関: intracellular adhesion molecule 3, ICAM-3:CD50

関: intracellular adhesion molecule 3, ICAM-3:CD50

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/09/22 11:52:40」(JST)

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Vascular cell adhesion protein 1 also known as vascular cell adhesion molecule 1 (VCAM-1) or cluster of differentiation 106 (CD106) is a protein that in humans is encoded by the VCAM1 gene.^[1] VCAM-1 functions as a cell adhesion molecule.

Structure

The VCAM-1 gene contains six or seven immunoglobulin domains, and is expressed on both large and small blood vessels only after the endothelial cells are stimulated by cytokines. It is alternatively spliced into two known RNA transcripts that encode different isoforms in humans.^[2] The gene product is a cell surface sialoglycoprotein, a type I membrane protein that is a member of the Ig superfamily.

Function

The VCAM-1 protein mediates the adhesion of lymphocytes, monocytes, eosinophils, and basophils to vascular endothelium. It also functions in leukocyte-endothelial cell signal transduction, and it may play a role in the development of atherosclerosis and rheumatoid arthritis.

Upregulation of VCAM-1 in endothelial cells by cytokines occurs as a result of increased gene transcription (e.g., in response to Tumor necrosis factor-alpha (TNF-α) and Interleukin-1 (IL-1)) and through stabilization of Messenger RNA (mRNA) (e.g., Interleukin-4 (IL-4)). The promoter region of the VCAM-1 gene contains functional tandem NF-κB (nuclear factor-kappa B) sites. The sustained expression of VCAM-1 lasts over 24 hours.

Primarily, the VCAM-1 protein is an endothelial ligand for VLA-4 (Very Late Antigen-4 or α4β1) of the β1 subfamily of integrins, and for integrin α4β7. VCAM-1 expression has also been observed in other cell types (e.g., smooth muscle cells). It has also been shown to interact with EZR^[3] and Moesin.^[3]

Pharmacology

Certain melanoma cells can use VCAM-1 to adhere to the endothelium,^[4] and VCAM-1 may participate in monocyte recruitment to atherosclerotic sites. As a result, VCAM-1 is a potential drug target.

References

^ Cybulsky M, Fries JW, Williams AJ, Sultan P, Eddy RL, Byers MG, Shows TB, Gimbrone MA Jr, Collins T (1991). "The human VCAM1 gene is assigned to chromosome 1p31-p32". Cytogenet. Cell Genet. 58: 1852. doi:10.1159/000133735.
^ "Entrez Gene: VCAM1 vascular cell adhesion molecule 1".
^ ^a ^b Barreiro, Olga; Yanez-Mo Maria, Serrador Juan M, Montoya Maria C, Vicente-Manzanares Miguel, Tejedor Reyes, Furthmayr Heinz, Sanchez-Madrid Francisco (Jun 2002). "Dynamic interaction of VCAM-1 and ICAM-1 with moesin and ezrin in a novel endothelial docking structure for adherent leukocytes". J. Cell Biol. (United States) 157 (7): 1233–45. doi:10.1083/jcb.200112126. ISSN 0021-9525. PMC 2173557. PMID 12082081. Cite uses deprecated parameters (help)
^ Eibl RH and Benoit M (2004). "Molecular resolution of cell adhesion forces.". IEE Proc Nanobiotechnol. 151 (3): 128-32. doi:10.1049/ip-nbt:20040707. PMID 16475855.

External links

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

UpToDate Contents

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1. BおよびTリンパ球の正常な発生 normal b and t lymphocyte development
2. 肥満細胞：増殖・分化、識別、および生理学的役割 mast cells development identification and physiologic roles

English Journal

Lipopolysaccharide induces the interactions of breast cancer and endothelial cells via activated monocytes.

