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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2016/02/24 08:45:00」(JST)

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CD166 antigen is a 100-105 kD typeI transmembrane glycoprotein that is a member of the immunoglobulin superfamily of proteins. In humans it is encoded by the ALCAM gene.^[1]^[2] It is also called CD166 (cluster of differentiation 166), MEMD, SC-1/DM-GRASP/BEN in the chicken, and KG-CAM in the rat. Some literature sources have also cited it as the CD6 ligand (CD6L). It is expressed on activated T cells, activated monocytes, epithelial cells, fibroblasts, neurons, melanoma cells, and also in sweat and sebaceous glands. CD166 protein expression is reported to be upregulated in a cell line deriving from a metastasizing melanoma. CD166 plays an important role in mediating adhesion interactions between thymic epithelial cells and CD6+ cells during intrathymic T cell development. Recently, CD166 has also been used as a potential cancer stem cell marker.

References

^ Bowen MA, Patel DD, Li X, Modrell B, Malacko AR, Wang WC, Marquardt H, Neubauer M, Pesando JM, Francke U; et al. (Jun 1995). "Cloning, mapping, and characterization of activated leukocyte-cell adhesion molecule (ALCAM), a CD6 ligand". J Exp Med 181 (6): 2213–20. doi:10.1084/jem.181.6.2213. PMC 2192054. PMID 7760007.
^ "Entrez Gene: ALCAM activated leukocyte cell adhesion molecule".

External links

ALCAM at the US National Library of Medicine Medical Subject Headings (MeSH)

This membrane protein–related article is a stub. You can help Wikipedia by expanding it.

English Journal

miR-483-5p promotes invasion and metastasis of lung adenocarcinoma by targeting RhoGDI1 and ALCAM.

Song Q1, Xu Y, Yang C, Chen Z, Jia C, Chen J, Zhang Y, Lai P, Fan X, Zhou X, Lin J, Li M, Ma W, Luo S, Bai X.Author information 1Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University.AbstractThe nodal regulatory properties of microRNAs in metastatic cancer may offer new targets for therapeutic control. Here we report that upregulation of miR-483-5p is correlated with the progression of human lung adenocarcinoma. miR-483-5p promotes epithelial-mesenchymal transition (EMT) accompanied by invasive and metastatic properties of lung adenocarcinoma. Mechanistically, miR-483-5p is activated by the WNT/β-catenin signaling pathway and exerts its pro-metastatic function by directly targeting the Rho GDP dissociation inhibitor alpha (RhoGDI1) and activated leukocyte cell adhesion molecule (ALCAM), two putative metastasis suppressors. What's more, we found that downregulation of RhoGDI1 enhances expression of Snail thereby promoting EMT. Importantly, miR-483-5p levels are positively correlated with β-catenin expression, but are negatively correlated with the levels of RhoGDI1 and ALCAM in human lung adenocarcinoma. Our findings reveal that miR-483-5p is a critical β-catenin-activated pro-metastatic microRNA and a negative regulator of the metastasis suppressors RhoGDI1 and ALCAM.
Cancer research.Cancer Res.2014 Apr 7. [Epub ahead of print]
The nodal regulatory properties of microRNAs in metastatic cancer may offer new targets for therapeutic control. Here we report that upregulation of miR-483-5p is correlated with the progression of human lung adenocarcinoma. miR-483-5p promotes epithelial-mesenchymal transition (EMT) accompanied by
PMID 24710410

Dynamic coupling of ALCAM to the actin cortex strengthens cell adhesion to CD6.

