Catalog Number:
CPTC-BRAF-7
RRID:
AB_2827860
Target Antigen:
B-Raf Proto-Oncogene, Serine/Threonine Kinase Peptide 5
Isotype:
IgG
Species:
Rabbit Monoclonal Antibody
Last Updated:
07/02/2025
Antigen Recognition(s):
Peptide, Recombinant Full-length, Endogenous, Phosphorylation
Thematic Panel(s):
Ras Pathway
Result: No Binding
Affinity and binding kinetics of CPTC-BRAF-7 and full length BRAF recombinant protein were measured using surface plasmon resonance. CPTC-BRAF-7 rabbit antibody was captured on series S protein A biosensor chip. BRAF recombinant protein at 1024 nM, 256 nM, 64 nM, 16 nM, 4 nM, 1 nM, 0.25 nM, and 0.0625 nM, was used as analyte.
Result: Negative
This antibody is not suitable for use in an Immunohistochemistry format as described in SOP M-106.
Result: Negative
Immunofluorescence staining of MCF10a cells stably transfected with KRAS (MCF10a-KRAS) using CPTC- BRAF-7 antibody. BRAF protein expression was not detected.
Result: Positive
Protein Array in which CPTC-BRAF-7 is screened against the NCI60 cell line panel for expression. Data is normalized to a mean signal of 1.0 and standard deviation of 0.5. Color conveys over-expression level (green), basal level (blue), under-expression level (red).
Result: Negative
Western Blot of CPTC-BRAF-7 against the over-expressed lysate of BRAF. Expected MW is 84 KDa. The antibody did not detect the target protein.
Result: Positive
Western Blot using CPTC-BRAF-7 as primary Ab against recombinant BRAF (lane 2). Also included are molecular wt. standards (lane 1).
Result: Positive
Western Blot using CPTC-BRAF-7 as primary Ab against MCF10A-KRas cell lysate (lane 2). Also included are molecular wt. standards (lane 1).
Result: Negative
Western blot using CPTC-BRAF-7 as primary antibody against the whole lysates of RPMI-8226, SNB-75, HL-60, NCI/ADR-RES, TK-10, and KM12. The antibody did not detect the target protein (~84 KDa) in any of the tested cell lysates.
NCI Identification Number:
00181
Antigen Name:
B-Raf Proto-Oncogene, Serine/Threonine Kinase Peptide 5
CPTC Name:
CPTC-BRAF Peptide 5
Aliases:
B-Raf Proto-Oncogene, Serine/Threonine Kinase; BRAF1; BRAF-1; V-Raf Murine Sarcoma Viral Oncogene Homolog B1; V-Raf Murine Sarcoma Viral Oncogene Homolog B; Serine/Threonine-Protein Kinase B-Raf; B-Raf Serine/Threonine-Protein; Proto-Oncogene B-Raf; RAFB1; B-Raf Proto-Oncogene Serine/Threonine-Protein Kinase (P94); V-Raf Murine Sarcoma Viral Oncogene-Like Protein B1; Murine Sarcoma Viral (V-Raf) Oncogene Homolog B1; Serine/Threonine-Protein Kinase B-Raf Variant; Non-Specific Serine/Threonine Protein Kinase; Uncharacterized Protein BRAF; 94 KDa B-Raf Protein; BRAF Protein; B-RAF1; B-Raf; NS7; P94
Function:
This gene encodes a protein belonging to the RAF family of serine/threonine protein kinases. This protein plays a role in regulating the MAP kinase/ERK signaling pathway, which affects cell division, differentiation, and secretion. Mutations in this gene, most commonly the V600E mutation, are the most frequently identified cancer-causing mutations in melanoma, and have been identified in various other cancers as well, including non-Hodgkin lymphoma, colorectal cancer, thyroid carcinoma, non-small cell lung carcinoma, hairy cell leukemia and adenocarcinoma of lung. Mutations in this gene are also associated with cardiofaciocutaneous, Noonan, and Costello syndromes, which exhibit overlapping phenotypes. A pseudogene of this gene has been identified on the X chromosome. BRAF mutations are found to be recurrent in many cancer types. Of these, the mutation of valine 600 to glutamic acid (V600E) is the most prevalent. V600E has been determined to be an activating mutation, and cells that harbor it, along with other V600 mutations are sensitive to the BRAF inhibitor dabrafenib. It is also common to use MEK inhibition as a substitute for BRAF inhibitors, and the MEK inhibitor trametinib has seen some success in BRAF mutant melanomas. BRAF mutations have also been correlated with poor prognosis in many cancer types, although there is at least one study that questions this conclusion in papillary thyroid cancer. Oncogenic BRAF mutations are divided into three categories that determine their sensitivity to inhibitors. Class 1 BRAF mutations (V600) are RAS-independent, signal as monomers and are sensitive to current RAF monomer inhibitors. Class 2 BRAF mutations (K601E, K601N, K601T, L597Q, L597V, G469A, G469V, G469R, G464V, G464E, and fusions) are RAS-independent, signaling as constitutive dimers and are resistant to vemurafenib. Such mutants may be sensitive to novel RAF dimer inhibitors or MEK inhibitors. Class 3 BRAF mutations (D287H, V459L, G466V, G466E, G466A, S467L, G469E, N581S, N581I, D594N, D594G, D594A, D594H, F595L, G596D, and G596R) with low or absent kinase activity are RAS-dependent and they activate ERK by increasing their binding to activated RAS and wild-type CRAF. Class 3 BRAF mutations coexist with mutations in RAS or NF1 in melanoma may be treated with MEK inhibitors. In epithelial tumors such as CRC or NSCLC may be effectively treated with combinations that include inhibitors of receptor tyrosine kinase.Raf kinases, a family of three serine/threonine kinases, are part of the Ras-MAPK signaling cascade and phosphorylate MEK. Upon growth factor stimulation, Raf-1 (c-Raf) is activated by GTP-bound Ras and recruited to the cell membrane. This activation process is tightly regulated.BRAF (B-Raf Proto-Oncogene, Serine/Threonine Kinase) is a Protein Coding gene. Diseases associated with BRAF include Cardiofaciocutaneous Syndrome 1 and Noonan Syndrome 7. Among its related pathways are In Progress: Dabrafenib Pathway, Pharmacokinetics/Pharmacodynamics and Signalling to p38 via RIT and RIN. An important paralog of this gene is RAF1.
Chromosomal Localization:
7q34
Accession Number:
UniProt Accession Number:
P15056
DNA Source:
N/A
Immunogen:
Synthetic Peptide
Vector Name:
N/A
Extinction Coefficient:
Buffers:
Expressed Sequence:
GDGGSTTGLSA(pT)PPASLPGSLTNVK
Native Sequence:
Calculated Isoelectric Point:
0
Molecular Weight:
2750
Last Updated:
07/01/2026
No SOPs available.
Get it for free at Adobe.com