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CD44 — JUN
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Foster et al., FASEB J 2000
:
Taken together, our studies demonstrate that
AP-1 proteins are a central regulatory component used by IL-1beta to modulate expression of CD44 during an inflammatory response in vascular smooth muscle cells and that transcription of
CD44 by AP-1 proteins is
enhanced by HMG-I(Y)
Kobayashi et al., Int J Cancer 2002
(Bone Neoplasms...) :
Our study indicates that ( i ) CD44 stimulation by fragmented HA upregulates expression of uPA and uPAR mRNA and protein but does not affect MMPs secretion or PAI-1 mRNA expression ; ( ii ) the effects of HA fragments are critically HA size dependent : high molecular weight HA is inactive, but lower molecular weight fragmented HA ( Mr 3.5 kDa ) is active ; ( iii ) cells can bind avidly Mr 3.5 kDa fragmented HA through a CD44 molecule, whereas cells do not effectively bind higher Mr HA ; ( iv ) a fragmented HA
induces phosphorylation of MAP kinase proteins ( MEK1/2, ERK1/2 and
c-Jun ) within 30 min ; ( v )
CD44 is critical for the response ( activation of MAP kinase and upregulation of uPA and uPAR expression ) ; and ( vi ) cell invasion induced by CD44 stimulation with a fragmented HA is inhibited by anti-CD44 mAb, MAP kinase inhibitors, neutralizing anti-uPAR pAb, anti-catalytic anti-uPA mAb or amiloride
Mishra et al., J Biol Chem 2005
(Calcium Signaling) :
Differential involvement of calmodulin dependent protein kinase II-activated
AP-1 and c-Jun N-terminal kinase
activated EGR-1 signaling pathways in tumor necrosis factor-alpha and lipopolysaccharide induced
CD44 expression in human monocytic cells ... We previously demonstrated that the
c-Jun N-terminal kinase (JNK) , a mitogen activated protein kinase ( MAPK ), differentially
regulated LPS- but not TNF-alpha induced
CD44 expression in monocytic cells ... Furthermore, TNF-alpha induced
CD44 expression was
regulated by
AP-1 through the activation of the CaMK-II pathway, whereas LPS induced CD44 transcription was regulated specifically by Egr-1 through JNK activation
Vendrov et al., J Biol Chem 2010
(Atherosclerosis) :
Thrombin induced
CD44 expression is
mediated by transcription factor
AP-1 in a NADPH oxidase dependent manner
Smith et al., PloS one 2012
(Breast Neoplasms) :
Cell specific
CD44 expression in breast cancer
requires the interaction of
AP-1 and NF?B with a novel cis-element
Lamb et al., Mol Cell Biol 1997
(Cell Transformation, Neoplastic...) :
We demonstrate that increased expression of
CD44 in Fos- and EGF transformed cells is
dependent upon
AP-1
Fujii et al., J Immunol 1999
(Arthritis, Rheumatoid) :
Briefly, we found that 1 ) rheumatoid synovial cells highly expressed CD44 ; 2 ) cross linking of CD44 markedly but transiently augmented VCAM-1 expression and its mRNA transcription much more than did IL-1beta and TNF-alpha ; 3 ) hyaluronan, especially when fragmented, also up-regulated VCAM-1 ; 4 )
CD44 activated the transcription factor
AP-1 ; and 5 ) the integrin dependent adhesive function of RA synovial cells to T cells was also amplified by CD44 cross linking