Ras signalling regulates differentiation and UCP1 expression in models of brown adipogenesis

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Ras signalling regulates differentiation and UCP1 expression in models of brown adipogenesis. / Murholm, Maria; Dixen, Karen; Hansen, Jacob B.

In: BBA General Subjects, Vol. 1800, No. 6, 2010, p. 619-627.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Murholm, M, Dixen, K & Hansen, JB 2010, 'Ras signalling regulates differentiation and UCP1 expression in models of brown adipogenesis', BBA General Subjects, vol. 1800, no. 6, pp. 619-627. https://doi.org/10.1016/j.bbagen.2010.03.008

APA

Murholm, M., Dixen, K., & Hansen, J. B. (2010). Ras signalling regulates differentiation and UCP1 expression in models of brown adipogenesis. BBA General Subjects, 1800(6), 619-627. https://doi.org/10.1016/j.bbagen.2010.03.008

Vancouver

Murholm M, Dixen K, Hansen JB. Ras signalling regulates differentiation and UCP1 expression in models of brown adipogenesis. BBA General Subjects. 2010;1800(6):619-627. https://doi.org/10.1016/j.bbagen.2010.03.008

Author

Murholm, Maria ; Dixen, Karen ; Hansen, Jacob B. / Ras signalling regulates differentiation and UCP1 expression in models of brown adipogenesis. In: BBA General Subjects. 2010 ; Vol. 1800, No. 6. pp. 619-627.

Bibtex

@article{497394d05c1e11df928f000ea68e967b,

title = "Ras signalling regulates differentiation and UCP1 expression in models of brown adipogenesis",

abstract = "BACKGROUND: The Ras/Raf/MEK/ERK pathway has been recognised as an important signalling module in adipogenesis and adipocyte function, but whether it promotes or inhibits the formation of fat cells has not been reconciled. METHODS: Here we investigate the significance of Ras signalling intensity on two unrelated models of mouse brown adipocyte differentiation. RESULTS: A constitutively active H-Ras mutant (Ras V12) caused a complete block of adipose conversion, as manifested by a lack of both lipid accumulation and induction of adipocyte gene expression. The Ras V12-mediated impediment of differentiation was inefficiently rescued by forced expression of the adipogenic transcription factors C/EBPalpha and PPARgamma. However, the defective differentiation was alleviated by MEK inhibitors, suggesting that the obstruction of differentiation was dependent on activation of ERK. A dominant interfering H-Ras mutant (Ras N17) did not inhibit differentiation, but led to increased expression of genes important for energy dissipation in brown fat cells, including UCP1. GENERAL SIGNIFICANCE: These data suggest that the intensity of Ras signalling is important for differentiation and UCP1 expression in models of brown adipogenesis.",

author = "Maria Murholm and Karen Dixen and Hansen, {Jacob B}",

year = "2010",

doi = "10.1016/j.bbagen.2010.03.008",

language = "English",

volume = "1800",

pages = "619--627",

journal = "B B A - General Subjects",

issn = "0304-4165",

publisher = "Elsevier",

number = "6",

}

RIS

TY - JOUR

T1 - Ras signalling regulates differentiation and UCP1 expression in models of brown adipogenesis

AU - Murholm, Maria

AU - Dixen, Karen

AU - Hansen, Jacob B

PY - 2010

Y1 - 2010

N2 - BACKGROUND: The Ras/Raf/MEK/ERK pathway has been recognised as an important signalling module in adipogenesis and adipocyte function, but whether it promotes or inhibits the formation of fat cells has not been reconciled. METHODS: Here we investigate the significance of Ras signalling intensity on two unrelated models of mouse brown adipocyte differentiation. RESULTS: A constitutively active H-Ras mutant (Ras V12) caused a complete block of adipose conversion, as manifested by a lack of both lipid accumulation and induction of adipocyte gene expression. The Ras V12-mediated impediment of differentiation was inefficiently rescued by forced expression of the adipogenic transcription factors C/EBPalpha and PPARgamma. However, the defective differentiation was alleviated by MEK inhibitors, suggesting that the obstruction of differentiation was dependent on activation of ERK. A dominant interfering H-Ras mutant (Ras N17) did not inhibit differentiation, but led to increased expression of genes important for energy dissipation in brown fat cells, including UCP1. GENERAL SIGNIFICANCE: These data suggest that the intensity of Ras signalling is important for differentiation and UCP1 expression in models of brown adipogenesis.

AB - BACKGROUND: The Ras/Raf/MEK/ERK pathway has been recognised as an important signalling module in adipogenesis and adipocyte function, but whether it promotes or inhibits the formation of fat cells has not been reconciled. METHODS: Here we investigate the significance of Ras signalling intensity on two unrelated models of mouse brown adipocyte differentiation. RESULTS: A constitutively active H-Ras mutant (Ras V12) caused a complete block of adipose conversion, as manifested by a lack of both lipid accumulation and induction of adipocyte gene expression. The Ras V12-mediated impediment of differentiation was inefficiently rescued by forced expression of the adipogenic transcription factors C/EBPalpha and PPARgamma. However, the defective differentiation was alleviated by MEK inhibitors, suggesting that the obstruction of differentiation was dependent on activation of ERK. A dominant interfering H-Ras mutant (Ras N17) did not inhibit differentiation, but led to increased expression of genes important for energy dissipation in brown fat cells, including UCP1. GENERAL SIGNIFICANCE: These data suggest that the intensity of Ras signalling is important for differentiation and UCP1 expression in models of brown adipogenesis.

U2 - 10.1016/j.bbagen.2010.03.008

DO - 10.1016/j.bbagen.2010.03.008

M3 - Journal article

C2 - 20307629

VL - 1800

SP - 619

EP - 627

JO - B B A - General Subjects

JF - B B A - General Subjects

SN - 0304-4165

IS - 6

ER -

ID: 19664151

Department of Biology