Literature DB >> 22987449

Janus kinase 2 and signal transducer and activator of transcription 3 activation is not essential for CCL3-, CCL5- or CCL8-induced chemotaxis.

S Khabbazi1, R O Jacques, C Moyano Cardaba, A Mueller.   

Abstract

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.

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Year:  2012        PMID: 22987449     DOI: 10.1002/cbf.2901

Source DB:  PubMed          Journal:  Cell Biochem Funct        ISSN: 0263-6484            Impact factor:   3.685


  2 in total

1.  Hepatocyte Growth Factor Receptor c-Met Instructs T Cell Cardiotropism and Promotes T Cell Migration to the Heart via Autocrine Chemokine Release.

Authors:  Izabela Komarowska; David Coe; Guosu Wang; Robert Haas; Claudio Mauro; Madhav Kishore; Dianne Cooper; Suchita Nadkarni; Hongmei Fu; Daniel A Steinbruchel; Costantino Pitzalis; Graham Anderson; Pat Bucy; Giovanna Lombardi; Ross Breckenridge; Federica M Marelli-Berg
Journal:  Immunity       Date:  2015-06-09       Impact factor: 31.745

2.  Cucurbitacin covalent bonding to cysteine thiols: the filamentous-actin severing protein Cofilin1 as an exemplary target.

Authors:  Mads Gabrielsen; Maike Schuldt; June Munro; Dagmara Borucka; Jenifer Cameron; Mark Baugh; Andrzej Mleczak; Sergio Lilla; Nicholas Morrice; Michael F Olson
Journal:  Cell Commun Signal       Date:  2013-08-14       Impact factor: 5.712

  2 in total

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