Relation Results

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-259921	Ser151	VARSNPKsPQKPIVR	Homo sapiens	Melanoma Cell
pmid	sentence
21478863	We show that overactivation of the MAPK pathway, induced by the oncogenic Ras in melanoma, induces constitutive phosphorylation of BRAF on Ser151 by ERK, which inhibits NRAS-BRAF interaction

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-259919	Ser151	VARSNPKsPQKPIVR	Homo sapiens	Melanoma Cell
pmid	sentence
21478863	We show that overactivation of the MAPK pathway, induced by the oncogenic Ras in melanoma, induces constitutive phosphorylation of BRAF on Ser151 by ERK, which inhibits NRAS-BRAF interaction

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, AML_TRIPLETS, Colorectal Carcinoma, EGFR Signaling, ErbB receptors in cancer, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, IL6 Signaling, Inhibition of Apoptosis, Luminal Breast Cancer, Malignant Melanoma, NPM1_new, Noonan syndrome, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, Rett syndrome, Rhabdomyosarcoma, RTKs in cancer, Thyroid cancer, T cell activation, VEGF Signaling

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-259920	Ser151	VARSNPKsPQKPIVR	Homo sapiens	Melanoma Cell
pmid	sentence
21478863	We show that overactivation of the MAPK pathway, induced by the oncogenic Ras in melanoma, induces constitutive phosphorylation of BRAF on Ser151 by ERK, which inhibits NRAS-BRAF interaction

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-236388	Thr753	YACASPKtPIQAGGY	Rattus norvegicus	PC-12 Cell
pmid	sentence
16508002	Erk-induced phosphorylation of b-raf on t753 promoted the disassembly of raf heterodimers, and the mutation of t753 prolonged growth factor-induced heterodimerization. The b-raf t753a mutant enhanced differentiation of pc12 cells, which was previously shown to be dependent on sustained erk signaling. Site is critical for v-src dependent modulation of slk kinase activity.

Publications:

2

Organism:

Homo Sapiens, Rattus Norvegicus

Identifier	Residue	Sequence	Organism
SIGNOR-278435	Ser205	APQSDEGsDIDSEPD	Homo sapiens
pmid	sentence
27906130	BRAF activates PAX3 to control muscle precursor cell migration during forelimb muscle development.\|We found that BRAF clearly induced phosphorylation of PAX3 at Ser205 in both cell types (XREF_FIG).

Publications:

1

Organism:

Homo Sapiens

Pathways:

Rhabdomyosarcoma

Identifier	Residue	Sequence	Organism
SIGNOR-276406	Ser21	GHVDSGKsTTTGHLI	in vitro
pmid	sentence
22378069	Mass spectrometry identified in vitro S21 and T88 as phosphorylation sites mediated by B-Raf but not C-Raf on eEF1A1 whereas S21 was phosphorylated on eEF1A2 by both B- and C-Raf.

Publications:

1

Organism:

In Vitro

Identifier	Residue	Sequence	Organism
SIGNOR-276404	Ser21	GHVDSGKsTTTGHLI	in vitro
pmid	sentence
22378069	Mass spectrometry identified in vitro S21 and T88 as phosphorylation sites mediated by B-Raf but not C-Raf on eEF1A1 whereas S21 was phosphorylated on eEF1A2 by both B- and C-Raf.

Identifier	Residue	Sequence	Organism
SIGNOR-276405	Thr88	ETSKYYVtIIDAPGH	in vitro
pmid	sentence
22378069	Mass spectrometry identified in vitro S21 and T88 as phosphorylation sites mediated by B-Raf but not C-Raf on eEF1A1 whereas S21 was phosphorylated on eEF1A2 by both B- and C-Raf.

Publications:

2

Organism:

In Vitro

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-235475	Ser218	VSGQLIDsMANSFVG	Mus musculus	NIH-3T3 Cell
pmid	sentence
8131746	Activation of mek family kinases requires phosphorylation of two conserved ser/thr residueserine residues 218 and 222 of human mek1 are the primary sites for phosphorylation by c-raf.

