1: Cell Cycle. 2004 Jun;3(6):774-8. Epub 2004 Jun 15.


Novel function of the retinoblastoma protein in fat: regulation of white versus brown adipocyte differentiation.

Hansen JB, te Riele H, Kristiansen K.

The Netherlands Cancer Institute, Division of Molecular Biology, The Netherlands.

The differentiation of white and brown fat cells is controlled by a similar set of transcription factors, including PPARgamma and C/EBPalpha. However, despite many similarities between the two types of fat cells, they carry out essentially opposite functions in vivo, with white adipocytes being the major energy store and brown adipocytes being potent energy-dissipaters through thermogenesis. Yet, little is known about factors differentially regulating the formation of white and brown fat cells. Members of the retinoblastoma protein family (pRB, p107, p130) have been implicated in the regulation of adipocyte differentiation, and expression and phosphorylation of the three retinoblastoma family proteins oscillate in a characteristic manner during differentiation of the white preadipocyte cell line 3T3-L1. We have recently demonstrated a surprising function of the retinoblastoma protein in the regulation of white versus brown adipocyte differentiation in vitro and possibly in vivo. Here we summarize the current knowledge on the retinoblastoma protein in fat cells, with particular emphasis on its potential role in adipocyte lineage commitment and differentiation.

Publication Types:
Research Support, Non-U.S. Gov't
Review

PMID: 15197340 [PubMed - indexed for MEDLINE]

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2: EMBO Rep. 2002 Feb;3(2):130-5.


Cell-nonautonomous function of the retinoblastoma tumour suppressor protein: new interpretations of old phenotypes.

Whyatt D, Grosveld F.

Erasmus University, Department of Cell Biology and Genetics, Medical Genetics Centre, PO Box 1738, 3000 DR Rotterdam, The Netherlands.

Loss of the retinoblastoma protein (pRb) induces a cell-nonautonomous defect in both erythroid and neuronal differentiation. It has previously been thought that this reflects a requirement for pRb function in cells that normally support erythropoiesis and neurogenesis, rather than in the erythrocytes or neurons themselves. However, recent studies have challenged this interpretation, and it appears that erythrocytes and neurons themselves have the intrinsic requirement for pRb function. This requirement can be bypassed by signals supplied by wild-type erythroid or neuronal cells. The existence of such a signalling mechanism has implications not only in understanding pRb function but also in the interpretation of other cell-nonautonomous phenotypes.

Publication Types:
Research Support, Non-U.S. Gov't
Review

PMID: 11839697 [PubMed - indexed for MEDLINE]

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3: Curr Top Microbiol Immunol. 2001;254:137-44.


Corepressors and retinoblastoma protein function.

Harbour JW, Dean DC.

Department of Ophthalmology and Visual Sciences, Division of Molecular Oncology, Washington University School of Medicine, St. Louis, MO 63110, USA.

Publication Types:
Review

PMID: 11190571 [PubMed - indexed for MEDLINE]

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4: Adv Cancer Res. 1993;61:115-41.


Unraveling the function of the retinoblastoma gene.

Zacksenhaus E, Bremner R, Jiang Z, Gill RM, Muncaster M, Sopta M, Phillips RA, Gallie BL.

Division of Immunology and Cancer Research, Hospital for Sick Children Research Institute, Toronto, Ontario, Canada.

Publication Types:
Review

PMID: 8346717 [PubMed - indexed for MEDLINE]