Proteome analysis of adipocyte lipid rafts reveals that gC1qR plays essential roles in adipogenesis and insulin signal transduction
- Authors
- Kim, Ki-Bum; Kim, Bong-Woo; Choo, Hyo-Jung; Kwon, Young-Chan; Ahn, Byung-Yoon; Choi, Jong-Soon; Lee, Jae-Seon; Ko, Young-Gyu
- Issue Date
- 5월-2009
- Publisher
- WILEY
- Keywords
- Insulin resistance; Lipid raft; Signal transduction; Two-dimensional difference gel electrophoresis
- Citation
- PROTEOMICS, v.9, no.9, pp.2373 - 2382
- Indexed
- SCIE
SCOPUS
- Journal Title
- PROTEOMICS
- Volume
- 9
- Number
- 9
- Start Page
- 2373
- End Page
- 2382
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/120157
- DOI
- 10.1002/pmic.200800811
- ISSN
- 1615-9853
- Abstract
- Since insulin receptors and their downstream signaling molecules are organized in lipid rafts, proteomic analysis of adipocyte lipid rafts may provide new insights into the function of lipid rafts in adipogenesis and insulin signaling. To search for proteins involved in adipocyte differentiation and insulin signaling, we analyzed detergent-resistant lipid raft proteins from 3T3-L1 preadipocytes and adipocytes by 2-DE. Eleven raft proteins were identified from adipocytes. One of the adipocyte-specific proteins was globular C1q receptor (gC1qR), an acidic 32 kDa protein known as the receptor for the globular domain of complement C1q. The targeting of gC1qR into lipid rafts was significantly increased during adipogenesis, as determined by immunoblotting and immunofluorescence. Since the silencing of gC1qR by small RNA interference abolished adipogenesis and blocked insulin-induced activation of insulin receptor, insulin receptor substrate-1 (IRS-1), Akt, and Erk1/2, we can conclude that gC1qR is an essential molecule involved in adipogenesis and insulin signaling.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - College of Life Sciences and Biotechnology > Division of Life Sciences > 1. Journal Articles
- Graduate School > Department of Life Sciences > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.