Gene interactions and pathways from curated databases and text-mining

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CD44 — ICAM1

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

  • STRING interaction: ICAM1 — CD44 (interaction, mapped from kegg_pathways)
  • STRING interaction: CD44 — ICAM1 (interaction, mapped from kegg_pathways)

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 ... 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
De Saint Jean et al., Exp Eye Res 2004 : In the primary cultured cells, TNFalpha induced an important upregulation of ICAM-1 , Fas and CD40 whereas CD44 and CD63 were significantly decreased
Patel et al., J Clin Immunol 1995 : While activation of TE cells with IFN-gamma for 48 hr induced a greater than fivefold increase in the expression of four surface molecules ( CD38, CD54 , MHC class I, and MHC class II ), it also induced a greater than 50 % increase in the expression of 14 other surface molecules ( CD12, CD29, CD40, CD44 , CD47, CD49b, CD49c, CD49e, CD55, CD66, CD87, CD104, TE4, and STE3 ) and a decrease in the expression of three molecules ( CDw65, CDw109, and STE2 )
Hawley et al., Clin Exp Metastasis 1993 (Neoplasm Metastasis...) : Despite higher ICAM-1 levels, cell aggregation assays revealed that LFA-1-ICAM-1 adhesive interactions were not involved in the homotypic adhesion of B9/BM1 cells but rather that binding of CD44 to endogenously synthesized hyaluronan was responsible