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Data indicate that the biosensor showed excellent analytical performance for the detection of the BCR/ABL oncogene in clinical samples of patients with leukemia.
Studies indicate that the prognosis of BCR-ABL (show ABL1 ELISA Kits)-positive acute myeloid leukemia (show BCL11A ELISA Kits) (BCR-ABL (show ABL1 ELISA Kits)+ AML (show RUNX1 ELISA Kits)) seems to depend on the cytogenetic and/or molecular background rather than on BCR-ABL (show ABL1 ELISA Kits) itself.
demonstrated that depletion of endogenous MAPK15 (show MAPK15 ELISA Kits) expression inhibited BCR-ABL1 (show ABL1 ELISA Kits)-dependent cell proliferation
Identify a novel BCR-ABL (show ABL1 ELISA Kits)/IkappaBalpha (show NFKBIA ELISA Kits)/p53 (show TP53 ELISA Kits) network, whereby BCR-ABL (show ABL1 ELISA Kits) functionally inactivates a key tumor suppressor in chronic myeloid leukemia (show BCL11A ELISA Kits).
Blockade of the interaction between Bcr-Abl and PTB1B by small molecule SBF-1 to overcomes imatinib-resistance of K562 cells.
BCR-ABL1 transcript types found in Syria were similar to that of Indian Far-Eastern, African or European populations. The M-BCR rearrangement types were not dependent on white blood count, platelet count, hemoglobin level or gender of the patients.
Data suggest elevated interleukin-1beta secretion from tyrosine kinase (show TXK ELISA Kits) inhibitor- (TKI-)resistant chronic myeloid leukemia (show BCL11A ELISA Kits) (CML) cells contributes to TKI/imatinib resistance via promotion of cell viability/migration; cells used lack BCR-ABL (show ABL1 ELISA Kits) mutation.
Higher incidence of BCR-ABL and lower incidence of TEL-AML1 are associated with acute lymphoblastic leukemia.
Suggest that AIC-47 in combination with imatinib strengthened the attack on cancer energy metabolism in BCR-ABL (show ABL1 ELISA Kits)-harboring leukemic cells.
Molecular rearrangements and the minimal residual disease follow-up for 5 chronic myeloid leukaemia patients; 3 resulted from new rearrangements between the BCR and ABL1 (show ABL1 ELISA Kits) sequences (the breakpoints being located within BCR exon 13 in 2 cases and within BCR exon 18 in one case). The other 2 cases revealed a complex e8-[ins (show INS ELISA Kits)]-a2 fusion transcript involving a 3rd partner gene.
BCR signaling elicits maximal cell death through upregulation of multiple BH3-only (show BBC3 ELISA Kits) proteins; namely Bim (show BCL2L11 ELISA Kits), Bik (show BIK ELISA Kits), and Noxa (show PMAIP1 ELISA Kits).
The resistance in BCR-ABL1 (show ABL1 ELISA Kits) cells resulted either from the Y253H mutation in the BCR-ABL1 (show ABL1 ELISA Kits) gene or incubation in increasing concentrations of imatinib.
PDZK1 (show PDZK1 ELISA Kits) has novel SR-BI (show SCARB1 ELISA Kits)-independent function in VSM that affords protection from neointima formation, and this involves PDZK1 (show PDZK1 ELISA Kits) suppression of VSM cell proliferation via an inhibitory interaction with Bcr
Hap1 (show HAP1 ELISA Kits) interacts with Bcr on microtubules to regulate neuronal differentiation.
Grb10 (show GRB10 ELISA Kits) is involved in BCR-ABL (show ABL1 ELISA Kits)-positive leukemia in mice.
Bcr is an integral member of the Par (show AFG3L2 ELISA Kits)-Tiam1 complex that controls polarized cell migration by locally restricting both Rac1 and PKCzeta (show PRKCZ ELISA Kits) function.
Loss of Bcr expression causes defects in spine development.
Suggest that HS-438 may be a novel drug candidate with the therapeutic potential to target BCR-ABL (show ABL1 ELISA Kits) and overcome imatinib resistance in patients with chronic myeloid leukemia (show BCL11A ELISA Kits).
IRF8 (show IRF8 ELISA Kits)-rescued BCR-ABL (show ABL1 ELISA Kits)-expressing dendritic cells were capable of inducing CTLs more efficiently than control dendritic cells.
study provided evidence for a novel, BCR-ABL (show ABL1 ELISA Kits)-mediated antiapoptotic mechanism, which results from the increased acetylation of p53 (show TP53 ELISA Kits) at the K317/K320 residue, thus preventing the nuclear export of p53 (show TP53 ELISA Kits) in response to DNA damage.
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 isoforms have been found for this gene.
breakpoint cluster region
, breakpoint cluster region protein-like
, BCR/FGFR1 chimera protein
, FGFR1/BCR chimera protein
, breakpoint cluster region protein
, renal carcinoma antigen NY-REN-26
, breakpoint cluster region homolog