Identifier	Residue	Sequence	Organism
SIGNOR-39054	Ser222	LIDSMANsFVGTRSY	in vitro
pmid	sentence
8413257	Raf-1 phosphorylation of MEK activated it, as judged by its ability to stimulate the phosphorylation of myelin basic protein by glutathione S-transferase-ERK1.

Identifier	Residue	Sequence	Organism
SIGNOR-39058	Ser248	SVQSDIWsMGLSLVE	in vitro
pmid	sentence
8413257	Raf-1 phosphorylation of MEK activated it, as judged by its ability to stimulate the phosphorylation of myelin basic protein by glutathione S-transferase-ERK1.

Identifier	Residue	Sequence	Organism
SIGNOR-39062	Ser252	DIWSMGLsLVEMAVG	in vitro
pmid	sentence
8413257	Raf-1 phosphorylation of MEK activated it, as judged by its ability to stimulate the phosphorylation of myelin basic protein by glutathione S-transferase-ERK1.

Publications:

4

Organism:

Mus Musculus, In Vitro

Identifier	Residue	Sequence	Organism
SIGNOR-42664	Ser222	VSGQLIDsMANSFVG	Homo sapiens
pmid	sentence
8668348	We show that, consequently, b-raf interacts with mek-1 and mek-2 with a better affinity than does c-raf-1, thus strengthening the notion that b-raf is a stronger mek activator than c-raf-l.

Identifier	Residue	Sequence	Organism
SIGNOR-42668	Ser226	LIDSMANsFVGTRSY	Homo sapiens
pmid	sentence
8668348	We show that, consequently, b-raf interacts with mek-1 and mek-2 with a better affinity than does c-raf-1, thus strengthening the notion that b-raf is a stronger mek activator than c-raf-l.

Publications:

2

Organism:

Homo Sapiens

Tissue:

Brain

Identifier	Residue	Sequence	Organism
SIGNOR-78681	Ser364	FGQRDRSsSAPNVHI	Homo sapiens
pmid	sentence
10869359	We show that phosphorylation of b-raf by akt occurs at multiple residues within its amino terminal regulatory domain, at both the conserved and unique phosphorylation sites. Akt phosphorylated b-raf on s364 and s428 to inactivate its kinase activity b-raf contains three akt consensus sites, table i. One site, ser364 is conserved with c-raf;however, two sites, ser428 and thr439, are unique to b-raf

Identifier	Residue	Sequence	Organism
SIGNOR-78685	Ser428	GPQRERKsSSSSEDR	Homo sapiens
pmid	sentence
10869359	We show that phosphorylation of b-raf by akt occurs at multiple residues within its amino terminal regulatory domain, at both the conserved and unique phosphorylation sites. Akt phosphorylated b-raf on s364 and s428 to inactivate its kinase activity b-raf contains three akt consensus sites, table i. One site, ser364 is conserved with c-raf;however, two sites, ser428 and thr439, are unique to b-raf

Identifier	Residue	Sequence	Organism
SIGNOR-78689	Thr440	EDRNRMKtLGRRDSS	Homo sapiens
pmid	sentence
10869359	We show that phosphorylation of b-raf by akt occurs at multiple residues within its amino terminal regulatory domain, at both the conserved and unique phosphorylation sites. Akt phosphorylated b-raf on s364 and s428 to inactivate its kinase activity b-raf contains three akt consensus sites, table i. One site, ser364 is conserved with c-raf;however, two sites, ser428 and thr439, are unique to b-raf

Publications:

3

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-78693	Ser364	FGQRDRSsSAPNVHI	Homo sapiens
pmid	sentence
10869359	We show that phosphorylation of b-raf by akt occurs at multiple residues within its aminoterminal regulatory domain, at both the conserved and unique phosphorylation sites. Akt phosphorylated b-raf on s364 and s428 to inactivate its kinase activity.

