Literature DB >> 27653985

RACK1 is required for adipogenesis.

Qinghua Kong1, Lan Gao1,2, Yanfen Niu1,3, Pianchou Gongpan1,2, Yuhui Xu1,2, Yan Li1,4, Wenyong Xiong5,4.   

Abstract

Adipose tissue plays a critical role in metabolic diseases and the maintenance of energy homeostasis. RACK1 has been identified as an adaptor protein involved in multiple intracellular signal transduction pathways and diseases. However, whether it regulates adipogenesis remains unknown. Here, we reported that RACK1 is expressed in 3T3-L1 cells and murine white adipose tissue and that RACK1 knockdown by shRNA profoundly suppressed adipogenesis by reducing the expression of PPAR-γ and C/EBP-β. Depletion of RACK1 increased β-catenin protein levels and activated Wnt signaling. Furthermore, RACK1 knockdown also suppressed the PI3K-Akt-mTOR-S6K signaling pathway by reducing the PI3K p85α, pAkt T473, and S6K p70. Taken together, these results demonstrate that RACK1 is a novel factor required for adipocyte differentiation by emerging Wnt/β-catenin signaling and PI3K-Akt-mTOR-S6K signaling pathway(s).
Copyright © 2016 the American Physiological Society.

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Keywords:  3T3-L1; PI3K-Akt-mTOR-S6K; RACK1; Wnt; adipogenesis

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Year:  2016        PMID: 27653985     DOI: 10.1152/ajpcell.00224.2016

Source DB:  PubMed          Journal:  Am J Physiol Cell Physiol        ISSN: 0363-6143            Impact factor:   4.249


  1 in total

1.  GNA14's interaction with RACK1 inhibits hepatocellular carcinoma progression through reducing MAPK/JNK and PI3K/AKT signaling pathway.

Authors:  Cong Xu; Yi-Ming Li; Bo Sun; Fang-Jing Zhong; Lian-Yue Yang
Journal:  Carcinogenesis       Date:  2021-11-12       Impact factor: 4.944

  1 in total

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