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Data indicate the Sp1 (show PSG1 Proteins) oncogene (show RAB1A Proteins) functions as a positive regulator for BCR/ABL (show ABL1 Proteins) expression.
dehydrocostus lactone significantly inhibits the phosphorylation expression of Bcr/Abl (show ABL1 Proteins), STAT5 (show STAT5A Proteins), JAK2 (show JAK2 Proteins), and STAT3 (show STAT3 Proteins) and downstream molecules including p-CrkL (show CRKL Proteins), Mcl-1 (show MCL1 Proteins), Bcl-XL (show BCL2L1 Proteins), and Bcl-2 (show BCL2 Proteins) proteins in K562 cells.
H19 (show NCKAP1 Proteins) overexpression, a frequent event in chronic myeloid leukemia (show BCL11A Proteins), was associated with higher BCR-ABL (show ABL1 Proteins) transcript and disease progression. H19 (show NCKAP1 Proteins) DMR (show WDR20 Proteins)/ICR hypomethylation in CML may be one of the mechanisms mediating H19 (show NCKAP1 Proteins) overexpression.
Frequent molecular monitoring and intervention are required for patients who do not show a reduction in BCR-ABL1 (show ABL1 Proteins) transcripts to these levels after stem cell transplantation.
this study shows that BCR regulates inflammation development via the alpha subunit of casein kinase II (show CSNK2A1 Proteins) associated with BCR
the e13a2 BCR-ABL1 (show ABL1 Proteins) 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 (show BCL11A Proteins) cells and can be regulated by BCR/ABL (show ABL1 Proteins) signal transduction through downstream phosphoinositide 3-kinase/Akt (show AKT1 Proteins) and Janus kinase/signal transducer and activator of transcription (show STAT1 Proteins) pathways, suggesting cell division cycle protein 6 as a potential therapeutic target in chronic myeloid leukemia (show BCL11A Proteins).
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.
In silico three-dimensional modeling of apoptin, molecular docking experiments between apoptin model and the known structure of Bcr-Abl (show ABL1 Proteins), and the 3D structures of SH2 domains of CrkL (show CRKL Proteins) and Bcr-Abl (show ABL1 Proteins), were performed.
The present study screened for the presence of bcr-abl (show ABL1 Proteins) transcripts in the blood of a group of healthy individuals.
BCR signaling elicits maximal cell death through upregulation of multiple BH3-only (show BBC3 Proteins) proteins; namely Bim (show BCL2L11 Proteins), Bik (show BIK Proteins), and Noxa (show PMAIP1 Proteins).
The resistance in BCR-ABL1 (show ABL1 Proteins) cells resulted either from the Y253H mutation in the BCR-ABL1 (show ABL1 Proteins) gene or incubation in increasing concentrations of imatinib.
PDZK1 (show PDZK1 Proteins) has novel SR-BI (show SCARB1 Proteins)-independent function in VSM that affords protection from neointima formation, and this involves PDZK1 (show PDZK1 Proteins) suppression of VSM cell proliferation via an inhibitory interaction with Bcr
Hap1 (show HAP1 Proteins) interacts with Bcr on microtubules to regulate neuronal differentiation.
Grb10 (show GRB10 Proteins) is involved in BCR-ABL (show ABL1 Proteins)-positive leukemia in mice.
Bcr is an integral member of the Par (show AFG3L2 Proteins)-Tiam1 (show TIAM1 Proteins) complex that controls polarized cell migration by locally restricting both Rac1 and PKCzeta (show PRKCZ Proteins) 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 Proteins) and overcome imatinib resistance in patients with chronic myeloid leukemia (show BCL11A Proteins).
IRF8 (show IRF8 Proteins)-rescued BCR-ABL (show ABL1 Proteins)-expressing dendritic cells were capable of inducing CTLs more efficiently than control dendritic cells.
study provided evidence for a novel, BCR-ABL (show ABL1 Proteins)-mediated antiapoptotic mechanism, which results from the increased acetylation of p53 (show TP53 Proteins) at the K317/K320 residue, thus preventing the nuclear export of p53 (show TP53 Proteins) 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