Mouse Anti-BCR Recombinant Antibody (CBYY-0455) (CBMAB-0458-YY)

Name: Mouse Anti-BCR Recombinant Antibody (CBYY-0455)
SKU: CBMAB-0458-YY
Rating: 5 (1 reviews)

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Published Data

Mouse Anti-BCR Recombinant Antibody (CBYY-0455) (CBMAB-0458-YY) in IP

Left panel shows tyrosine-phosphorylation of p85 PI3K in HL-60.Bcr ± Abl observed in the same blot. ...View More

Amarante-Mendes, G. P., Jascur, T., Nishioka, W. K., Mustelin, T., & Green, D. R. (1997). Bcr-Abl-mediated resistance to apoptosis is independent of PI 3-kinase activity. Cell Death & Differentiation, 4(7), 548-554.

Mouse Anti-BCR Recombinant Antibody (CBYY-0455) (CBMAB-0458-YY) in IP

The indicated cell lysates were subjected to anti-Runx1 or IgG immunoprecipitation and immunoblotted using the
indicated antibodies. ...View More

Liu, H., Cui, Y., Wang, G. F., Dong, Q., Yao, Y., Li, P., ... & Liu, X. (2018). The nonreceptor tyrosine kinase c-Abl phosphorylates Runx1 and regulates Runx1-mediated megakaryocyte maturation. Biochimica et Biophysica Acta (BBA)-Molecular Cell Research, 1865(8), 1060-1072.

Mouse Anti-BCR Recombinant Antibody (CBYY-0455) (CBMAB-0458-YY) in IF

K562 cells were treated with imatinib (2 mM for 48 hrs) in the presence and absence of 3-MA (5 mM). Following treatment, these cells were assessed for expression of Bcr-Abl (red-left panels), LC3 (green-second set of panels from the left), and co-localization of Bcr-Abl and LC3 (third set of panels from the left) using immunofluorescence. To enable the visualization of the co-localization images more clearly, Bcr-Abl and LC3 images are merged without the nuclei (right set of panels). ...View More

Elzinga, B. M., Nyhan, M. J., Crowley, L. C., O'Donovan, T. R., Cahill, M. R., & McKenna, S. L. (2013). Induction of autophagy by Imatinib sequesters Bcr-Abl in autophagosomes and down-regulates Bcr-Abl protein. American journal of hematology, 88(6), 455-462.

Mouse Anti-BCR Recombinant Antibody (CBYY-0455) (CBMAB-0458-YY) in IP

Western blot analyses of proteins extracted from PLAT-gp cells were performed with an anti-BCR antibody (a) or with an anti-IKAROS antibody (b) (see Materials and methods). The expression of α-tubulin served as a loading control. ...View More

Suzuki, K., Ono, R., Ohishi, K., Masuya, M., Kataoka, I., Liu, B., ... & Nosaka, T. (2012). IKAROS isoform 6 enhances BCR-ABL1-mediated proliferation of human CD34+ hematopoietic cells on stromal cells. International journal of oncology, 40(1), 53-62.

Datasheet

SDS

Request for COA

Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Host Animal

Mouse

Clone

CBYY-0455

Application

WB, IP, IF, IHC-P

Immunogen

Synthetic peptide from the amino acid sequence of the Bcr gene product.

Host Species

Mouse

Specificity

Human, Mouse, Rat

Antibody Isotype

IgG1, κ

Clonality

Monoclonal

Application Notes

The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Application	Note
WB	1:100-1:1,000
IP	1-2 µg per 100-500 µg of total protein (1 ml of cell lysate)
IF(ICC)	1:50-1:500
IHC-P	1:50-1:500

Formulations & Storage [For reference only, actual COA shall prevail!]

Format

Liquid

Buffer

PBS, 0.1% gelatin

Preservative

< 0.1% sodium azide

Concentration

0.2 mg/ml

Storage

Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

More Infomation

Target

Full Name

BCR, RhoGEF And GTPase Activating Protein

Introduction

A reciprocal translocation between chromosomes 22 and 9 produces the Philadelphia chromosome, which is often found in patients with chronic myelogenous leukemia. The chromosome 22 breakpoint for this translocation is located within the BCR gene. The translocation produces a fusion protein which is encoded by sequence from both BCR and ABL, the gene at the chromosome 9 breakpoint. Although the BCR-ABL fusion protein has been extensively studied, the function of the normal BCR gene product is not clear. The protein has serine/threonine kinase activity and is a GTPase-activating protein for p21rac. Two transcript variants encoding different isoforMouse have been found for this gene.

