U.S. flag

An official website of the United States government

Format

Send to:

Choose Destination
    • Showing Current items.

    Braf B-Raf proto-oncogene, serine/threonine kinase [ Rattus norvegicus (Norway rat) ]

    Gene ID: 114486, updated on 4-Jan-2025

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Cardiomyocyte BRAF and type 1 RAF inhibitors promote cardiomyocyte and cardiac hypertrophy in mice in vivo.

    Cardiomyocyte BRAF and type 1 RAF inhibitors promote cardiomyocyte and cardiac hypertrophy in mice in vivo.
    Clerk A, Meijles DN, Hardyman MA, Fuller SJ, Chothani SP, Cull JJ, Cooper STE, Alharbi HO, Vanezis K, Felkin LE, Markou T, Leonard SJ, Shaw SW, Rackham OJL, Cook SA, Glennon PE, Sheppard MN, Sembrat JC, Rojas M, McTiernan CF, Barton PJ, Sugden PH., Free PMC Article

    03/5/2022
    stimulation of B-Raf strongly activated the transcription factor AP-1 which is accompanied by increased c-Jun and c-Fos promoter activities, an upregulation of c-Jun and c-Fos biosynthesis, and elevated transcriptional activation potentials of c-Jun and c-Fos.

    Stimulation of B-Raf increases c-Jun and c-Fos expression and upregulates AP-1-regulated gene transcription in insulinoma cells.
    Langfermann DS, Rössler OG, Thiel G.

    04/27/2019
    The gliomas were immunoreactive to BRAF V600E antibody. These results indicate that Braf mutation is a frequent early event in the development of rat gliomas caused by a single dose of N-ethyl-N-nitrosourea (ENU).

    Braf Mutations Initiate the Development of Rat Gliomas Induced by Postnatal Exposure to N-Ethyl-N-Nitrosourea.
    Wang Q, Satomi K, Oh JE, Hutter B, Brors B, Diessl N, Liu HK, Wolf S, Wiestler O, Kleihues P, Koelsch B, Kindler-Röhrborn A, Ohgaki H.

    10/14/2017
    Study provides evidence that transcriptional and post-translational modification of B-Raf may contribute to the progression of tuberous sclerosis renal cell carcinoma.

    Transcriptional and post-translational modifications of B-Raf in quinol-thioether induced tuberous sclerosis renal cell carcinoma.
    Cohen JD, Labenski M, Mastrandrea NJ, Canatsey RD, Monks TJ, Lau SS., Free PMC Article

    07/22/2017
    B-RAF kinase activity is essential for cardiac hypertrophy and RCN1, its newly identified negative regulator

    B-RAF and its novel negative regulator reticulocalbin 1 (RCN1) modulates cardiomyocyte hypertrophy.
    Kramann N, Hasenfuß G, Seidler T.

    11/29/2014
    BRAF alternative splicing is dispensable for development but required for learning and memory associated with the hippocampus. Exons 8b and 9b are expressed in rodent species.

    B-raf alternative splicing is dispensable for development but required for learning and memory associated with the hippocampus in the adult mouse.
    Valluet A, Hmitou I, Davis S, Druillennec S, Larcher M, Laroche S, Eychène A., Free PMC Article

    01/26/2011
    B-raf is required for extracellular signal-regulated kinase activation by thyrotropin, and is necessary for thyrotropin-stimulated DNA synthesis.

    Protein kinase A and B-Raf mediate extracellular signal-regulated kinase activation by thyrotropin.
    Vuchak LA, Tsygankova OM, Prendergast GV, Meinkoth JL., Free PMC Article

    01/21/2010
    selective modulation of c-Raf-1 but not B-Raf activation by RKIP can limit the dynamic range of the MAPK signaling response to growth factors and may play a critical role in growth and development

    Raf kinase inhibitory protein regulates Raf-1 but not B-Raf kinase activation.
    Trakul N, Menard RE, Schade GR, Qian Z, Rosner MR.

    01/21/2010
    DYRK1A prolongs the kinetics of ERK activation by interacting with Ras, B-Raf, and MEK1 to facilitate the formation of a Ras/B-Raf/MEK1 multiprotein complex

    DYRK1A enhances the mitogen-activated protein kinase cascade in PC12 cells by forming a complex with Ras, B-Raf, and MEK1.
    Kelly PA, Rahmani Z., Free PMC Article

    01/21/2010
    observations establish Rin as a neuronal specific regulator of neurotrophin signaling, required to couple NGF stimulation to sustain activation of p38 MAP kinase and b-Raf signaling cascades required for neuronal development

    Rin GTPase couples nerve growth factor signaling to p38 and b-Raf/ERK pathways to promote neuronal differentiation.
    Shi GX, Han J, Andres DA.

    01/21/2010
    The preferential induction of MMPs by BRAF could explain in part the more invasive behavior of thyroid cancers with BRAF mutations.

    Conditional activation of RET/PTC3 and BRAFV600E in thyroid cells is associated with gene expression profiles that predict a preferential role of BRAF in extracellular matrix remodeling.
    Mesa C Jr, Mirza M, Mitsutake N, Sartor M, Medvedovic M, Tomlinson C, Knauf JA, Weber GF, Fagin JA.

    01/21/2010
    firstprevious page of 1 nextlast