Chen C1, Khismatullin DB2.Author information 1Department of Biomedical Engineering, Tulane University, New Orleans, LA 70118, USA.2Department of Biomedical Engineering, Tulane University, New Orleans, LA 70118, USA. Electronic address: damir@tulane.edu.AbstractThe adhesion of circulating cancer cells to vascular endothelium is a key step in hematogenous metastasis. Cancer cell-endothelium interactions are mediated by cell adhesion molecules that can also be involved in the arrest of monocytes and other circulating leukocytes on endothelium in inflammation. Static and microfluidic flow adhesion assays as well as flow cytometry were conducted in this study to elucidate the role of monocytes, bacterial lipopolysaccharide (LPS), and histamine in breast cancer cell adhesion to vascular endothelial cells. Tumor necrosis factor-α (TNF-α) released from LPS-treated monocytes triggered the expression of intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) on endothelial cells. Histamine augmented the TNF-α effect, leading to a high number of arrested breast cancer cells under both static and shear flow conditions. LPS-treated monocytes were shown to enhance the arrest of breast cancer cells by anchoring the cancer cells to activated endothelial cells. This anchorage was achieved by binding cancer cell ICAM-1 to monocyte β2 integrins and binding endothelial ICAM-1 and VCAM-1 to monocyte β1 and β2 integrins. The results of this study imply that LPS is an important risk factor for cancer metastasis and that the elevated serum level of histamine further increases the risk of LPS-induced cancer metastasis. Preventing bacterial infections is essential in cancer treatment, and it is particularly vital for cancer patients affected by allergy.
Cancer letters.Cancer Lett.2014 Apr 1;345(1):75-84. doi: 10.1016/j.canlet.2013.11.022. Epub 2013 Dec 11.
The adhesion of circulating cancer cells to vascular endothelium is a key step in hematogenous metastasis. Cancer cell-endothelium interactions are mediated by cell adhesion molecules that can also be involved in the arrest of monocytes and other circulating leukocytes on endothelium in inflammation
PMID 24333719

Cell-cell adhesion through N-cadherin enhances VCAM-1 expression via PDGFRβ in a ligand-independent manner in mesenchymal stem cells.

Aomatsu E1, Chosa N1, Nishihira S1, Sugiyama Y2, Miura H3, Ishisaki A1.Author information 1Division of Cellular Biosignal Sciences, Department of Biochemistry, Iwate Medical University, Yahaba, Iwate 028-3694, Japan.2Division of Oral Surgery, Department of Oral and Maxillofacial Surgery, Iwate Medical University School of Dentistry, Morioka, Iwate 020-8505, Japan.3Division of Orthodontics, Department of Developmental Oral Health Science, Iwate Medical University School of Dentistry, Morioka, Iwate 020-8505, Japan.AbstractCell-cell adhesions induce various intracellular signals through hierarchical and synergistic molecular interactions. Recently, we demonstrated that a high cell density induces the expression of vascular cell adhesion molecule-1 (VCAM-1) through the nuclear factor-κB (NF-κB) pathway in human bone marrow-derived mesenchymal stem cells (MSCs). However, the specific molecules that activated the NF-κB pathway were not determined. In the present study, in experiments with receptor tyrosine kinase inhibitors, VCAM-1 expression was completely suppressed by platelet-derived growth factor (PDGF) receptor (PDGFR) inhibitors. In addition, VCAM-1 expression was significantly suppressed by knockdown with PDGFRβ siRNA, but not with PDGFRα siRNA. However, VCAM-1 expression did not increase following treatment with PDGF. The overexpression of N-cadherin, a structural molecule in adherence junctions in MSCs, promoted VCAM-1 expression and induced the marked phosphorylation of the intracellular signaling factor, Src. In addition, VCAM-1 expression and Src phosphorylation were reduced by the overexpression of a dominant negative mutant of N-cadherin. These results suggest that cell-cell adhesion, through N-cadherin, enhances the expression of VCAM-1 via PDGFRβ and the activation of Src in a ligand-independent manner in MSCs.
International journal of molecular medicine.Int J Mol Med.2014 Mar;33(3):565-72. doi: 10.3892/ijmm.2013.1607. Epub 2013 Dec 27.
Cell-cell adhesions induce various intracellular signals through hierarchical and synergistic molecular interactions. Recently, we demonstrated that a high cell density induces the expression of vascular cell adhesion molecule-1 (VCAM-1) through the nuclear factor-κB (NF-κB) pathway in human bone
PMID 24378362

Improved adhesion and differentiation of endothelial cells on surface-attached fibrin structures containing extracellular matrix proteins.

