

The protein encoded by this gene is a transmembrane (type I) heparan sulfate proteoglycan and is a member of the syndecan proteoglycan family. The syndecans mediate cell binding, cell signaling, and cytoskeletal organization and syndecan receptors are required for internalization of the HIV-1 tat protein. The syndecan-1 protein functions as an integral membrane protein and participates in cell proliferation, cell migration and cell-matrix interactions via its receptor for extracellular matrix proteins. Altered syndecan-1 expression has been detected in several different tumor types. While several transcript variants may exist for this gene, the full-length natures of only two have been described to date. These two represent the major variants of this gene and encode the same protein.

Application

It is a useful marker for plasma cells, but only if the cells tested are already known to be derived from blood.

References

Further reading

• David G (1992). "Structural and functional diversity of the heparan sulfate proteoglycans". Adv. Exp. Med. Biol. 313: 69–78. PMID 1442271. 
• Jaakkola P, Jalkanen M (1999). "Transcriptional regulation of Syndecan-1 expression by growth factors". Prog. Nucleic Acid Res. Mol. Biol.. Progress in Nucleic Acid Research and Molecular Biology 63: 109–38. doi:10.1016/S0079-6603(08)60721-7. ISBN 978-0-12-540063-3. PMID 10506830. 
• Wijdenes J, Dore JM, Clement C, Vermot-Desroches C (2003). "CD138". J. Biol. Regul. Homeost. Agents 16 (2): 152–5. PMID 12144130. 
• Lories V, Cassiman JJ, Van den Berghe H, David G (1992). "Differential expression of cell surface heparan sulfate proteoglycans in human mammary epithelial cells and lung fibroblasts". J. Biol. Chem. 267 (2): 1116–22. PMID 1339431. 
• Vainio S, Jalkanen M, Bernfield M, Saxén L (1992). "Transient expression of syndecan in mesenchymal cell aggregates of the embryonic kidney". Dev. Biol. 152 (2): 221–32. doi:10.1016/0012-1606(92)90130-9. PMID 1644217. 
• Kiefer MC, Ishihara M, Swiedler SJ et al. (1992). "The molecular biology of heparan sulfate fibroblast growth factor receptors". Ann. N. Y. Acad. Sci. 638: 167–76. doi:10.1111/j.1749-6632.1991.tb49027.x. PMID 1664683. 
• Ala-Kapee M, Nevanlinna H, Mali M et al. (1990). "Localization of gene for human syndecan, an integral membrane proteoglycan and a matrix receptor, to chromosome 2". Somat. Cell Mol. Genet. 16 (5): 501–5. doi:10.1007/BF01233200. PMID 2173154. 
• Mali M, Jaakkola P, Arvilommi AM, Jalkanen M (1990). "Sequence of human syndecan indicates a novel gene family of integral membrane proteoglycans". J. Biol. Chem. 265 (12): 6884–9. PMID 2324102. 
