880: Interactions of immunoglobulin-like cell adhesion molecule hepaCAM with CD137 in cell-matrix interactions, cell motility and escape from immune surveillance in Hodgkin Lymphoma

2014 ◽  
Vol 50 ◽  
pp. S215
Author(s):  
J. Seah
Keyword(s):  
Cell Adhesion ◽  
Cell Motility ◽  
Hodgkin Lymphoma ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Immune Surveillance ◽  
Cell Matrix ◽  
Matrix Interactions ◽  
Cell Matrix Interactions

Effects of collagenase-cleavage of type I collagen on alpha2beta1 integrin-mediated cell adhesion

1998 ◽  
Vol 111 (8) ◽  
pp. 1127-1135 ◽  
Author(s):  
A.J. Messent ◽  
D.S. Tuckwell ◽  
V. Knauper ◽  
M.J. Humphries ◽  
G. Murphy ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Type I Collagen ◽  
Cell Attachment ◽  
Heat Denaturation ◽  
Type I ◽  
Cell Matrix ◽  
Matrix Interactions ◽  
Triple Helices ◽  
Collagen Fragment ◽  
Cell Matrix Interactions

In this paper we show that collagenase-3 cleavage of type I collagen has a marked effect on alpha2beta1 integrin-mediated interactions with the collagen fragments generated. Isolated alpha2beta1 integrin and alpha2 integrin A-domain were found to bind to both native collagen and native 3/4 fragment and, to a lesser degree, native 1/4 fragment. Whole integrin and integrin A-domain binding were lost after heat denaturation of the collagen fragments. At physiological temperature, cell adhesion to triple-helical 3/4 fragment via alpha2beta1 integrin was still possible; however, no alpha2beta1 integrin-mediated adhesion to the 1/4 fragment was observed. Unwinding of the collagen fragment triple helices by heating to physiological temperatures prior to adsorption to plastic tissue culture plates resulted in total abrogation of HT1080 cell attachment to either fragment. These results provide significant evidence in support of a role for matrix-metalloproteinase cleavage of the extracellular matrix in modifying cell-matrix interactions.

scholarly journals Soluble forms of the cell adhesion molecule L1 produced by insect and baculovirus-transduced mammalian cells enhance Schwann cell motility

2010 ◽  
Vol 115 (5) ◽  
pp. 1137-1149 ◽  
Author(s):  
Alexandros A. Lavdas ◽  
Rodica Efrose ◽  
Vassilis Douris ◽  
Maria Gaitanou ◽  
Florentia Papastefanaki ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Schwann Cell ◽  
Cell Motility ◽  
Adhesion Molecule ◽  
Mammalian Cells ◽  
Cell Adhesion Molecule ◽  
Cell Adhesion Molecule L1

scholarly journals Oncogenic Deregulation of Cell Adhesion Molecules in Leukemia

Cancers ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 311 ◽  
Author(s):  
Roland Windisch ◽  
Nina Pirschtat ◽  
Christian Kellner ◽  
Linping Chen-Wichmann ◽  
Jörn Lausen ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cell Adhesion ◽  
Progenitor Cells ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Gene Products ◽  
Hematopoietic Stem ◽  
Cell Matrix ◽  
Matrix Interactions ◽  
Cell Matrix Interactions

Numerous cell–cell and cell–matrix interactions within the bone marrow microenvironment enable the controlled lifelong self-renewal and progeny of hematopoietic stem and progenitor cells (HSPCs). On the cellular level, this highly mutual interaction is granted by cell adhesion molecules (CAMs) integrating differentiation, proliferation, and pro-survival signals from the surrounding microenvironment to the inner cell. However, cell–cell and cell–matrix interactions are also critically involved during malignant transformation of hematopoietic stem/progenitor cells. It has become increasingly apparent that leukemia-associated gene products, such as activated tyrosine kinases and fusion proteins resulting from chromosomal translocations, directly regulate the activation status of adhesion molecules, thereby directing the leukemic phenotype. These observations imply that interference with adhesion molecule function represents a promising treatment strategy to target pre-leukemic and leukemic lesions within the bone marrow niche. Focusing on myeloid leukemia, we provide a current overview of the mechanisms by which leukemogenic gene products hijack control of cellular adhesion to subsequently disturb normal hematopoiesis and promote leukemia development.

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