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In melanoma, RAS mutations are accompanied by switching signaling from BRAF to CRAF and disrupted cyclic AMP signaling.

Dumaz N, Hayward R, Martin J, Ogilvie L, Hedley D, Curtin JA, Bastian BC, Springer C, Marais R.

Cancer Res. 2006 Oct 1;66(19):9483-91.


V599EB-RAF is an oncogene in melanocytes.

Wellbrock C, Ogilvie L, Hedley D, Karasarides M, Martin J, Niculescu-Duvaz D, Springer CJ, Marais R.

Cancer Res. 2004 Apr 1;64(7):2338-42.


ERK and PDE4 cooperate to induce RAF isoform switching in melanoma.

Marquette A, André J, Bagot M, Bensussan A, Dumaz N.

Nat Struct Mol Biol. 2011 May;18(5):584-91. doi: 10.1038/nsmb.2022. Epub 2011 Apr 10.


Extracellular signal-regulated kinase-dependent proliferation is mediated through the protein kinase A/B-Raf pathway in human uveal melanoma cells.

Calipel A, Mouriaux F, Glotin AL, Malecaze F, Faussat AM, Mascarelli F.

J Biol Chem. 2006 Apr 7;281(14):9238-50. Epub 2006 Feb 1.


SPRY2 is an inhibitor of the ras/extracellular signal-regulated kinase pathway in melanocytes and melanoma cells with wild-type BRAF but not with the V599E mutant.

Tsavachidou D, Coleman ML, Athanasiadis G, Li S, Licht JD, Olson MF, Weber BL.

Cancer Res. 2004 Aug 15;64(16):5556-9.


Combined targeting of BRAF and CRAF or BRAF and PI3K effector pathways is required for efficacy in NRAS mutant tumors.

Jaiswal BS, Janakiraman V, Kljavin NM, Eastham-Anderson J, Cupp JE, Liang Y, Davis DP, Hoeflich KP, Seshagiri S.

PLoS One. 2009 May 27;4(5):e5717. doi: 10.1371/journal.pone.0005717.


BRAF, HRAS, KRAS, NRAS and CDKN2A genes analysis in cultured melanocytes used for vitiligo treatment.

Czajkowski R.

Int J Dermatol. 2011 Feb;50(2):180-3. doi: 10.1111/j.1365-4632.2010.04675.x.


Elastin peptides activate extracellular signal-regulated kinase 1/2 via a Ras-independent mechanism requiring both p110gamma/Raf-1 and protein kinase A/B-Raf signaling in human skin fibroblasts.

Duca L, Lambert E, Debret R, Rothhut B, Blanchevoye C, Delacoux F, Hornebeck W, Martiny L, Debelle L.

Mol Pharmacol. 2005 Apr;67(4):1315-24. Epub 2005 Jan 13.


Adhesion-dependent activation of the ERK1/2 cascade is by-passed in melanoma cells.

Conner SR, Scott G, Aplin AE.

J Biol Chem. 2003 Sep 5;278(36):34548-54. Epub 2003 Jun 23.


Ras mediates the cAMP-dependent activation of extracellular signal-regulated kinases (ERKs) in melanocytes.

Buscà R, Abbe P, Mantoux F, Aberdam E, Peyssonnaux C, Eychène A, Ortonne JP, Ballotti R.

EMBO J. 2000 Jun 15;19(12):2900-10.


Mechanism of RAF isoform switching induced by oncogenic RAS in melanoma.

Dumaz N.

Small GTPases. 2011 Sep;2(5):289-292. Epub 2011 Sep 1.


Calcium restriction allows cAMP activation of the B-Raf/ERK pathway, switching cells to a cAMP-dependent growth-stimulated phenotype.

Yamaguchi T, Wallace DP, Magenheimer BS, Hempson SJ, Grantham JJ, Calvet JP.

J Biol Chem. 2004 Sep 24;279(39):40419-30. Epub 2004 Jul 19.


The Brn-2 transcription factor links activated BRAF to melanoma proliferation.

Goodall J, Wellbrock C, Dexter TJ, Roberts K, Marais R, Goding CR.

Mol Cell Biol. 2004 Apr;24(7):2923-31.


NRAS and BRAF mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression.

Omholt K, Platz A, Kanter L, Ringborg U, Hansson J.

Clin Cancer Res. 2003 Dec 15;9(17):6483-8.


Cyclic AMP-independent involvement of Rap1/B-Raf in the angiotensin II AT2 receptor signaling pathway in NG108-15 cells.

Gendron L, Oligny JF, Payet MD, Gallo-Payet N.

J Biol Chem. 2003 Feb 7;278(6):3606-14. Epub 2002 Dec 2.


The PI3K/Akt and mTOR/P70S6K signaling pathways in human uveal melanoma cells: interaction with B-Raf/ERK.

Babchia N, Calipel A, Mouriaux F, Faussat AM, Mascarelli F.

Invest Ophthalmol Vis Sci. 2010 Jan;51(1):421-9. doi: 10.1167/iovs.09-3974. Epub 2009 Aug 6.


Cyclic AMP blocks cell growth through Raf-1-dependent and Raf-1-independent mechanisms.

Dumaz N, Light Y, Marais R.

Mol Cell Biol. 2002 Jun;22(11):3717-28.


A genome-based strategy uncovers frequent BRAF mutations in melanoma.

Pollock PM, Meltzer PS.

Cancer Cell. 2002 Jul;2(1):5-7.


BRAF V600E disrupts AZD6244-induced abrogation of negative feedback pathways between extracellular signal-regulated kinase and Raf proteins.

Friday BB, Yu C, Dy GK, Smith PD, Wang L, Thibodeau SN, Adjei AA.

Cancer Res. 2008 Aug 1;68(15):6145-53. doi: 10.1158/0008-5472.CAN-08-1430.

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