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Invitrogen
BCR-ABL Monoclonal Antibody (7C6)
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BCR-ABL Antibody (MA1-153) in WB
Knockout of BCR was achieved by CRISPR-Cas9 genome editing using LentiArray™ Lentiviral sgRNA (Product # A32042, Assay ID CRISPR981967_LV) and LentiArray Cas9 Lentivirus (Product # A32064). Western blot analysis of BCR was performed by loading 30 µg of A-431 Wild Type (Lane 1), A-431 Cas9 (Lane 2) andA-431 BCR KO (Lane 3) whole cell extracts. The samples were electrophoresed using NuPAGE™ 3-8% Tris-Acetate Protein Gel (Product # EA0378BOX). Resolved proteins were then transferred onto a nitrocellulose membrane (Product # IB23001) by iBlot®... View More
Product Details
MA1-153
Applications
Tested Dilution
Publications
Product Specifications
Species Reactivity
Human,
Mouse
Published species
Human
Host/Isotype
Mouse
/ IgG2a
Class
Monoclonal
Type
Antibody
Clone
7C6
Immunogen
Bcr686 thyroglobulin conjugate corresponding to human BCR sequence 686-696 (SSINEEITPRRQS)
Conjugate
Form
Liquid
Concentration
1 mg/mL
Purification
Protein A
Storage buffer
PBS with 1mg/mL BSA
Contains
0.05% sodium azide
Storage conditions
-20°C
Shipping conditions
Ambient (domestic); Wet ice (international)
RRID
AB_2536861
Product Specific Information
Western blot analysis of MA1-153 detects ~130-160 kDa and a 210-250 kDa protein in K562 cells. In addition to BCR-ABL, BCR and ABL are also expressed in these cells and full length BCR is also detected by the antibody. For detection purposes, non-reducing conditions resulted in enhanced detection of BCR-ABL.
Target Information
A reciprocal translocation between chromosomes 22 and 9 produces the BCR-ABL fusion oncoprotein, which is found in patients with chronic myelogenous leukemia (CML). Although there are various versions, p210 is the most commonly found BCR-ABL form. The fusion to BCR, results in deregulated/constitutively active tyrosine kinase activity of BCR-ABL which is sufficient of oncogenic transformation of myeloid cells. Inhibition of BCR-ABL oncogenic activity by the ABL-kinase inhibitor STI-571 (also known as gleevec, imatinib) became the first and best example for successful targeted therapy of cancer, and specifically CML. In recent years, several mutations (such as the T351I mutation) were found in CML patients that resulted in STI-571 resistance and the need for additional drug development.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
Bioinformatics
Protein Aliases: BCR/FGFR1 chimera protein; breakpoint cluster region; breakpoint cluster region homolog; Breakpoint cluster region protein; FGFR1/BCR chimera protein; Renal carcinoma antigen NY-REN-26
Gene Aliases: 5133400C09Rik; AI561783; AI853148; ALL; BCR; BCR1; CML; D22S11; D22S662; Kiaa3017; mKIAA3017; PHL
UniProt ID: (Human) P11274, (Mouse) Q6PAJ1
Entrez Gene ID: (Human) 613, (Mouse) 110279
negative regulation of cellular extravasation
protein phosphorylation
signal transduction
brain development
peptidyl-tyrosine phosphorylation
actin cytoskeleton organization
response to lipopolysaccharide
regulation of Rho protein signal transduction
intracellular signal transduction
inner ear morphogenesis
regulation of vascular permeability
negative regulation of neutrophil degranulation
positive regulation of GTPase activity
protein autophosphorylation
platelet-derived growth factor receptor signaling pathway
negative regulation of inflammatory response
positive regulation of phagocytosis
neuromuscular process controlling balance
regulation of small GTPase mediated signal transduction
regulation of cell cycle
negative regulation of blood vessel remodeling
phosphorylation
negative regulation of cell migration
Performance Guarantee
If an Invitrogen™ antibody doesn't perform as described on our website or datasheet,we'll replace the product at no cost to you, or provide you with a credit for a future purchase.*
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