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We report the clinical evolution of a Philadelphia-positive ALL patient co-expressing the e1a2 and e14a2 BCR-ABL transcript at diagnosis
LY294002 treatment had no effect on decreased expression of Bach2 induced by BCR-ABL.
The combination of BCR-ABL1 transcript type and spleen size at diagnosis is significantly predictive for achieving an overall MMR and FFS. Incorporating these predictors could be important when making clinical decisions regarding changing therapy for CML patients treated initially with IM.
expression of WASP inversely correlates with BCR-ABL1 levels and the progression of the disease in Chronic myeloid leukemia patients. BCR-ABL1 downregulates WASP in part by epigenetic modification of its proximal promoter.
The imaging method achieved ultrasensitive detection of BCR/ABL fusion gene with a low detection limit down to 23 fM. And this method exhibited wide linear ranges over seven orders of magnitude and excellent discrimination ability toward target
This is the first report evaluating the role of SOD2 in native and T351-mutated BCR-ABL-expressing cells and in a large cohort of chronic myeloid leukemia patients. In leukemic cells silenced for SOD2 expression a specific down-regulation of the expression of PRDX2 gene was found.
The compound missense mutations in BCR-ABL kinase domain responsible to elicit disease progression, drug resistance or disease relapse in chronic myeloid leukemia.
JNJ-26854165, an inhibitor of MDM2, inhibits proliferation and triggers cell death in a p53-independent manner in various BCR/ABL-expressing cells, which include primary leukemic cells from patients with CML blast crisis and cells expressing the Imatinib-resistant T315I BCR/ABL mutant.
Double inhibition of the N- and C-terminal termini can disrupt Hsp90 chaperone function synergistically, but not antagonistically, in Bcr-Abl-positive human leukemia cells.
this study identifies different BCR/Abl protein suppression patterns as a converging trait of chronic myeloid leukemia cell adaptation to energy restriction
BGB324 does not inhibit BCR-ABL1 and consequently inhibits chronic myeloid leukemia (CML)independent of BCR-ABL1 mutational status. Our data show that Axl inhibition has therapeutic potential in BCR-ABL TKI-sensitive as well as -resistant CML and support the need for clinical trials
BCR-ABL1-positive microvesicles from chronic myeloid leukemias malignantly transform human bone marrow mesenchymal stem cells.
Data indicate the Sp1 oncogene functions as a positive regulator for BCR/ABL expression.
dehydrocostus lactone significantly inhibits the phosphorylation expression of Bcr/Abl, STAT5, JAK2, and STAT3 and downstream molecules including p-CrkL, Mcl-1, Bcl-XL, and Bcl-2 proteins in K562 cells.
H19 overexpression, a frequent event in chronic myeloid leukemia, was associated with higher BCR-ABL transcript and disease progression. H19 DMR/ICR hypomethylation in CML may be one of the mechanisms mediating H19 overexpression.
Frequent molecular monitoring and intervention are required for patients who do not show a reduction in BCR-ABL1 transcripts to these levels after stem cell transplantation.
this study shows that BCR regulates inflammation development via the alpha subunit of casein kinase II associated with BCR
the e13a2 BCR-ABL1 fusion transcript affects the rate, the depth, and the speed of the response to treatment with imatinib firstline, and that including the transcript type in the calculation of the baseline risk scores may improve prognostic stratification and may help the choice of the best treatment policy.
6 overexpression may contribute to the high proliferation and low apoptosis in chronic myeloid leukemia cells and can be regulated by BCR/ABL signal transduction through downstream phosphoinositide 3-kinase/Akt and Janus kinase/signal transducer and activator of transcription pathways, suggesting cell division cycle protein 6 as a potential therapeutic target in chronic myeloid leukemia.
though our data support the previous findings that co-expression of BCR-ABL transcripts is due to the occurrence of exonic and intronic polymorphisms in the BCR gene, it also shows that the intronic polymorphism can arise without the linked exonic polymorphism. The occurrence of ABL kinase domain mutation is less frequent in Indian population.
BCR signaling elicits maximal cell death through upregulation of multiple BH3-only proteins; namely Bim, Bik, and Noxa.
The resistance in BCR-ABL1 cells resulted either from the Y253H mutation in the BCR-ABL1 gene or incubation in increasing concentrations of imatinib.
PDZK1 has novel SR-BI-independent function in VSM that affords protection from neointima formation, and this involves PDZK1 suppression of VSM cell proliferation via an inhibitory interaction with Bcr
Hap1 interacts with Bcr on microtubules to regulate neuronal differentiation.
Grb10 is involved in BCR-ABL-positive leukemia in mice.
Bcr is an integral member of the Par-Tiam1 complex that controls polarized cell migration by locally restricting both Rac1 and PKCzeta 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 and overcome imatinib resistance in patients with chronic myeloid leukemia.
IRF8-rescued BCR-ABL-expressing dendritic cells were capable of inducing CTLs more efficiently than control dendritic cells.
study provided evidence for a novel, BCR-ABL-mediated antiapoptotic mechanism, which results from the increased acetylation of p53 at the K317/K320 residue, thus preventing the nuclear export of p53 in response to DNA damage.
Intrafemoral transplantation of BCR-ABL-transduced Cbl-b(-/-) cells revealed equivalent latency of disease development to the wild-type transplants
Data show that T315I-mutated BCR-ABL is functional at the stem cell level, conferring to murine embryonic stem cell (mESC)-derived leukemic cells a long-term hematopoietic repopulation ability.
Bcr and Abr play a critical role in down-regulating hypoxia-induced pulmonary hypertension by deactivating Rac1.
BCR is a novel substrate of PTPRT .
BCR signalling as a mechanism to cause biased cellular and Ig repertoire selection, ultimately contributing to B cell-mediated autoimmune predisposition.
Essential role for telomerase in chronic myeloid leukemia induced by BCR-ABL in mice.
BCR-JAK2 codes for a protein containing the BCR oligomerization domain fused to the JAK2 tyrosine-kinase domain
STAT5a/b is essential for the induction of CML-like leukemia by BCR-ABL1 and of polycythemia by JAK2(V617F).
The data confirm that BCR-ABL promotes ROS and demonstrate that NF-kappaB prevents excessive levels.
CDK1-mediated phosphorylation of Abi1 attenuates Bcr-Abl-induced F-actin assembly and tyrosine phosphorylation of WAVE complex during mitosis
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