Filová E, Brynda E, Riedel T, Chlupáč J, Vandrovcová M, Svindrych Z, Lisá V, Houska M, Pirk J, Bačáková L.Author information Department of Biomaterials and Tissue Engineering, Institute of Physiology, Academy of Sciences of the Czech Republic, v.v.i., 142 20 Prague 4, Czech Republic.AbstractCurrently used vascular prostheses are hydrophobic and do not allow endothelial cell (EC) adhesion and growth. The aim of this study was to prepare fibrin (Fb)-based two-dimensional (2D) and three-dimensional (3D) assemblies coated with extracellular matrix (ECM) proteins and to evaluate the EC adhesion, proliferation and differentiation on these assemblies in vitro. Coating of Fb with collagen, laminin (LM), and fibronectin (FN) was proved using the surface plasmon resonance technique. On all Fb assemblies, ECs reached higher cell densities than on polystyrene after 3 and 7 days of culture. Immunoflurescence staining showed better assembly of talin and vinculin into focal adhesion plaques, and also more apparent staining of vascular endothelial cadherin on surface-attached 3D Fb and protein-coated Fb assemblies. On these samples, ECs also contained a lower concentration of intercellular adhesion molecule-1, measured by enzyme-linked immunosorbent assay. Higher concentrations of CD31 (platelet-endothelial cell adhesion molecule-1) were found on 3D Fb coated with LM, and higher concentrations of von Willebrand factor were found on 3D Fb coated with type I collagen or LM in comparison to 2D Fb layers. The results indicate that ECM protein-coated 2D and 3D Fb assemblies can be used for versatile applications in various tissue replacements where endothelialization is desirable, for example, vascular prostheses and heart valves. © 2013 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 102A: 698-712, 2014.
Journal of biomedical materials research. Part A.J Biomed Mater Res A.2014 Mar;102(3):698-712. doi: 10.1002/jbm.a.34733. Epub 2013 May 30.
Currently used vascular prostheses are hydrophobic and do not allow endothelial cell (EC) adhesion and growth. The aim of this study was to prepare fibrin (Fb)-based two-dimensional (2D) and three-dimensional (3D) assemblies coated with extracellular matrix (ECM) proteins and to evaluate the EC adhe
PMID 23723042

Japanese Journal

Changes in the expression of CD106, osteogenic genes, and transcription factors involved in the osteogenic differentiation of human bone marrow mesenchymal stem cells

LIU Feng,AKIYAMA Yasuto,TAI Sachiko,MARUYAMA Kouji,KAWAGUCHI Yoshihiro,MURAMATSU Kouji,YAMAGUCHI Ken
Journal of bone and mineral metabolism 26(4), 312-320, 2008-07-30
NAID 10024458551

Increased expression of soluble form of vascular cell adhesion molecule-1 aggravates autoimmune arthritis in MRL-Fas^<Ipr> mice

OISHI Hisashi,MIZUKI Shinichi,TERADA Miho,KUDO Megumi,ARAKI Kimi,ARAKI Masatake,NOSE Masato,TAKAHASHI Satoru
Pathology international 57(11), 734-740, 2007-11-01
NAID 10021234200

