First Author | Kumagai N | Year | 2004 |
Journal | Biochem Biophys Res Commun | Volume | 325 |
Issue | 3 | Pages | 758-68 |
PubMed ID | 15541355 | Mgi Jnum | J:93822 |
Mgi Id | MGI:3505810 | Doi | 10.1016/j.bbrc.2004.10.094 |
Citation | Kumagai N, et al. (2004) Induction of mouse c-src in RAW264 cells is dependent on AP-1 and NF-kappaB and important for progression to multinucleated cell formation. Biochem Biophys Res Commun 325(3):758-68 |
abstractText | c-src is known to play an essential role in osteoclastogenesis. We studied the regulatory mechanism as well as the significance of c-src induction in RANKL-induced differentiation of mouse monocytic RAW264 cells to TRAP-positive-multinucleated cells. We determined the genomic organization of the 5'-terminal region of mouse c-src. Mutational and biochemical analyses in the region 0.9kb upstream of the transcription start site revealed that c-Fos and JNK pathways, in addition to NF-kappaB, participate in c-src induction in response to RANKL. On the other hand, when the expression of c-src was suppressed by introducing antisense src, the number of multinucleated cells formed was significantly reduced. Together, these findings show that the expression of c-src is under the control of AP-1 and NF-kappaB in the differentiation of RAW264 cells and that c-src plays an essential role at the stage of progression to multinucleated cell formation. |