Selective expression of cell type specific cell-cell adhesion molecules in mouse hybrid cells

1983 ◽  
Vol 24 (1-3) ◽  
pp. 140-144 ◽  
Author(s):  
Tadao Atsumi ◽  
Masatoshi Takeichi ◽  
T.S. Okada
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Specific Cell ◽  
Hybrid Cells ◽  
Cell Type ◽  
Selective Expression ◽  
Cell Type Specific ◽  
Cell Cell

scholarly journals Molecular Expression of bone marrow angiogenic factors, cell-cell adhesion molecules and matrix-metallo-proteinase plasma cellular disorders: a molecular panel to investigate disease progression

2018 ◽  
Vol 10 ◽  
pp. e2018059
Author(s):  
Maria Cristina Rapanotti
Keyword(s):  
Multiple Myeloma ◽  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Plasma Cells ◽  
Angiogenic Factors ◽  
Specific Cell ◽  
Angiogenic Potential ◽  
E Cadherin ◽  
Cell Cell

Increasing levels of angiogenesis play an important role in the pathogenesis and progression of multiple myeloma (MM). Malignant plasma cells promote a gradual increase in the degree of angiogenesis, modulation of specific cell-cell adhesion molecules and secretion of matrix-metallo-proteinases (MMPs), changing the BM composition from benign conditions, such as MGUS, to smouldering multiple myeloma (SM) and to active MM. We aimed to identify a gene expression profile, helpful to discriminate the “angiogenic potential” in BM and PB plasma cells from MGUS, SMM and active MM patients analyzed at diagnosis. We analyzed the expression of cell-cell adhesion molecules such as VE-Cadherin, E-Cadherin MCAM/MUC18/CD146 and of the MMP-2 and MMP-9. MCAM/MUC18 expression resulted mostly associated with that of the pivotal angiogenic factors VEGF and Ang2, and in MGUS the pattern was different in steady state, compared to progression towards SM. Furthermore, E-Cadherin, the main epithelial cell-cell-adhesion molecule, unexpectedly resulted overexpressed in MM.                                                                                                                                                                                                                                                

An inhibition of gap-junctional communication by cadherins

1997 ◽  
Vol 110 (3) ◽  
pp. 301-309 ◽  
Author(s):  
Y. Wang ◽  
B. Rose
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Hepatoma Cells ◽  
Cell Type ◽  
Gap Junctional Communication ◽  
L Cells ◽  
Junctional Communication ◽  
Gap Junctional ◽  
Cell Cell

The action of Ca(2+)-dependent cell-cell adhesion molecules (cadherins) on cell-to-cell channel-mediated intercellular communication was investigated in mouse L and rat Morris hepatoma cells. These cells fail to adhere to one another in aggregation assays and thus seem to lack cell adhesion molecules. Expression of exogenous cadherin induced strong cell-cell adhesion in both cell types, but had opposite effects of communication, causing inhibition in L cells and improvement in hepatoma cells. Both cells express the connexin43 cell-to-cell channel protein. By western blot we found no cadherin-specific changes in connexin43 protein in either cell type, but connexin43 gap junctional plaque staining, i.e. connexin43 localization to cell-cell junctions, was inhibited in L cells and facilitated in hepatoma cells. In addition we found that the inhibitory effect is largely abolished by blockers of glycosylation. Cadherin-cadherin interactions are known to trigger cell type-specific intracellular signal cascades resulting in diverse end effects, and gap junctional communication/plaque formation seems a further example of such cell type-specificity.

scholarly journals Stick around: Cell–Cell Adhesion Molecules during Neocortical Development

Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 118
Author(s):  
David de Agustín-Durán ◽  
Isabel Mateos-White ◽  
Jaime Fabra-Beser ◽  
Cristina Gil-Sanz
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Neural Cells ◽  
Surface Receptors ◽  
Cellular Processes ◽  
Neocortical Development ◽  
Classical Cadherins ◽  
Adhesive Interactions ◽  
Cell Cell

The neocortex is an exquisitely organized structure achieved through complex cellular processes from the generation of neural cells to their integration into cortical circuits after complex migration processes. During this long journey, neural cells need to establish and release adhesive interactions through cell surface receptors known as cell adhesion molecules (CAMs). Several types of CAMs have been described regulating different aspects of neurodevelopment. Whereas some of them mediate interactions with the extracellular matrix, others allow contact with additional cells. In this review, we will focus on the role of two important families of cell–cell adhesion molecules (C-CAMs), classical cadherins and nectins, as well as in their effectors, in the control of fundamental processes related with corticogenesis, with special attention in the cooperative actions among the two families of C-CAMs.

Expression of Cadherin/Catenin Cell—Cell Adhesion Molecules in a Onychomatricoma

2008 ◽  
Vol 16 (3) ◽  
pp. 349-353 ◽  
Author(s):  
James L. Burchette ◽  
Tram T. Pham ◽  
Steven P. Higgins ◽  
Jonathan L. Cook ◽  
Alejandro Peralta Soler
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Cell Cell

scholarly journals Nectin-3, a New Member of Immunoglobulin-like Cell Adhesion Molecules That Shows Homophilic and Heterophilic Cell-Cell Adhesion Activities

2000 ◽  
Vol 275 (14) ◽  
pp. 10291-10299 ◽  
Author(s):  
Keiko Satoh-Horikawa ◽  
Hiroyuki Nakanishi ◽  
Kenichi Takahashi ◽  
Masako Miyahara ◽  
Miyuki Nishimura ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Cell Cell

scholarly journals The Role of Immunoglobulin Superfamily Cell Adhesion Molecules in Cancer Metastasis

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Chee Wai Wong ◽  
Danielle E. Dye ◽  
Deirdre R. Coombe
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Cancer Progression ◽  
Cell Adhesion Molecules ◽  
Cancer Metastasis ◽  
Clinical Problem ◽  
Metastatic Lesion ◽  
Immunoglobulin Superfamily ◽  
Metastatic Pathway ◽  
Cell Cell

Metastasis is a major clinical problem and results in a poor prognosis for most cancers. The metastatic pathway describes the process by which cancer cells give rise to a metastatic lesion in a new tissue or organ. It consists of interconnecting steps all of which must be successfully completed to result in a metastasis. Cell-cell adhesion is a key aspect of many of these steps. Adhesion molecules belonging to the immunoglobulin superfamily (Ig-SF) commonly play a central role in cell-cell adhesion, and a number of these molecules have been associated with cancer progression and a metastatic phenotype. Surprisingly, the contribution of Ig-SF members to metastasis has not received the attention afforded other cell adhesion molecules (CAMs) such as the integrins. Here we examine the steps in the metastatic pathway focusing on how the Ig-SF members, melanoma cell adhesion molecule (MCAM), L1CAM, neural CAM (NCAM), leukocyte CAM (ALCAM), intercellular CAM-1 (ICAM-1) and platelet endothelial CAM-1 (PECAM-1) could play a role. Although much remains to be understood, this review aims to raise the profile of Ig-SF members in metastasis formation and prompt further research that could lead to useful clinical outcomes.

Analysis of Cell‐Cell Contact Mediated by Ig Superfamily Cell Adhesion Molecules

2001 ◽  
Vol 11 (1) ◽  
Author(s):  
Peter Sonderegger ◽  
Stefan Kunz ◽  
Christoph Rader ◽  
Daniel M. Suter ◽  
Esther T. Stoeckli
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Cell Contact ◽  
Ig Superfamily ◽  
Cell Cell
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