Entrez Gene ID

Human	613
Mouse	110279
Rat	309696

UniProt ID

Human	P11274
Mouse	Q6PAJ1
Rat	F1LXF1

Alternative Names

BCR, RhoGEF And GTPase Activating Protein; Renal Carcinoma Antigen NY-REN-26; Breakpoint Cluster Region; EC 2.7.11.1; D22S11; BCR1; Breakpoint Cluster Region Protein;

Function

Protein with a unique structure having two opposing regulatory activities toward small GTP-binding proteins. The C-terminus is a GTPase-activating protein (GAP) domain which stimulates GTP hydrolysis by RAC1, RAC2 and CDC42. Accelerates the intrinsic rate of GTP hydrolysis of RAC1 or CDC42, leading to down-regulation of the active GTP-bound form (PubMed:7479768, PubMed:1903516, PubMed:17116687).
The central Dbl homology (DH) domain functions as guanine nucleotide exchange factor (GEF) that modulates the GTPases CDC42, RHOA and RAC1. Promotes the conversion of CDC42, RHOA and RAC1 from the GDP-bound to the GTP-bound form (PubMed:7479768, PubMed:23940119).
The amino terminus contains an intrinsic kinase activity (PubMed:1657398).
Functions as an important negative regulator of neuronal RAC1 activity (By similarity).
Regulates macrophage functions such as CSF1-directed motility and phagocytosis through the modulation of RAC1 activity (PubMed:17116687).
Plays a major role as a RHOA GEF in keratinocytes being involved in focal adhesion formation and keratinocyte differentiation (PubMed:23940119).

Biological Process

Activation of GTPase activity Source: UniProtKB
Focal adhesion assembly Source: UniProtKB
Keratinocyte differentiation Source: UniProtKB
Modulation of chemical synaptic transmission Source: UniProtKB
Platelet-derived growth factor receptor signaling pathway Source: Ensembl
Protein autophosphorylation Source: Ensembl
Protein phosphorylation Source: ProtInc
Regulation of Rho protein signal transduction Source: UniProtKB
Regulation of small GTPase mediated signal transduction Source: Reactome
Signal transduction Source: ProtInc
Small GTPase mediated signal transduction Source: UniProtKB

Cellular Location

Postsynaptic density; Dendritic spine; Axon; Synapse

Involvement in disease

Leukemia, chronic myeloid (CML): A clonal myeloproliferative disorder of a pluripotent stem cell with a specific cytogenetic abnormality, the Philadelphia chromosome (Ph), involving myeloid, erythroid, megakaryocytic, B-lymphoid, and sometimes T-lymphoid cells, but not marrow fibroblasts.
A chromosomal aberration involving BCR has been found in patients with chronic myeloid leukemia. Translocation t(9;22)(q34;q11) with ABL1. The translocation produces a BCR-ABL found also in acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL).

PTM

Autophosphorylated. Phosphorylated by FES/FPS on tyrosine residues, leading to down-regulation of the BCR kinase activity. Phosphorylation at Tyr-177 by HCK is important for interaction with GRB2.

Chen, J. A., Hou, Y., Roskin, K. M., Arber, D. A., Bangs, C. D., Baughn, L. B., ... & Gotlib, J. (2021). Lymphoid blast transformation in an MPN with BCR-JAK2 treated with ruxolitinib: putative mechanisms of resistance. Blood Advances, 5(17), 3492-3496.

Scott, S., Cartwright, A., Francis, S., Whitby, L., Sanzone, A. P., Mulder, A., ... & Chantry, A. (2021). Assessment of droplet digital polymerase chain reaction for measuring BCR‐ABL1 in chronic myeloid leukaemia in an international interlaboratory study. British journal of haematology.

Mokhtar, A. M. A., & binti Hashim, I. F. (2021). Small Rho GTPases and their associated RhoGEFs mutations promote immunological defects in Primary Immunodeficiencies. The International Journal of Biochemistry & Cell Biology, 106034.

Ciccarelli, B. T., Hu, T., Wang, Q., Kim, J. J., & Whitehead, I. P. (2020). Examination of clinically-derived p210 BCR/ABL1 RhoGEF mutations in a murine bone marrow transplantation model of CML. Leukemia Research, 97, 106440.

Peiris, M. N., Li, F., & Donoghue, D. J. (2019). BCR: a promiscuous fusion partner in hematopoietic disorders. Oncotarget, 10(28), 2738.

Mousinho, F., Azevedo, A. P., Mendes, T., Santos, P. S. E., Cerqueira, R., Matos, S., ... & Lima, F. (2018). Concomitant presence of JAK2V617F mutation and BCR‑ABL translocation in two patients: A new entity or a variant of myeloproliferative neoplasms (Case report). Molecular medicine reports, 18(1), 1001-1006.

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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme-Linked Immunospot (ELISpot)
Proteogenomics
Other Protocols

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For research use only. Not intended for any clinical use.

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