Retinoblastoma protein phosphorylation via PI 3-kinase and mTOR pathway regulates adipocyte differentiation

Biochemical and Biophysical Research Communications

Volumn 275, Issue 1, 2000, Pages 115-120

  Usui, Isao ^a   Haruta, Tetsuro ^a   Iwata, Minoru ^a   Takano, Atsuko ^a   Uno, Tatsuhito ^a   Kawahara, Junko ^a   Ueno, Eiichi ^a   Sasaoka, Toshiyasu ^a   Kobayashi, Masashi ^a  

^a UNIVERSITY OF TOYAMA   (Japan)

Author keywords

3T3 L1 adipocyte; Adipocyte differentiation; Clonal expansion; Insulin; mTOR; PI 3 kinase; Retinoblastoma protein

Indexed keywords

INSULIN; PHOSPHATIDYLINOSITOL 3 KINASE; RETINOBLASTOMA PROTEIN;

ADIPOCYTE; ANIMAL CELL; ARTICLE; CELL DIFFERENTIATION; CELL STRAIN 3T3; CONTROLLED STUDY; ENZYME ACTIVITY; ENZYME INHIBITION; ENZYME REGULATION; HORMONE ACTION; NONHUMAN; PRIORITY JOURNAL; PROTEIN PHOSPHORYLATION;

ANIMALIA;

EID: 0034682970     PISSN: 0006291X     EISSN: None     Source Type: Journal    
DOI: 10.1006/bbrc.2000.3201     Document Type: Article

References (28)

1. CSF-1 receptor/insulin receptor chimera permits CSF-l-dependent differentiation of 3T3-L1 preadipocytes
2. Insulin-like growth factor-I is an essential regulator of the differentiation of 3T3-L1 adipocytes
3. Peroxisome proliferator activated receptor γ, CCAAT/enhancer-binding protein α, and cell cycle status regulate the commitment to adipocyte differentiation
4. Enforced expression of the c-myc oncogene inhibits cell differentiation by precluding entry into a distinct predifferentiation state in G0/G1
5. Transcriptional control of adipogenesis
6. Wortmannin, a specific phosphatidylinositol 3-kinase inhibitor, inhibits adipocytic differentiation of 3T3-L1 cells
7. Posttranscriptional control of adipocyte differentiation through activation of phosphoinositide 3-kinase
8. Expression of a constitutively active Akt Ser/Thr kinase in 3T3-L1 adipocytes stimulates glucose uptake and glucose transporter 4 translocation
9. Expression of a constitutively activated form of protein kinase B (c-Akt) in 3T3-L1 preadipose cells causes spontaneous differentiation
10. Rapamycin inhibits clonal expansion and adipogenic differentiation of 3T3-L1 cells
11. The transcription factor E2F is required for S phase during Drosophila embryogenesis
12. Expression of dominant-negative mutant DP-1 blocks cell cycle progression in G1
13. Retinoblastoma protein positively regulates terminal adipocyte differentiation through direct interaction with C/EBPs
14. Insulin-stimulated GLUT4 translocation is mediated by a divergent intracellular signaling pathway
15. Mitogen-activated protein kinase kinase inhibition does not block the stimulation of glucose utilization by insulin
16. Role of ERK1/ERK2 and p70(S6K) pathway in insulin signaling of protein synthesis
17. Interaction of myogenic factors and the retinoblastoma protein mediates muscle cell commitment and differentiation
18. Dual roles of the retinoblastoma protein in cell cycle regulation and neuron differentiation
19. Mitotic clonal expansion during preadipocyte differentiation: Calpain-mediated turnover of 27
20. CCAAT-enhancer binding protein: A component of a differentiation switch
21. An established preadipose cell line and its differentiation in culture. II. Factors affecting the adipose conversion
22. The 3-phosphorylated phosphoinositide response of 3T3-L1 preadipose cells exposed to insulin, insulin-like growth factor-1, or platelet-derived growth factor
23. Phosphatidylinositol 3-kinase is a requirement for insulin-like growth factor I-induced differentiation, but not for mitogenesis, in fetal brown adipocytes
24. Cyclin D expression is controlled post-transcriptionally via a phosphatidylinositol 3-kinase/Akt-dependent pathway
25. Evidence of insulin-stimulated phosphorylation and activation of the mammalian target of rapamycin mediated by a protein kinase B signaling pathway
26. Mammalian target of rapamycin is a direct target for protein kinase B: Identification of a convergence point for opposing effects of insulin and amino-acid deficiency on protein translation
27. Rapamycin blocks the phosphorylation of 4E-BP1 and inhibits cap-dependent initiation of translation
28. The insulin-induced signaling pathway leading to S6 and initiation factor 4E binding protein 1 phophorylation bifurcates at a rapamycin-sensitive point immediately upstream of p70 (S6 k)