• Sanderson RD, Lalor P, Bernfield M (1992). "B lymphocytes express and lose syndecan at specific stages of differentiation". Cell Regul. 1 (1): 27–35. PMC 361422. PMID 2519615. //www.ncbi.nlm.nih.gov/pmc/articles/PMC361422/. 
• Asundi VK, Carey DJ (1995). "Self-association of N-syndecan (syndecan-3) core protein is mediated by a novel structural motif in the transmembrane domain and ectodomain flanking region". J. Biol. Chem. 270 (44): 26404–10. doi:10.1074/jbc.270.44.26404. PMID 7592855. 
• Zhang L, David G, Esko JD (1995). "Repetitive Ser-Gly sequences enhance heparan sulfate assembly in proteoglycans". J. Biol. Chem. 270 (45): 27127–35. doi:10.1074/jbc.270.45.27127. PMID 7592967. 
• Barillari G, Gendelman R, Gallo RC, Ensoli B (1993). "The Tat protein of human immunodeficiency virus type 1, a growth factor for AIDS Kaposi sarcoma and cytokine-activated vascular cells, induces adhesion of the same cell types by using integrin receptors recognizing the RGD amino acid sequence". Proc. Natl. Acad. Sci. U.S.A. 90 (17): 7941–5. doi:10.1073/pnas.90.17.7941. PMC 47263. PMID 7690138. //www.ncbi.nlm.nih.gov/pmc/articles/PMC47263/. 
• Spring J, Goldberger OA, Jenkins NA et al. (1994). "Mapping of the syndecan genes in the mouse: linkage with members of the myc gene family". Genomics 21 (3): 597–601. doi:10.1006/geno.1994.1319. PMID 7959737. 
• Sneed TB, Stanley DJ, Young LA, Sanderson RD (1994). "Interleukin-6 regulates expression of the syndecan-1 proteoglycan on B lymphoid cells". Cell. Immunol. 153 (2): 456–67. doi:10.1006/cimm.1994.1042. PMID 8118875. 
• Maruyama K, Sugano S (1994). "Oligo-capping: a simple method to replace the cap structure of eukaryotic mRNAs with oligoribonucleotides". Gene 138 (1–2): 171–4. doi:10.1016/0378-1119(94)90802-8. PMID 8125298. 
• Kokenyesi R, Bernfield M (1994). "Core protein structure and sequence determine the site and presence of heparan sulfate and chondroitin sulfate on syndecan-1". J. Biol. Chem. 269 (16): 12304–9. PMID 8163535. 
• Albini A, Benelli R, Presta M et al. (1996). "HIV-tat protein is a heparin-binding angiogenic growth factor". Oncogene 12 (2): 289–97. PMID 8570206. 
• Bonaldo MF, Lennon G, Soares MB (1997). "Normalization and subtraction: two approaches to facilitate gene discovery". Genome Res. 6 (9): 791–806. doi:10.1101/gr.6.9.791. PMID 8889548. 
• Kaukonen J, Alanen-Kurki L, Jalkanen M, Palotie A (1997). "The mapping and visual ordering of the human syndecan-1 and N-myc genes near the telomeric region of chromosome 2p". Hum. Genet. 99 (3): 295–7. doi:10.1007/s004390050360. PMID 9050911. 