Te Riet J1, Helenius J, Strohmeyer N, Cambi A, Figdor CG, Müller DJ.Author information 1Department of Tumor Immunology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Geert Grooteplein 28, 6525 GA Nijmegen, The Netherlands.AbstractAt the immunological synapse, the activated leukocyte cell adhesion molecule (ALCAM) on a dendritic cell (DC) and CD6 molecules on a T cell contribute to sustained DC-T-cell contacts. However, little is known about how ALCAM-CD6 bonds resist and adapt to mechanical stress. Here, we combine single-cell force spectroscopy (SCFS) with total-internal reflection fluorescence microscopy to examine ALCAM-CD6-mediated cell adhesion. The combination of cells expressing ALCAM constructs with certain cytoplasmic tail mutations and improved SCFS analysis processes reveal that the affinity of ALCAM-CD6 bonds is not influenced by the linking of the intracellular domains of ALCAM to the actin cortex. By contrast, the recruitment of ALCAM to adhesion sites and the propensity of ALCAM to anchor plasma membrane tethers depend on actin cytoskeletal interactions. Furthermore, linking ALCAM to the actin cortex through adaptor proteins stiffens the cortex and strengthens cell adhesion. We propose a framework for how ALCAMs contribute to DC-T-cell adhesion, stabilize DC-T-cell contacts and form a mechanical link between CD6 and the actin cortex to strengthen cell adhesion at the immunological synapse.
Journal of cell science.J Cell Sci.2014 Apr 1;127(Pt 7):1595-606. doi: 10.1242/jcs.141077. Epub 2014 Feb 4.
At the immunological synapse, the activated leukocyte cell adhesion molecule (ALCAM) on a dendritic cell (DC) and CD6 molecules on a T cell contribute to sustained DC-T-cell contacts. However, little is known about how ALCAM-CD6 bonds resist and adapt to mechanical stress. Here, we combine single-ce
PMID 24496453

Functional role of endothelial adhesion molecules in the early stages of brain metastasis.

Soto MS1, Serres S, Anthony DC, Sibson NR.Author information 1CR-UK/MRC Gray Institute for Radiation Oncology and Biology, Department of Oncology, University of Oxford, Churchill Hospital, Oxford, UK (M.S.S., S. S., N.R.S.; Department of Pharmacology, University of Oxford, Oxford UK (D.C.A.).AbstractBACKGROUND: Cellular adhesion molecules (CAMs), which are normally associated with leukocyte trafficking, have also been shown to play an essential role in tumor metastasis to non-CNS sites. However, the role played by CAMs in brain metastasis is largely unexplored. It is known that leukocyte recruitment to the brain is very atypical and that mechanisms of disease in peripheral tissues cannot be extrapolated to the brain. Here, we have established the spatiotemporal expression of 12 key CAMs in the initial phases of tumor seeding in 2 different models of brain metastasis.
Neuro-oncology.Neuro Oncol.2014 Apr;16(4):540-51. doi: 10.1093/neuonc/not222. Epub 2013 Dec 4.
BACKGROUND: Cellular adhesion molecules (CAMs), which are normally associated with leukocyte trafficking, have also been shown to play an essential role in tumor metastasis to non-CNS sites. However, the role played by CAMs in brain metastasis is largely unexplored. It is known that leukocyte recrui
PMID 24311639

Japanese Journal

Hematopoietic stem cells and niche cell populations

Inflammation and Regeneration 32(4), 152-157, 2012
NAID 130004943821

9-24.ヒト胚および子宮内膜上皮におけるactivated leukocyte cell adhesion molecule(ALCAM/CD166)の発現(第40群生殖生理・病理5)(一般演題)

日本産科婦人科學會雜誌 56(2), 438, 2004-02-01
NAID 110002101237

胚との相互作用における着床期子宮内膜の機能変化とその分子機構の解析(子宮内膜機能の調節機構 : 着床機構の視点から)

日本産科婦人科學會雜誌 55(8), 1047-1057, 2003-08-01
NAID 110002100222

Related Pictures

Flow Cytometry Mouse ALCAM/CD166 APC ALCAM Industrial Supplies Dynamic coupling of ALCAM to the actin Photos de alcam à Garges les gonesse Flow Cytometry Human ALCAM/CD166 Alexa leukocyte cell adhesion molecule (ALCAM

★リンクテーブル★

リンク元	「活性化白血球細胞接着分子」「activated-leukocyte cell adhesion molecule」

「活性化白血球細胞接着分子」

Activated leukocyte cell adhesion molecule
Available structures
PDB	Ortholog search: PDBe, RCSB
List of PDB id codes
	1KJC
Identifiers
Symbols	ALCAM ; CD166; MEMD
External IDs	OMIM: 601662 MGI: 1313266 HomoloGene: 1229 GeneCards: ALCAM Gene
Gene ontology
Molecular function	• receptor binding; • protein binding;
Cellular component	• focal adhesion; • external side of plasma membrane; • integral component of membrane; • axon; • neuronal cell body; • extracellular exosome;
Biological process	• cell adhesion; • signal transduction; • axon guidance; • motor neuron axon guidance;
	Sources: Amigo / QuickGO
Orthologs
	v; t; e;