Identifier	Residue	Sequence	Organism
SIGNOR-78697	Ser428	GPQRERKsSSSSEDR	Homo sapiens
pmid	sentence
10869359	We show that phosphorylation of b-raf by akt occurs at multiple residues within its aminoterminal regulatory domain, at both the conserved and unique phosphorylation sites. Akt phosphorylated b-raf on s364 and s428 to inactivate its kinase activity.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-244152	Ser364	FGQRDRSsSAPNVHI	Homo sapiens
pmid	sentence
10869359	We show that phosphorylation of b-raf by akt occurs at multiple residues within its amino terminal regulatory domain, at both the conserved and unique phosphorylation sites. Akt phosphorylated b-raf on s364 and s428 to inactivate its kinase activity b-raf contains three akt consensus sites, table i. One site, ser364 is conserved with c-raf;however, two sites, ser428 and thr439, are unique to b-raf

Identifier	Residue	Sequence	Organism
SIGNOR-244160	Ser428	GPQRERKsSSSSEDR	Homo sapiens
pmid	sentence
10869359	We show that phosphorylation of b-raf by akt occurs at multiple residues within its amino terminal regulatory domain, at both the conserved and unique phosphorylation sites. Akt phosphorylated b-raf on s364 and s428 to inactivate its kinase activity b-raf contains three akt consensus sites, table i. One site, ser364 is conserved with c-raf;however, two sites, ser428 and thr439, are unique to b-raf

Identifier	Residue	Sequence	Organism
SIGNOR-244156	Thr440	EDRNRMKtLGRRDSS	Homo sapiens
pmid	sentence
10869359	We show that phosphorylation of b-raf by akt occurs at multiple residues within its amino terminal regulatory domain, at both the conserved and unique phosphorylation sites. Akt phosphorylated b-raf on s364 and s428 to inactivate its kinase activity b-raf contains three akt consensus sites, table i. One site, ser364 is conserved with c-raf;however, two sites, ser428 and thr439, are unique to b-raf

Publications:

3

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, AML_TRIPLETS, EGFR Signaling, ErbB receptors in cancer, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, Inhibition of Apoptosis, Luminal Breast Cancer, Malignant Melanoma, NPM1_new, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, Rhabdomyosarcoma, RTKs in cancer, Thyroid cancer, T cell activation, VEGF Signaling

Identifier	Residue	Sequence	Organism
SIGNOR-251471	Ser365	GQRDRSSsAPNVHIN	Homo sapiens
pmid	sentence
10869359	Akt phosphorylates both S364 and S428. Akt downregulates B-Raf activity in vivo

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-251472	Ser429	PQRERKSsSSSEDRN	Homo sapiens	HEK-293 Cell
pmid	sentence
10869359	Akt phosphorylates both S364 and S428. Akt downregulates B-Raf activity in vivo

Publications:

2

Organism:

Homo Sapiens

Pathways:

FLT3-ITD signaling, Glioblastoma Multiforme

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-259922	Ser429	PQRERKSsSSSEDRN	Rattus norvegicus	PC-12 Cell
pmid	sentence
11510412	The in vitro phosphorylation of a site unique to B-Raf (Ser429) has been proposed to be responsible for the negative regulation of the isoenzyme by Akt. Using phosphopetide mapping and site-directed mutagenesis we showed that Ser429 is phosphorylated upon cAMP elevation in PC12 cells and proposed that PKA is a major kinase phosphorylating the B-Raf-specific site in vivo

Identifier	Residue	Sequence	Organism
SIGNOR-250339	Ser429	PQRERKSsSSSEDRN	in vitro
pmid	sentence
11510412	Direct phosphorylation of B-Raf by PKA exerts a negative effect on its kinase activity, essentially via phosphorylation of Ser429

Publications:

2

Organism:

Rattus Norvegicus, In Vitro

Identifier	Residue	Sequence	Organism
SIGNOR-277498	Ser465	TVGQRIGsGSFGTVY	Homo sapiens
pmid	sentence
31929109	We previously identified that BRAFWT can autophosphorylate its P-loop (Ser-465/Ser-467) to inactivate itself in the absence of native substrate MEK

Identifier	Residue	Sequence	Organism
SIGNOR-277499	Ser467	GQRIGSGsFGTVYKG	Homo sapiens
pmid	sentence
31929109	We previously identified that BRAFWT can autophosphorylate its P-loop (Ser-465/Ser-467) to inactivate itself in the absence of native substrate MEK

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-277255	Ser614	SHQFEQLsGSILWMA	Homo sapiens	HEK-293T Cell
pmid	sentence
27345148	The phosphorylation of S614 is mitogen inducible and the result of autophosphorylation. These data suggest that phosphorylation at this site is inhibitory, and part of the physiological shut-down mechanism of BRAF signalling.