External links

• Syndecan-1 at the US National Library of Medicine Medical Subject Headings (MeSH)

UpToDate Contents

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• 1. リンパ形質細胞性リンパ腫の臨床症状、病理学的特徴、および診断 clinical manifestations pathologic features and diagnosis of lymphoplasmacytic lymphoma
• 2. 形質細胞白血病 plasma cell leukemia
• 3. AIDS関連リンパ腫：疫学、危険因子、および病理学 aids related lymphomas epidemiology risk factors and pathobiology
• 4. BおよびTリンパ球の正常な発生 normal b and t lymphocyte development
• 5. びまん性大細胞型B細胞性リンパ腫の疫学、臨床症状、病理学的特徴、および診断 epidemiology clinical manifestations pathologic features and diagnosis of diffuse large b cell lymphoma

English Journal

• Irradiation-induced angiogenesis is associated with an MMP-9-miR-494-syndecan-1 regulatory loop in medulloblastoma cells.

• Asuthkar S1, Velpula KK1, Nalla AK1, Gogineni VR1, Gondi CS1, Rao JS2.Author information 1Department of Cancer Biology and Pharmacology, University of Illinois College of Medicine at Peoria, Peoria, IL, USA.21] Department of Cancer Biology and Pharmacology, University of Illinois College of Medicine at Peoria, Peoria, IL, USA [2] Department of Neurosurgery, University of Illinois College of Medicine at Peoria, Peoria, IL, USA.AbstractMatrix metalloproteinase-9 (MMP-9) represents one of the most prominent proteins associated with tumorigenesis and is a modulator of the tumor microenvironment during angiogenesis. Recently, syndecan-1 (SDC1), a transmembrane heparan sulfate-bearing proteoglycan, was also speculated to have a critical role in contributing to angiogenesis when associated with MMP-9. However, the mechanism behind their synergistic regulation is not fully understood. In the current study, we report for the first time that ionizing radiation (IR)-induced MMP-9 enhances SDC1 shedding, corroborating to tube-inducing ability of medulloblastoma (MB) cells. Furthermore, we observed that the tumor angiogenesis is associated with higher MMP-9-SDC1 interactions on both the cell surface and extracellular medium. Our results also revealed the existence of a novel regulatory mechanism where MMP-9 drives the suppression of miR-494, resulting in enhanced SDC1 shedding and angiogenesis. From the in situ hybridization analysis, we found that MMP-9-specific shRNA (shMMP-9) treatment of mouse intracranial tumors resulted in elevated expression of miR-494. This negative correlation between MMP-9 and miR-494 levels was observed to be dependent on the methylation status of a miR-494 promoter-associated CpG island region (-186 to -20), which was confirmed by bisulfite-sequencing and methylation-specific PCR (MSP) analysis. Further, validation of MMP-9 and SDC1 3'-untranslated region (3'-UTR) targets with luciferase reporter assay provided a more favorable result for miR-494-mediated regulation of SDC1 but not of MMP-9, suggesting that the 3'-UTR of SDC1 mRNA is a direct target of miR-494. Overall, our results indicate that angiogenesis induced by radiotherapy is associated with an MMP-9-miR-494-SDC1 regulatory loop and that MMP-9-SDC1 activity creates a negative feedback loop by regulating the expression of miR-494.
• Oncogene.Oncogene.2014 Apr 10;33(15):1922-33. doi: 10.1038/onc.2013.151. Epub 2013 Jun 3.
• Matrix metalloproteinase-9 (MMP-9) represents one of the most prominent proteins associated with tumorigenesis and is a modulator of the tumor microenvironment during angiogenesis. Recently, syndecan-1 (SDC1), a transmembrane heparan sulfate-bearing proteoglycan, was also speculated to have a critic
• PMID 23728345

• Loss of Syndecan-1 Induces a Pro-inflammatory Phenotype in Endothelial Cells with a Dysregulated Response to Atheroprotective Flow.

• Voyvodic PL1, Min D, Liu R, Williams E, Chitalia V, Dunn AK, Baker AB.Author information 1From the Department of Biomedical Engineering, University of Texas at Austin, Austin, Texas 78712 and.AbstractFluid shear stresses are potent regulators of vascular homeostasis and powerful determinants of vascular disease progression. The glycocalyx is a layer of glycoaminoglycans, proteoglycans, and glycoproteins that lines the luminal surface of arteries. The glycocalyx interacts directly with hemodynamic forces from blood flow and, consequently, is a prime candidate for the mechanosensing of fluidic shear stresses. Here, we investigated the role of the glycocalyx component syndecan-1 (sdc-1) in controlling the shear stress-induced signaling and flow-mediated phenotypic modulation in endothelial cells. We found that knock-out of sdc-1 abolished several key early signaling events of endothelial cells in response to shear stress including the phosphorylation of Akt, the formation of a spatial gradient in paxillin phosphorylation, and the activation of RhoA. After exposure to atheroprotective flow, we found that sdc-1 knock-out endothelial cells had a phenotypic shift to an inflammatory/pro-atherosclerotic phenotype in contrast to the atheroprotective phenotype of wild type cells. Consistent with these findings, we found increased leukocyte adhesion to sdc-1 knock-out endothelial cells in vitro that was reduced by re-expression of sdc-1. In vivo, we found increased leukocyte recruitment and vascular permeability/inflammation in sdc-1 knock-out mice. Taken together, our studies support a key role for sdc-1 in endothelial mechanosensing and regulation of endothelial phenotype.
• The Journal of biological chemistry.J Biol Chem.2014 Apr 4;289(14):9547-59. doi: 10.1074/jbc.M113.541573. Epub 2014 Feb 19.
• Fluid shear stresses are potent regulators of vascular homeostasis and powerful determinants of vascular disease progression. The glycocalyx is a layer of glycoaminoglycans, proteoglycans, and glycoproteins that lines the luminal surface of arteries. The glycocalyx interacts directly with hemodynami
• PMID 24554698

• BAFF and APRIL as TNF superfamily molecules and angiogenesis parallel progression of human multiple myeloma.

