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Frequent molecular monitoring and intervention are required for patients who do not show a reduction in BCR-ABL1 (显示 ABL1 ELISA试剂盒) transcripts to these levels after stem cell transplantation.
this study shows that BCR regulates inflammation development via the alpha subunit of casein kinase II (显示 CSNK2A1 ELISA试剂盒) associated with BCR
the e13a2 BCR-ABL1 (显示 ABL1 ELISA试剂盒) 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 (显示 BCL11A ELISA试剂盒) cells and can be regulated by BCR/ABL (显示 ABL1 ELISA试剂盒) signal transduction through downstream phosphoinositide 3-kinase/Akt (显示 AKT1 ELISA试剂盒) and Janus kinase/signal transducer and activator of transcription (显示 STAT1 ELISA试剂盒) pathways, suggesting cell division cycle protein 6 as a potential therapeutic target in chronic myeloid leukemia (显示 BCL11A ELISA试剂盒).
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 (显示 ABL1 ELISA试剂盒), and the 3D structures of SH2 domains of CrkL (显示 CRKL ELISA试剂盒) and Bcr-Abl (显示 ABL1 ELISA试剂盒), were performed.
The present study screened for the presence of bcr-abl (显示 ABL1 ELISA试剂盒) transcripts in the blood of a group of healthy individuals.
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 (显示 ABL1 ELISA试剂盒)-positive acute myeloid leukemia (显示 BCL11A ELISA试剂盒) (BCR-ABL (显示 ABL1 ELISA试剂盒)+ AML (显示 RUNX1 ELISA试剂盒)) seems to depend on the cytogenetic and/or molecular background rather than on BCR-ABL (显示 ABL1 ELISA试剂盒) itself.
demonstrated that depletion of endogenous MAPK15 (显示 MAPK15 ELISA试剂盒) expression inhibited BCR-ABL1 (显示 ABL1 ELISA试剂盒)-dependent cell proliferation
BCR signaling elicits maximal cell death through upregulation of multiple BH3-only (显示 BBC3 ELISA试剂盒) proteins; namely Bim (显示 BCL2L11 ELISA试剂盒), Bik (显示 BIK ELISA试剂盒), and Noxa (显示 PMAIP1 ELISA试剂盒).
The resistance in BCR-ABL1 (显示 ABL1 ELISA试剂盒) cells resulted either from the Y253H mutation in the BCR-ABL1 (显示 ABL1 ELISA试剂盒) gene or incubation in increasing concentrations of imatinib.
PDZK1 (显示 PDZK1 ELISA试剂盒) has novel SR-BI (显示 SCARB1 ELISA试剂盒)-independent function in VSM that affords protection from neointima formation, and this involves PDZK1 (显示 PDZK1 ELISA试剂盒) suppression of VSM cell proliferation via an inhibitory interaction with Bcr
Hap1 (显示 HAP1 ELISA试剂盒) interacts with Bcr on microtubules to regulate neuronal differentiation.
Grb10 (显示 GRB10 ELISA试剂盒) is involved in BCR-ABL (显示 ABL1 ELISA试剂盒)-positive leukemia in mice.
Bcr is an integral member of the Par (显示 AFG3L2 ELISA试剂盒)-Tiam1 complex that controls polarized cell migration by locally restricting both Rac1 and PKCzeta (显示 PRKCZ ELISA试剂盒) 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 (显示 ABL1 ELISA试剂盒) and overcome imatinib resistance in patients with chronic myeloid leukemia (显示 BCL11A ELISA试剂盒).
IRF8 (显示 IRF8 ELISA试剂盒)-rescued BCR-ABL (显示 ABL1 ELISA试剂盒)-expressing dendritic cells were capable of inducing CTLs more efficiently than control dendritic cells.
study provided evidence for a novel, BCR-ABL (显示 ABL1 ELISA试剂盒)-mediated antiapoptotic mechanism, which results from the increased acetylation of p53 (显示 TP53 ELISA试剂盒) at the K317/K320 residue, thus preventing the nuclear export of p53 (显示 TP53 ELISA试剂盒) 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