Publications:

3

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, AML_TRIPLETS, Colorectal Carcinoma, EGFR Signaling, ErbB receptors in cancer, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, IL6 Signaling, Inhibition of Apoptosis, Luminal Breast Cancer, Malignant Melanoma, NPM1_new, Noonan syndrome, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, Rett syndrome, Rhabdomyosarcoma, RTKs in cancer, Thyroid cancer, T cell activation, VEGF Signaling

Identifier	Residue	Sequence	Organism
SIGNOR-278352	Thr219	AEHQYFMtEYVATRW	Homo sapiens
pmid	sentence
29483645	Our data indicate that oncogenic BRAF increases ERK5 protein level, phosphorylation at several residues and kinase activity.\|Overexpression of oncogenic BRAF induced ERK5 phosphorylation at Thr218 and Tyr220, although to a lower level than that induced by MEK5DD.

Identifier	Residue	Sequence	Organism
SIGNOR-278353	Tyr221	HQYFMTEyVATRWYR	Homo sapiens
pmid	sentence
29483645	Our data indicate that oncogenic BRAF increases ERK5 protein level, phosphorylation at several residues and kinase activity.\|Overexpression of oncogenic BRAF induced ERK5 phosphorylation at Thr218 and Tyr220, although to a lower level than that induced by MEK5DD.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Sequence	Organism
SIGNOR-170339	Thr401	STTGLSAtPPASLPG	Homo sapiens
pmid	sentence
21135229	We show that b-raf is a calcineurin substrate;among calcineurin target residues on b-raf is t401, a site of negative feedback phosphorylation by erk1/2. Blocking calcineurin activity in _ cells prevents dephosphorylation of b-raf t401 and decreases b-raf and erk1/2 activities.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, AML_TRIPLETS, Colorectal Carcinoma, EGFR Signaling, ErbB receptors in cancer, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, IL6 Signaling, Inhibition of Apoptosis, Luminal Breast Cancer, Malignant Melanoma, NPM1_new, Noonan syndrome, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, Rett syndrome, Rhabdomyosarcoma, RTKs in cancer, Thyroid cancer, T cell activation, VEGF Signaling

Identifier	Residue	Sequence	Organism
SIGNOR-161819	Thr753	YACASPKtPIQAGGY	Homo sapiens
pmid	sentence
19933846	Erk-induced phosphorylation of b-raf on t753 promoted the disassembly of raf heterodimers, and the mutation of t753 prolonged growth factor-induced heterodimerization. The b-raf t753a mutant enhanced differentiation of pc12 cells, which was previously shown to be dependent on sustained erk signaling. Site is critical for v-src dependent modulation of slk kinase activity.

Identifier	Residue	Sequence	Organism
SIGNOR-144827	Thr753	YACASPKtPIQAGGY	Homo sapiens
pmid	sentence
16508002	Erk-induced phosphorylation of b-raf on t753 promoted the disassembly of raf heterodimers, and the mutation of t753 prolonged growth factor-induced heterodimerization. The b-raf t753a mutant enhanced differentiation of pc12 cells, which was previously shown to be dependent on sustained erk signaling. Site is critical for v-src dependent modulation of slk kinase activity.

Publications:

2

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-174036		Homo sapiens	Melanoma Cell
pmid	sentence
21654832	Inhibition of map kinases mek, jnk, p38, and multikinases (braf, craf, vegfp by sorafenib) in wm-115 and m14 human melanoma cell lines led to either significant reduction or complete inhibition of the plk-1 protein expression.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-244827		Mus musculus
pmid	sentence
8131746	Activation of mek family kinases requires phosphorylation of two conserved ser/thr residueserine residues 218 and 222 of human mek1 are the primary sites for phosphorylation by c-raf.

Identifier	Residue	Organism
SIGNOR-251988		Homo sapiens
pmid	sentence
21900390	BRAFV600E has been shown to initiate thyroid follicular cell transformation. The BRAFV600E mutation disrupts the hydrophobic interaction, enabling the BRAF kinase to fold into a catalytically active formation, resulting in an almost 500-fold increase in kinase activity. Mutant BRAF can dimerize and activate MEK without Ras activation.

