Human BRAF blocking peptide

Name: Human BRAF blocking peptide
SKU: CDBP0627
Rating: 5 (1 reviews)

Synthetic Human BRAF blocking peptide for BL

COA

SDS

Datasheet

Summary

Product Overview

Blocking peptide for anti-B-raf antibody

Target

B-raf

Nature

Synthetic

Tag/Conjugate

Unconjugated

Application Notes

For in vitro research use only. Not intended for any diagnostic or therapeutic purpose. Not suitable for human or animal consumption.

Format

Liquid

Concentration

200 μg/ml

Buffer

PBS containing 0.02% sodium azide

Preservative

0.02% Sodium Azide

Storage

Store at -20℃, stable for one year.

Entrez Gene ID

673

Antigen Description

This gene encodes a protein belonging to the raf/mil family of serine/threonine protein kinases. This protein plays a role in regulating the MAP kinase/ERKs signaling pathway, which affects cell division, differentiation, and secretion. Mutations in this gene are associated with cardiofaciocutaneous syndrome, a disease characterized by heart defects, mental retardation and a distinctive facial appearance. Mutations in this gene have also been associated with various cancers, including non-Hodgkin lymphoma, colorectal cancer, malignant melanoma, thyroid carcinoma, non-small cell lung carcinoma, and adenocarcinoma of lung. A pseudogene, which is located on chromosome X, has been identified for this gene. [provided by RefSeq, Jul 2008]

Function

ATP binding; MAP kinase kinase kinase activity; calcium ion binding; identical protein binding; mitogen-activated protein kinase kinase binding; protein binding; protein heterodimerization activity; protein kinase activity; protein serine/threonine kinase

Synonyms

BRAF; v-raf murine sarcoma viral oncogene homolog B; NS7; BRAF1; RAFB1; B-RAF1; serine/threonine-protein kinase B-raf; 94 kDa B-raf protein; proto-oncogene B-Raf; v-raf murine sarcoma viral oncogene homolog B1; murine sarcoma viral (v-raf) oncogene homolog B1; B-Raf proto-oncogene serine/threonine-protein kinase (p94);

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Combination of Dabrafenib and Trametinib for the Treatment of Relapsed and Refractory Multiple Myeloma Harboring BRAF V600E Mutation

CASE REPORTS IN HEMATOLOGY

Authors: Cepulyte, Ruta; Zucenka, Andrius; Peceliunas, Valdas

Abstract

Multiple myeloma (MM) is an incurable plasma cell neoplasia characterized by relapsed and/or refractory (R/R) disease course, which poses a major therapeutic challenge. New therapies, including BRAF V600E mutation targeting, may become a new treatment option for R/R MM. In combination with mitogen-activated protein kinase inhibitors (MEKi), BRAF inhibitors (BRAFi) could provide better tailored clinical management, although experience in this field is lacking. To this date, there is only one case describing R/R MM treatment with BRAFi vemurafenib and MEKi cobimetinib. This is the first case presenting a R/R MM patient treated with BRAFi dabrafenib and MEKi trametinib.

Oncogenic signaling pathways associated with immune evasion and resistance to immune checkpoint inhibitors in cancer

SEMINARS IN CANCER BIOLOGY

Authors: Kobayashi, Yoshie; Lim, Seung-Oe; Yamaguchi, Hirohito

Abstract

Immune checkpoint inhibitors (ICIs) are novel class of anti-cancer drugs that exhibit significant therapeutic effects even in patients with advanced-stage cancer. However, the efficacy of ICIs is limited due to resistance. Therefore, appropriate biomarkers to select patients who are likely to respond to these drugs as well as combination therapy to overcome the resistance are urgently necessary. Cancer is caused by various genetic alterations that lead to abnormalities in oncogenic signaling pathways. The aberrant oncogenic signaling pathways serve as not only prognostic and predictive biomarkers, but also targets for molecularly targeted therapy. Growing evidence shows that the aberrant oncogenic signaling pathways in cancer cells facilitate the resistance to ICIs by modulating the regulation of immune checkpoint and cancer immune surveillance. Indeed, it has been demonstrated that some molecular targeted therapies significantly improve the efficacy of ICIs in preclinical and clinical studies. In this review, we highlighted several oncogenic signaling pathways including receptor tyrosine kinases (RTKs), MAPK, PI3K-AKT-mTOR, JAK-STAT, Hippo, and Wnt pathways, and summarized the recent findings of the mechanisms underlying the regulation of cancer immunity and the ICI resistance induced by these aberrant oncogenic signaling pathways in cancer cells. Moreover, we discussed potential combination therapies with ICIs and molecularly targeted drugs to overcome the resistance and increase the efficacy of ICIs.