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Janus kinase 2 and signal transducer and activator of transcription 3 activation is not essential for CCL3‐, CCL5‐ or CCL8‐induced chemotaxis
Author(s) -
Khabbazi S.,
Jacques R.O.,
Moyano Cardaba C.,
Mueller A.
Publication year - 2013
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.2901
Subject(s) - microbiology and biotechnology , janus kinase , stat protein , ccl5 , actin cytoskeleton , stat3 , rac gtp binding proteins , chemotaxis , ccl3 , signal transduction , chemokine receptor , chemokine , chemistry , cytoskeleton , activator (genetics) , biology , rac1 , cell , t cell , receptor , immunology , ccl2 , biochemistry , immune system , il 2 receptor
Chemokine receptors induce cell migration, but the molecular basis of the signal cascade involved is not completely understood. Therefore, we investigated here the molecular mechanisms of CCL3‐, CCL5‐ and CCL8‐induced cells migration and investigated whether the Janus kinase/signal transducer and activator of transcription (STAT) signalling pathway is involved. Some STAT3 inhibitors, like Cucurbitacin I, destroy the actin cytoskeleton inside the cells and therefore prevent any cellular migration. However, for inhibitors that do not affect the actin cytoskeleton or induce cell death, we show that chemokine‐induced cell migration is not dependent on activation of Janus kinase 2 or STAT3. Copyright © 2012 John Wiley & Sons, Ltd.