BCR-ABL1 Fusion Expression Plasmid Vectors

RGBiotech offers BCR-ABL1 fusion expression plasmid vectors to assist researchers to study the resistance mechanisms to tyrosine kinase inhibitors (TKIs), and to develop new treatment strategies to improve outcomes for patients with Philadelphia chromosome (Ph)-positive leukemias.

The BCR activator of RhoGEF and GTPase (BCR), also known as the breakpoint cluster region protein, is a protein that in humans is encoded by the BCR gene (Gene ID: 613) located on chromosome 22 and has two different isoforms.

The ABL proto-oncogene 1, non-receptor tyrosine kinase (ABL1), also known as tyrosine-protein kinase ABL, is a protein that in humans is encoded by the ABL1 gene (Gene ID: 25) located on chromosome 9 and has two different isoforms. ABL1 is involved in a variety of cellular processes which include cell division, cell adhesion, cell differentiation, and cell response to stress. ABL1 gene has been found fused to a variety of translocation partner genes in many cases of leukemias, most notably the t(9;22) translocation that leads to a fusion with the 5' end of the BCR gene.

BCR-ABL1, also known as BCR-ABL, is a fusion gene that is formed by a translocation between chromosome 9 and chromosome 22, specifically t(9;22)(q34;q11), where the ABL1 gene from chromosome 9 fuses with the BCR gene on chromosome 22. This translocation produces the Philadelphia chromosome which has been found in patients with chronic myelogenous leukemia (CML), acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), B-Cell acute lymphoblastic leukemia (B-ALL). The resulted BCR-ABL fusion protein is a constitutively active tyrosine kinase enzyme, which promotes cell survival and growth while inhibiting apoptosis (programmed cell death) thus contributes to the development of leukemia. The activities of BCR-ABL fusion proteins can be inhibited by tyrosine kinase inhibitors (TKIs) such as imatinib (Gleevec), dasatinib and nilotinib. However, the evolution of mutations in the BCR-ABL1 fusion gene transcript renders patients resistant to tyrosine kinase inhibitor (TKI) based therapy.

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