Identifier	Residue	Organism
SIGNOR-244831		in vitro
pmid	sentence
8413257	Raf-1 phosphorylation of MEK activated it, as judged by its ability to stimulate the phosphorylation of myelin basic protein by glutathione S-transferase-ERK1.

Publications:

3

Organism:

Mus Musculus, Homo Sapiens, In Vitro

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, AML_TRIPLETS, Colorectal Carcinoma, EGFR Signaling, ErbB receptors in cancer, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, IL6 Signaling, Inhibition of Apoptosis, Luminal Breast Cancer, Malignant Melanoma, NPM1_new, Noonan syndrome, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, Rett syndrome, Rhabdomyosarcoma, RTKs in cancer, Thyroid cancer, T cell activation, VEGF Signaling

Identifier	Residue	Organism
SIGNOR-258267		in vitro
pmid	sentence
22037378	Our data set represents the most detailed comprehensive assessment of the reactivity of known and clinical kinase inhibitors across the kinome published to date. \| The data also show that for at least 15 of the 27 kinases that are the primary, intended targets for the compounds tested and that are represented in the assay panel, selective inhibitors, as assessed by both absolute selectivity across the kinome and selectivity relative to the primary target, are among the 72 tested here.

Publications:

1

Organism:

In Vitro

Identifier	Residue	Organism	Cell Line
SIGNOR-276608		Homo sapiens	HEK-293T Cell
pmid	sentence
24290981	Our data are consistent with a pathway involving the cAMP-mediated activation of Rapgef2, which then stimulates Rap1, leading to increases in B-Raf, MEK, and ERK activity.Increased intracellular concentrations of cAMP enhanced the Rapgef2-dependent activation of Rap1, which in turn associated with B-Raf to enable the activation of ERK and subsequent neuronal- and endocrine-specific cellular outcomes, such as induction of neuroendocrine-specific genes and extension of neuritic processes (neuritogenesis).

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-261986		in vitro
pmid	sentence
32069833	HG6-64-1 is a specific BRAF inhibitor

Publications:

1

Organism:

In Vitro

Identifier	Residue	Organism	Cell Line
SIGNOR-272043		Homo sapiens	HCT-116 Cell
pmid	sentence
22628551	We showed that RNF149 bound directly to the C-terminal kinase-containing domain of wild-type BRAF and induced ubiquitination, followed by proteasome-dependent degradation, of the latter protein. Functionally, RNF149 attenuated the increase in cell growth induced by wild-type BRAF.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-259373		Homo sapiens	Colonic Cancer Cell Line
pmid	sentence
27340238	These alterations corresponded to mutant KRAS and BRAF-dependent increases in glucose uptake and lactate production. Metabolic reprogramming and glucose conversion to lactate in RKO cells were proportional to levels of BRAF V600E protein.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism	Cell Line
SIGNOR-235478		Mus musculus	NIH-3T3 Cell
pmid	sentence
7706312	Association of B-Raf with immobilized Ras occurred independently of prior stimulation of cells with serum, suggesting that primarily the production of GTP-Ras by mitogen stimulation is critical for the formation of B-Raf_GTP-Ras complexes.

Identifier	Residue	Organism
SIGNOR-160043		Homo sapiens
pmid	sentence
18098337	BRAF kinase is a downstream target of KRAS and activates the MAPK pathway.

Publications:

2

Organism:

Mus Musculus, Homo Sapiens

Pathways:

EGFR Signaling, ErbB receptors in cancer, Glioblastoma Multiforme, Hepatocellular Tumor, Noonan syndrome, Non-small-cell lung cancer (NSCLC), PI3K/AKT Signaling, Rett syndrome, RTKs in cancer, T cell activation, VEGF Signaling

Identifier	Residue	Organism
SIGNOR-251989		Homo sapiens
pmid	sentence
19861538	The BRAFV600E oncogene induces transforming growth factor beta secretion leading to sodium iodide symporter repression and increased malignancy in thyroid cancer. BRAF induces TGFβ secretion leading to NIS repression in a MEK-ERK–independent manner but cooperating with the MEK-ERK pathway to induce strong tumor invasion, two major traits acquired during PTC progression.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Thyroid cancer

Identifier	Residue	Organism
SIGNOR-258112		in vitro
pmid	sentence
22037378	Our data set represents the most detailed comprehensive assessment of the reactivity of known and clinical kinase inhibitors across the kinome published to date. \| The data also show that for at least 15 of the 27 kinases that are the primary, intended targets for the compounds tested and that are represented in the assay panel, selective inhibitors, as assessed by both absolute selectivity across the kinome and selectivity relative to the primary target, are among the 72 tested here.

