| Selective BRAFV600E inhibitor PLX4720, requires TRAIL assistance to overcome oncogenic PIK3CA resistance. | None |
| Oncogenic Ras and B-Raf proteins positively regulate death receptor 5 expression through co-activation of ERK and JNK signaling. | None |
| These data support a model where the continuous regenerative process initiated by oncogenic B-RAF-driven alveolar disruption provides a tumor-promoting environment associated with chronic inflammation. | None |
| Targeting oncogenic serine/threonine-protein kinase BRAF in cancer cells inhibits angiogenesis and abrogates hypoxia. | None |
| These results provide a functional link between oncogenic BRAF and angiogenesis. | None |
| The findings show mutant BRAF-induced oncogenic stress manifests itself by DNA damage and growth arrest by activating the pCHK2-p53-p21 pathway.It also confers tumor-promoting phenotypes such as the up-regulation of GLUT1 and enhances glucose metabolism. | None |
| Report of oncogenic BRAF/KRAS mutations in sporadic glomus tumors. | None |
| expression of these oncogenes markedly stimulated ERK1/2 activities and morphologically transformed IECs. Importantly however | None |
| The intermediate-activity (L597V)BRAF mutant acts as an epistatic modifier of oncogenic RAS by enhancing signaling through the RAF/MEK/ERK pathway. | None |
| This report is the first to identify the rare, variant BRAF V600D mutation in LCH, and provides support for constitutively activated BRAF oncogene-induced cell senescence as a mechanism of regression in congenital, benign LCH. | None |
| Identification of the V600D mutation in Exon 15 of the BRAF oncogene in congenital, benign langerhans cell histiocytosis. | None |
| demonstrate dose-dependent effects of oncogenic signaling, with physiologic Braf(V600E) expression being sufficient for hyperplasia induction | None |
| Our studies have identified a previously unrecognized regulatory role of Lys63-linked polyubiquitination in BRAF-mediated normal and oncogenic signalings. | None |
| Data show that a high proportion of cases of non-pulmonary Langerhans cell histiocytosis (LCH) and pulmonary LCH (PLCH) expressed the proto-oncogene protein B-raf (BRAF) V600E mutant protein. | None |
| BRAFV600E-mutation is invariably present and associated to oncogene-induced senescence in Erdheim-Chester disease. | None |
| Data support a central role of BRAF V600E mutation in Erdheim-Chester disease and suggest oncogene-induced senescense as a link to both inflammation and oncogenic mutation in histiocytes playing a role in the disease. | None |
| Mig-6 reduces pRb phosphorylation at Ser249/ Thr252 in both primary and B-Raf V600E oncogene expressing. | None |
| Transgenic expression of oncogenic BRAF induces loss of stem cells in the mouse intestine, which is antagonized by beta-catenin activity. | None |
| loss of stem cell identity upon induction of BRAF/MAPK activity may represent a novel fail-safe mechanism protecting intestinal tissue from oncogene activation | None |
| The BRAF oncoprotein functions through the transcriptional repressor MAFG to mediate the CpG Island Methylator phenotype. | None |