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CD44 — ITGA4
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Chute et al., Exp Hematol 1999
:
Despite the high level of cellular activation and proliferation induced by PMVEC coculture, the surface expression of adhesion molecules CD11a ( LFA-1 ), CD11b, CD15s ( sialyl-Lewis x ), CD43, and
CD44 ( HCAM ) on the total CD34+ population was maintained, and the surface expression of
CD49d ( VLA-4 ), CD54 ( ICAM ), CD58, and CD62L ( L selectin )
increased after ex vivo expansion
Kawakami et al., J Immunol 1999
:
The data suggest that integrin alpha4 and CD44 play different roles, i.e.,
integrin alpha4 is required for the adhesion of FL cells to the thymus lobe and
CD44 is
required for the migration of the cells into the thymus
Wang et al., Exp Cell Res 2005
(Breast Neoplasms) :
Using flow cytometric analysis and immunofluorescence staining, we demonstrated that cross linking of
CD44 resulted in a marked induction of the expression of lymphocyte function associated antigen-1 ( LFA-1 ) and
very late antigen-4 (VLA-4) by exocytosis ... This shows that
CD44 cross linking
induces LFA-1 and
VLA-4 expression in MDA-MB-435S cells and increases integrin mediated adhesion to endothelial cells, resulting in the transendothelial migration of breast cancer cells
Sackstein et al., Curr Opin Hematol 2011
:
Engagement of
CD44 or of HCELL directly
induces VLA-4 activation via G-protein dependent signaling, triggering a ` step 2-bypass pathway ' of cell migration, and extravascular lodgment, in absence of chemokine receptor engagement