Publications:

1

Organism:

In Vitro

Identifier	Residue	Organism	Cell Line
SIGNOR-273878		Homo sapiens	HEK-293 Cell
pmid	sentence
29433126	In mammals, RAF family kinases include three catalytically competent enzymes (ARAF, BRAF and CRAF) and two pseudokinases (KSR1 and KSR2) that have been described as scaffolds owing to their apparent ability to bridge RAF isoforms and their substrate, mitogen-activated protein kinase kinase (MEK).Kinase suppressor of Ras (KSR) pseudokinases were also shown to dimerize with kinase-competent RAFs to stimulate catalysis allosterically.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-277160		Homo sapiens
pmid	sentence
29335436	To address whether PP1\u03b1 activates B-Raf through these inhibitory sites, we made use of B-Raf protein mutants in which an individual inhibitory site, as well as all four sites (4A), were mutated to alanine.\|We confirmed that GST-B-Raf was phosphorylated by ERK2 in vitro xref , mainly on S151 and T753 (Fig.\u00a0 xref ), and found that PP1\u03b1 dephosphorylated B-Raf on both ERK phosphorylation sites (Fig.\u00a0 xref ).

Publications:

1

Organism:

Homo Sapiens

Pathways:

Noonan syndrome

Identifier	Residue	Organism	Cell Line
SIGNOR-251650		Mus musculus	NIH-3T3 Cell
pmid	sentence
23791108	It is possible that RIT1 interacts with RAF1 and that gain-of-function mutations in RIT1 and RAF1 exert similar effects in heart development.

Publications:

1

Organism:

Mus Musculus

Pathways:

Noonan syndrome

Identifier	Residue	Organism
SIGNOR-190907		Homo sapiens
pmid	sentence
Other

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-192592		Homo sapiens
pmid	sentence
Other

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-260082		Homo sapiens
pmid	sentence
21900390	RAF, a cytoplasmic serine-threonine protein kinase, is a member of the RAS-RAF-MEK-ERK cell-signaling pathway [also known as the MAP kinase (MAPK) pathway], and it plays an essential role in mediating cellular differentiation, proliferation, senescence, and survival in response to extracellular cues. Raf phosphorylates and activates MAP-ERK kinase (MEK), which phosphorylates and activates extracellular signal-regulated kinase (ERK).

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, AML_TRIPLETS, Colorectal Carcinoma, EGFR Signaling, ErbB receptors in cancer, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, IL6 Signaling, Inhibition of Apoptosis, Luminal Breast Cancer, Malignant Melanoma, NPM1_new, Noonan syndrome, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, Rett syndrome, Rhabdomyosarcoma, RTKs in cancer, Thyroid cancer, T cell activation, VEGF Signaling

Identifier	Residue	Organism
SIGNOR-258283		in vitro
pmid	sentence
22037378	Our data set represents the most detailed comprehensive assessment of the reactivity of known and clinical kinase inhibitors across the kinome published to date. \| The data also show that for at least 15 of the 27 kinases that are the primary, intended targets for the compounds tested and that are represented in the assay panel, selective inhibitors, as assessed by both absolute selectivity across the kinome and selectivity relative to the primary target, are among the 72 tested here.

Publications:

1

Organism:

In Vitro

Identifier	Residue	Organism
SIGNOR-258097		in vitro
pmid	sentence
22037378	Our data set represents the most detailed comprehensive assessment of the reactivity of known and clinical kinase inhibitors across the kinome published to date. \| The data also show that for at least 15 of the 27 kinases that are the primary, intended targets for the compounds tested and that are represented in the assay panel, selective inhibitors, as assessed by both absolute selectivity across the kinome and selectivity relative to the primary target, are among the 72 tested here.