• Bolkun L1, Lemancewicz D, Jablonska E, Kulczynska A, Bolkun-Skornicka U, Kloczko J, Dzieciol J.Author information 1Department of Haematology, Medical University of Bialystok, 24a Sklodowskiej-Curie, Bialystok, 15-276, Poland, lbolkun@gmail.com.AbstractTumour necrosis factor alpha (TNF-α) is an inflammatory cytokine with a wide spectrum of biological activity, including angiogenesis. B cell activating factor (BAFF) and a proliferation-inducing ligand (APRIL) are members of the TNF-α family. Vascular endothelial growth factor (VEGF), on the other hand, is one of the most characteristic pro-angiogenic cytokines produced by multiple cell types in multiple myeloma (MM). We have analysed BAFF and APRIL concentrations in parallel with pro-angiogenic cytokines in serum and trephine biopsy, and the bone marrow microvascular density (MVD) in 50 patients with newly diagnosed IgG MM and 24 healthy volunteers. The study showed statistically higher concentrations of BAFF, APRIL and TNF-α, as well as VEGF and its receptor, in MM patients compared to healthy volunteers and patients in advanced stages of the disease. A statistically positive correlation between the concentration of TNF-α and the expression of VEGF was demonstrated, and so was a positive link between BAFF, APRIL, MVD and lactate dehydrogenase (LDH). Furthermore, we observed a significant decrease in all studied cytokines after anti-angiogenic therapy, with meaningful differences between responders (at least partial remission) and patients with stable disease. It was also established that APRIL, but not BAFF, correlated with pro-angiogenic cytokines such as VEGF with its receptor, MVD and syndecan-1. Finally, our results showed that serum BAFF and APRIL levels could be useful biomarkers of MM disease activity and its progression which suggests that APRIL could be a possible novel therapeutic target in MM.
• Annals of hematology.Ann Hematol.2014 Apr;93(4):635-44. doi: 10.1007/s00277-013-1924-9. Epub 2013 Oct 19.
• Tumour necrosis factor alpha (TNF-α) is an inflammatory cytokine with a wide spectrum of biological activity, including angiogenesis. B cell activating factor (BAFF) and a proliferation-inducing ligand (APRIL) are members of the TNF-α family. Vascular endothelial growth factor (VEGF), on the other
• PMID 24141333

Japanese Journal

• Peritoneum from Trypanosoma cruzi-infected mice is a homing site of Syndecan-1^<neg> plasma cells which mainly provide non-parasite-specific antibodies

• MERINO Maria C.,MONTES Carolina L.,ACOSTA-RODRIGUEZ Eva V.,BERMEJO Daniela A.,AMEZCUA-VESELY Maria C.,GRUPPI Adriana
• International immunology 22(5), 399-410, 2010-05-01
• NAID 10027580026

• Role of syndecan-1 (CD138) in cell survival of human urothelial carcinoma

• SHIMADA Keiji,NAKAMURA Mitsutoshi,DE VELASCO Marco A.,TANAKA Motoyoshi,OUJI Yukiteru,MIYAKE Makito,FUJIMOTO Kiyohide,HIRAO Kazuya,KONISHI Noboru
• Cancer science 101(1), 155-160, 2010-01-10
• NAID 10027199949

Related Links

• 抗CD138抗体/サイトメトリー専門Webサイト

CD138 【Syndecan-1】 CD138抗原（syndecan-1としても知られている）は､4種類の膜貫通型ヘパラン硫酸化プロテオグリカン高分子（Syndecan-1､Syndecan-2またはfibroglycan､Syndecan-3またはN-syndecan､Syndecan-4または ...

• 糖質科学のことば / Proteoglycan-A02

シンデカンとグリピカン - 細胞表面プロテオグリカン 膜貫通型ヘパラン硫酸プロテオグリカン（HSPG）であるシンデカン（Syndecan）ファミリーは、4つのメンバー（Syndecan-1/Syndecan, Syndecan-2/Fibroglycan, Syndecan-3/N ...

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