Related Pictures

★リンクテーブル★

リンク元	「接着分子」「T細胞」「VCAM-1」
関連記事	「CD1」「CD10」

「接着分子」

Vascular cell adhesion molecule 1
	; PDB rendering based on 1ij9.
Available structures
PDB	Ortholog search: PDBe, RCSB
List of PDB id codes
	1IJ9, 1VCA, 1VSC
Identifiers
Symbols	VCAM1 ; CD106; INCAM-100
External IDs	OMIM: 192225 MGI: 98926 HomoloGene: 838 ChEMBL: 3735 GeneCards: VCAM1 Gene
Gene ontology
Molecular function	• integrin binding; • primary amine oxidase activity; • cell adhesion molecule binding;
Cellular component	• podosome; • extracellular space; • early endosome; • endoplasmic reticulum; • Golgi apparatus; • plasma membrane; • microvillus; • external side of plasma membrane; • cell surface; • integral component of membrane; • filopodium; • sarcolemma; • apical part of cell; • extracellular vesicular exosome; • alpha9-beta1 integrin-vascular cell adhesion molecule-1 complex;
Biological process	• response to hypoxia; • acute inflammatory response; • chronic inflammatory response; • cell adhesion; • heterophilic cell-cell adhesion; • leukocyte cell-cell adhesion; • heart development; • aging; • response to nutrient; • amine metabolic process; • response to zinc ion; • response to ionizing radiation; • viral process; • cytokine-mediated signaling pathway; • membrane to membrane docking; • B cell differentiation; • extracellular matrix organization; • response to lipopolysaccharide; • response to nicotine; • cellular response to vascular endothelial growth factor stimulus; • positive regulation of T cell proliferation; • response to ethanol; • regulation of immune response; • leukocyte tethering or rolling; • oxidation-reduction process; • cell chemotaxis; • interferon-gamma-mediated signaling pathway; • chorio-allantoic fusion; • cellular response to glucose stimulus; • cellular response to tumor necrosis factor;
	Sources: Amigo / QuickGO
RNA expression pattern
	More reference expression data
Orthologs
	This box: view; talk; edit;

　　[★]

英: adhesion molecule
同: 接着因子
関

接着分子のファミリー

インテグリンファミリー
Igスーパーファミリー
セレクチンファミリー
CD44ファミリー
カドヘリンファミリー

白血球の相互作用に関与している接着分子 (IMM.87)

グループ名	機能	名称	別名		組織分布	リガンド
セレクチン	炭化水素鎖に結合。白血球-内皮細胞の反応を開始	P-selectin	PADGEN	CD62P	活性化した内皮細胞、活性化した血小板	PSGL-1, sialyl-Lewisx
セレクチン	炭化水素鎖に結合。白血球-内皮細胞の反応を開始	E-selectin	ELAM-1	CD62E	活性化した内皮細胞	sialyl-Lewisx
インテグリン	CAMや細胞外マトリックスに結合。強い結合	LFA-1	αL:β2	CD11a:CD18	単球、T細胞、マクロファージ、好中球、樹状細胞	ICAMs
		CR3, Mac-1	αM:β2	CD11b:CD18	好中球、単球、マクロファージ	ICAM-1, iC3b, fibrinogen
		CR4, p150.95	αX:β2	CD11c:CD18	樹状細胞、マクロファージ、好中球	iC3b
		VLA-5	α5:β1	CD49d:CD29	単球、マクロファージ	fibronectin
免疫グロブリンスーパーファミリー	細胞結合で様々に働く。インテグリンの基質	ICAM-1		CD54	活性化した内皮細胞	LFA-1, MAC1
		ICAM-2		CD102	非活性化状態の内皮細胞、樹状細胞	LFA-1
		VCAM-1		CD106	活性化した内皮細胞	VLA-4
		PECAM		CD31	活性化した白血球、内皮細胞間の結合	CD31

白血球の相互作用に関与している免疫グロブリンスーパーファミリーの接着分子 (IMM.329)

名称		分布組織	リガンド
CD2	LFA-2	T細胞	LFA-1	CD53
ICAM-1	CD54	活性化した血管、リンパ球、樹状細胞	LFA-1, Mac-1
ICAM-2	CD102	非活性化状態の血管	LFA-1
ICAM-3	CD50	Naive T cells	DC-SIGN, LFA-1
LFA-3	CD58	リンパ球、APC	CD2
VCAM-1	CD106	活性化した内皮細胞	VLA-4