Publications:

1

Organism:

In Vitro

Identifier	Residue	Organism
SIGNOR-267362		Homo sapiens
pmid	sentence
29731393	Oncogenic proteins that regulate proliferation, such as KRAS, BRAF, and MYC increase the transcription of NRF2

Publications:

1

Organism:

Homo Sapiens

Pathways:

Hepatocellular Tumor

Identifier	Residue	Organism
SIGNOR-259220		in vitro
pmid	sentence
16757355	This effort culminated in the identification of the clinical candidate BAY 43-9006 (Sorafenib, Nexavar), which has recently been approved by the FDA for advanced renal cell carcinoma in phase III clinical trials. Sorafenib inhibited the kinase activity of both C-RAF and B-RAF (wild type and V600E mutant).

Publications:

1

Organism:

In Vitro

Identifier	Residue	Organism
SIGNOR-175219		Homo sapiens
pmid	sentence
21779497	The raf family of proteins (raf-1, a-raf, and b-raf) is serine/threonine kinases that bind to the effector region of ras-gtp, thus inducing translocation of the protein to the plasma membrane. Once there, raf proteins are activated and phosphorylated by different protein kinases.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, KIT in AML, AML_TRIPLETS, IL6 Signaling, Inhibition of Apoptosis, Malignant Melanoma, NPM1_new, Noonan syndrome

Identifier	Residue	Organism
SIGNOR-259215		in vitro
pmid	sentence
24720932	Dabrafenib is known to inhibit V600E, V600K and V600D BRAF enzymes with in vitro IC50 values of 0.65, 0.5 and 1.84 nM, respectively. Dabrafenib can inhibit wild-type BRAF and CRAF kinases with IC50 values of 3.2 and 5.0 nM. Other kinases (SIK1, NEK111 and LIMK1) can be inhibited by dabrafenib when administered in high concentrations

Publications:

1

Organism:

In Vitro

Identifier	Residue	Organism	Cell Line
SIGNOR-273877		Homo sapiens	HEK-293 Cell
pmid	sentence
29433126	In mammals, RAF family kinases include three catalytically competent enzymes (ARAF, BRAF and CRAF) and two pseudokinases (KSR1 and KSR2) that have been described as scaffolds owing to their apparent ability to bridge RAF isoforms and their substrate, mitogen-activated protein kinase kinase (MEK).Kinase suppressor of Ras (KSR) pseudokinases were also shown to dimerize with kinase-competent RAFs to stimulate catalysis allosterically.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-259281		Homo sapiens
pmid	sentence
23094782	Metastatic melanoma is an aggressive disease resistant to chemotherapy. Recent clinical trials have reported improved survival for two novel agents; ipilimumab, a humanized, IgG1 monoclonal antibody that blocks cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) and vemurafenib , a BRAF (v-raf murine sarcoma viral oncogene homolog B1) inhibitor targeting an activating mutation in the serine-threonine-protein kinase BRAF gene.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-156906		Homo sapiens
pmid	sentence
21779497	The raf family of proteins (raf-1, a-raf, and b-raf) is serine/threonine kinases that bind to the effector region of ras-gtp, thus inducing translocation of the protein to the plasma membrane. Once there, raf proteins are activated and phosphorylated by different protein kinases.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, Colorectal Carcinoma, FLT3-ITD signaling, Glioblastoma Multiforme, Luminal Breast Cancer, Noonan syndrome, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), Rhabdomyosarcoma, Thyroid cancer

Identifier	Residue	Organism
SIGNOR-251987		Homo sapiens
pmid	sentence
19861538	The BRAFV600E oncogene induces transforming growth factor beta secretion leading to sodium iodide symporter repression and increased malignancy in thyroid cancer. BRAF induces TGFβ secretion leading to NIS repression in a MEK-ERK–independent manner but cooperating with the MEK-ERK pathway to induce strong tumor invasion, two major traits acquired during PTC progression.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Colorectal Carcinoma, Thyroid cancer

