Publicacions en què col·labora amb MARÍA ALMUDENA PORRAS GALLO (21)

2010

  1. C3G down-regulates p38 MAPK activity in response to stress by Rap-1 independent mechanisms: Involvement in cell death

    Cellular Signalling, Vol. 22, Núm. 3, pp. 533-542

2007

  1. Negative regulation of Akt activity by p38α MAP kinase in cardiomyocytes involves membrane localization of PP2A through interaction with caveolin-1

    Cellular Signalling, Vol. 19, Núm. 1, pp. 62-74

  2. p38α MAPK can positively or negatively regulate Rac-1 activity depending on the presence of serum

    FEBS Letters, Vol. 581, Núm. 20, pp. 3819-3825

2004

  1. p38α Mitogen-activated Protein Kinase Sensitizes Cells to Apoptosis Induced by Different Stimuli

    Molecular Biology of the Cell, Vol. 15, Núm. 2, pp. 922-933

2003

  1. Long-Term Treatment with Insulin Induces Apoptosis in Brown Adipocytes: Role of Oxidative Stress

    Endocrinology, Vol. 144, Núm. 12, pp. 5390-5401

2002

  1. Differential role of PPARγ in the regulation of UCP-1 and adipogenesis by TNF-α in brown adipocytes

    FEBS Letters, Vol. 520, Núm. 1-3, pp. 58-62

  2. Regulation of proliferation, differentiation and apoptosis of brown adipocytes: Signal transduction pathways involved

    Cell and Molecular Response to Stress, pp. 269-282

2001

  1. Activation of p38MAPK by TGF-β in fetal rat hepatocytes requires radical oxygen production, but is dispensable for cell death

    FEBS Letters, Vol. 499, Núm. 3, pp. 225-229

  2. TNF-α inhibits UCP-1 expression in brown adipocytes via ERKs - Opposite effect of p38MAPK

    FEBS Letters, Vol. 493, Núm. 1, pp. 6-11

2000

  1. Noradrenaline induces brown adipocytes cell growth via β-receptors by a mechanism dependent on ERKs but independent of cAMP and PKA

    Journal of Cellular Physiology, Vol. 185, Núm. 3, pp. 324-330

  2. p38 mitogen-activated protein kinase mediates tumor necrosis factor-α-induced apoptosis in rat fetal brown adipocytes

    Endocrinology, Vol. 141, Núm. 12, pp. 4383-4395

1998

  1. P42/p44 mitogen-activated protein kinases activation is required for the insulin-like growth factor-i/insulin induced proliferation, but inhibits differentiation, in rat fetal brown adipocytes

    Molecular Endocrinology, Vol. 12, Núm. 6, pp. 825-834

1997

  1. TNF-α-induced apoptosis in rat fetal brown adipocytes in primary culture

    FEBS Letters, Vol. 416, Núm. 3, pp. 324-328

1996

  1. Ras proteins mediate induction of uncoupling protein, IGF-I, and IGF-I receptor in rat fetal brown adipocyte cell lines

    DNA and Cell Biology, Vol. 15, Núm. 11, pp. 921-928

  2. Triiodothyronine induces the transcription of the uncoupling protein gene and stabilizes its mRNA in fetal rat brown adipocyte primary cultures

    Journal of Biological Chemistry, Vol. 271, Núm. 4, pp. 2076-2081

1994

  1. Triiodothyronine induces the expression of the uncoupling protein in long term fetal rat brown adipocyte primary cultures: Role of nuclear thyroid hormone receptor expression

    Endocrinology, Vol. 134, Núm. 3, pp. 1067-1074

1993

  1. Establishment of permanent brown adipocyte cell lines achieved by transfection with SV40 large T antigen and ras genes

    Experimental Cell Research, Vol. 209, Núm. 2, pp. 248-254

1992

  1. Activation of Ras by insulin in 3T3 L1 cells does not involve GTPase- activating protein phosphorylation

    Journal of Biological Chemistry, Vol. 267, Núm. 29, pp. 21124-21131

1991

  1. Differentiation of 3T3-L1 fibroblasts to adipocytes induced by transfection of ras oncogenes

    Science, Vol. 253, Núm. 5019, pp. 565-568

1990

  1. Development of the uncoupling protein in the rat brown‐adipose tissue during the perinatal period: Its relationship with the mitochondrial GDP‐binding and GDP‐sensitive ion permeabilities and respiration

    European Journal of Biochemistry, Vol. 187, Núm. 3, pp. 671-675