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Cot/Tpl2 Is Essential for RANKL Induction by Lipid A in Osteoblasts

Cot/Tpl2 Is Essential for RANKL Induction by Lipid A in Osteoblasts

T Kikuchi, Y Yoshikai, J Miyoshi, M Katsuki, T Musikacharoen, A Mitani, S Tanaka, T Noguchi, T Matsuguchi

J Dent Res. 2003 Jul;82(7):546-50.

PMID: 12821717

Abstract:

Lipopolysaccharide (LPS) is a pathogenic factor that increases bone resorption in periodontal diseases. LPS treatment of osteoblasts was shown to induce the receptor activator of NF-kappa B ligand (RANKL), an essential secretory or membrane-bound factor for osteoclast function, in a manner dependent on extracellular signal-regulated kinase (ERK) activation. However, the mechanisms regulating this process remained unknown. Here, we show that RANKL mRNA induction and ERK activation, when treated with synthetic lipid A (an active center of LPS), were markedly reduced in mouse osteoblasts lacking Cot/Tpl2, which was recently recognized as an essential kinase for the induction of TNF-alpha by LPS in macrophages. In contrast, c-Jun N-terminal kinase (JNK), p38 kinase, Raf-1, and NF-kappa B were normally activated in cot/tpl2-/- osteoblasts. These findings indicate that Cot/Tpl2 is essential for LPS-induced ERK activation and RANKL induction in osteoblasts.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR42411970	Cot active mouse			Price

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