Identifier	Residue	Organism
SIGNOR-244843		Homo sapiens
pmid	sentence
8668348	We show that, consequently, b-raf interacts with mek-1 and mek-2 with a better affinity than does c-raf-1, thus strengthening the notion that b-raf is a stronger mek activator than c-raf-l.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, AML_TRIPLETS, Colorectal Carcinoma, EGFR Signaling, ErbB receptors in cancer, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, IL6 Signaling, Inhibition of Apoptosis, Luminal Breast Cancer, Malignant Melanoma, NPM1_new, Noonan syndrome, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, Rett syndrome, Rhabdomyosarcoma, RTKs in cancer, Thyroid cancer, T cell activation, VEGF Signaling

Identifier	Residue	Organism
SIGNOR-270043		Homo sapiens
pmid	sentence
16508002	Erk-induced phosphorylation of b-raf on t753 promoted the disassembly of raf heterodimers, and the mutation of t753 prolonged growth factor-induced heterodimerization. The b-raf t753a mutant enhanced differentiation of pc12 cells, which was previously shown to be dependent on sustained erk signaling. Site is critical for v-src dependent modulation of slk kinase activity.

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-259176		Homo sapiens
pmid	sentence
26254357	A novel multi-kinase inhibitor, regorafenib (Figure 1), inhibits vascular endothelial growth factor receptor (VEGFR) 1, VEGFR2, and VEGFR3, that play key roles in angiogenesis, and fibroblast growth factor receptor (FGFR) 1, platelet-derived growth factor receptor-β (PDGFR-β), tyrosine kinase with immunoglobulin and epidermal growth factor homology domain 2 (TIE2) and the mutant oncogenic kinase KIT, RET, B-RAF

Publications:

1

Organism:

Homo Sapiens

Identifier	Residue	Organism
SIGNOR-147327		Homo sapiens
pmid	sentence
21779497	The raf family of proteins (raf-1, a-raf, and b-raf) is serine/threonine kinases that bind to the effector region of ras-gtp, thus inducing translocation of the protein to the plasma membrane. Once there, raf proteins are activated and phosphorylated by different protein kinases.

Publications:

1

Organism:

Homo Sapiens

Pathways:

EGFR Signaling, ErbB receptors in cancer, Glioblastoma Multiforme, Hepatocellular Tumor, Noonan syndrome, Non-small-cell lung cancer (NSCLC), PI3K/AKT Signaling, Rett syndrome, RTKs in cancer, T cell activation, VEGF Signaling

Name	BRAF View Modifications
Full Name	Serine/threonine-protein kinase B-raf
Synonyms	Proto-oncogene B-Raf, p94, v-Raf murine sarcoma viral oncogene homolog B1 \| BRAF1, RAFB1
Primary ID	P15056
Links	- -
Type	protein
Relations	67
Pathways	Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, AML_TRIPLETS, Colorectal Carcinoma, EGFR Signaling, ErbB receptors in cancer, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, IL6 Signaling, Inhibition of Apoptosis, Luminal Breast Cancer, LIF in PDAC, Mitochondrial dynamics in T cell exhaustion, Malignant Melanoma, NPM1_new, Noonan syndrome, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, Rett syndrome, Rhabdomyosarcoma, RTKs in cancer, Thyroid cancer, T cell activation, VEGF Signaling
Inhibitors	sorafenib; PLX-4720; N-[4-[(4-Ethylpiperazin-1-yl)methyl]-3-(trifluoromethyl)phenyl]-3-[(E)-2-(4-methoxy-1H-pyrrolo[2,3-b]pyridin-5-yl)ethenyl]-4-methylbenzamide; 5-[1-(2-hydroxyethyl)-3-pyridin-4-yl-4-pyrazolyl]-2,3-dihydroinden-1-one oxime; CCT239065; GDC-0879; 1-methyl-5-[[2-[5-(trifluoromethyl)-1H-imidazol-2-yl]-4-pyridinyl]oxy]-N-[4-(trifluoromethyl)phenyl]-2-benzimidazolamine; sorafenib tosylate; dabrafenib; vemurafenib; regorafenib
Function	Protein kinase involved in the transduction of mitogenic signals from the cell membrane to the nucleus (Probable). Phosphorylates MAP2K1, and thereby activates the MAP kinase signal transduction pathway (PubMed:21441910, PubMed:29433126). May play a role in the postsynaptic responses of hippocampal neurons (PubMed:1508179).

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