| protein
| interacts with MEK1 |
|
interacts with PLCepsilon1 (PLCE1)  |
|
BRAF associates with and stimulates SLC9A1 activity and BRAF(V600E) also increases SLC9A1 activity that raises intracellular pH |
|
association of BRAF with RAF1 induces the activation of RAF1 |
|
bound to the cytosolic regulatory tail of SLC9A1 (can directly bind to the C-terminal 182 AAs of SLC9A1 protein) |
|
bound directly to the C-terminal kinase-containing domain of BRAF and induced ubiquitination, followed by proteasome-dependent degradation, of the latter protein |
|
BRAF enhanced the Na+-coupled glucose transporter SLC5A1 protein abundance in the cell membrane |
|
NF1 cooperates with BRAF mutations in melanoma |
|
target of BRAF, the melanocyte lineage factor MITF, directly regulates the expression of PPARGC1A |
|
MITF is a target of BRAF, directly regulating the expression of PPARGC1A |
|
regulatory role for BRAF in the MAPK pathway independent of its kinase activity but dependent on interaction with MAP2K1 |
|
RHEB interaction with BRAF is crucial for inhibiting RAF/MEK/ERK signaling |
| Other morbid association(s)
|
| Type | Gene Modification | Chromosome rearrangement | Protein expression | Protein Function
|
|---|
| tumoral
| fusion
|
|
|
| |
fused with TIF1A to form the oncoprotein T18 | | tumoral
| somatic mutation
|
|
|
| |
in malignant melanoma of the skin UV-exposed and in naevus, rarely in colorectal cancer with mismatch repair deficiency and in lung adenocarcinoma | | tumoral
| somatic mutation
|
|
|
| |
a missense transversion T1796A in lung, head and neck cancers | | tumoral
| somatic mutation
|
|
|
| |
V599E mutation in adult sporadic papillary thyroid carcinomas, with poorer clinicopathological outcomes | | constitutional
| germinal mutation
|
|
|
| |
de novo missense mutation in CFC, at the interface of the ATP binding cleft and altering the catalytic activity of kinase domain | | tumoral
|
|
| --low
|
| |
by aberrant DNA methylation in colorectal cancer | | tumoral
|
|
|
| gain of function
| |
in melanomas, mutation gain de function V600E (which encodes an amino acid substitution mutant of BRAF) in the neural crest lineage | | tumoral
| fusion
|
|
|
| |
tandem duplication at 7q34 leading to a fusion between KIAA1549 and BRAF occurs in the majority of Pilocytic astrocytomas | | tumoral
|
| amplification
|
|
| |
duplication was the most frequent genomic aberration in constitutes a mechanism of MAPK pathway activation in low-grade astrocytoma | | tumoral
| fusion
|
|
|
| |
KIAA1549-BRAF fusion gene in cells forming microvascular proliferations in pilocytic astrocytoma | |
