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Frequent molecular monitoring and intervention are required for patients who do not show a reduction in BCR-ABL1 (show ABL1 ELISA Kits) 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 ELISA Kits) associated with BCR
the e13a2 BCR-ABL1 (show ABL1 ELISA Kits) 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 ELISA Kits) cells and can be regulated by BCR/ABL (show ABL1 ELISA Kits) signal transduction through downstream phosphoinositide 3-kinase/Akt (show AKT1 ELISA Kits) and Janus kinase/signal transducer and activator of transcription (show STAT1 ELISA Kits) pathways, suggesting cell division cycle protein 6 as a potential therapeutic target in chronic myeloid leukemia (show BCL11A ELISA Kits).
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 ELISA Kits), and the 3D structures of SH2 domains of CrkL (show CRKL ELISA Kits) and Bcr-Abl (show ABL1 ELISA Kits), were performed.
The present study screened for the presence of bcr-abl (show ABL1 ELISA Kits) 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 (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
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