-接着分子

-細胞接着分子

-カドヘリン

「T細胞」

　　[★]

英: T cell
同: Tリンパ球、T lymphocyte
関: TCR、B細胞、MHC

図：IMM.315(T細胞の成熟)
胸腺で成熟したT細胞は血流によって移動し、リンパ節の傍皮質、白脾髄のリンパ性動脈周囲鞘、パイエル板の傍濾胞域に集まる(人間の正常構造と機能 VIIA血管・免疫 p.28)

種類

T細胞の抗原認識 (SP.248)

	CD	TCRが抗原と共に認識する分子	認識する細胞
Tc細胞	CD8	MHCクラスI	感染細胞
Th細胞	CD4	MHCクラスII	抗原提示細胞

CD4+ T細胞のサイトカイン放出とその原因

DCが認識する外来異物	DCが分泌する物質	DCに反応する細胞	この細胞が分泌するサイトカイン	NK系の細胞が放出したサイトカインに反応するTh細胞	Th細胞が分泌するサイトカイン
ウイルス、一部の細菌	IL-12	NK細胞(IL-12による)	INF-γ	Th1	IL-2, IFN-γ, TNF-β
原虫など		NKT細胞	IL-4	Th2	IL-4, IL-13, IL-5

Th細胞活性化と接着分子

	抗原提示細胞	Th細胞
主シグナル	MHC classII	TCR, CD3
主シグナル	MHC classII	CD4
副シグナル	B7{B7-1(CD80)/B7-2(CD86)}	CD28
	VCAM-1(CD106)	VLA-4
	ICAM-1	LFA-1
	LFA-3(CD58)	CD2

「VCAM-1」

　　[★]

同: vascular cell adhesion molecule 1; CD106

インテグリン(VLA-1 integlin)と接着

同: CD106

同: vascular cell adhesion molecule 1

「CD1」

　　[★]

同: leucine-6, CD1A through E

種類

CD1a, CD1b, CD1c, CD1d

発現組織

胸腺皮質、ランゲルハンス細胞、樹状細胞、B細胞(CD1c)、腸上皮、平滑筋、血管上皮(CD1d)

分子量

43-49

機能

MHC class I-like molecule, associated with β2-microgloulin. Has specialized role in presentation of lipid antigens

「CD10」

　　[★]

同: common acute lymphoid leukemia antigen, nephrilysin

発現細胞

B細胞やT細胞前駆体。骨髄間質細胞(bone marrow stromal cell)

分子量

100kDa

機能

Zinc metalloproteinase, marker for pre-B acute lymphatic leukemia (ALL)

別名

Neutral endopeptidase, common acute lymphocytic leukemia antigen(CALLA)

[Cybulsky_1991-1] Cybulsky M, Fries JW, Williams AJ, Sultan P, Eddy RL, Byers MG, Shows TB, Gimbrone MA Jr, Collins T (1991). "The human VCAM1 gene is assigned to chromosome 1p31-p32". Cytogenet. Cell Genet. 58: 1852. doi:10.1159/000133735.

[2] "Entrez Gene: VCAM1 vascular cell adhesion molecule 1".

[pmid12082081-3] Barreiro, Olga; Yanez-Mo Maria, Serrador Juan M, Montoya Maria C, Vicente-Manzanares Miguel, Tejedor Reyes, Furthmayr Heinz, Sanchez-Madrid Francisco (Jun 2002). "Dynamic interaction of VCAM-1 and ICAM-1 with moesin and ezrin in a novel endothelial docking structure for adherent leukocytes". J. Cell Biol. (United States) 157 (7): 1233–45. doi:10.1083/jcb.200112126. ISSN 0021-9525. PMC 2173557. PMID 12082081. Cite uses deprecated parameters (help)

[4] Eibl RH and Benoit M (2004). "Molecular resolution of cell adhesion forces.". IEE Proc Nanobiotechnol. 151 (3): 128-32. doi:10.1049/ip-nbt:20040707. PMID 16475855.

匿名

検索

案内

案内

CD106