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Human Monoclonal BCR Primary Antibody for IA, IF - ABIN2192147
Bruynzeel, Abou El Hassan, Schalkwijk, Berkhof, Bast, Niessen, van der Vijgh: Anti-inflammatory agents and monoHER protect against DOX-induced cardiotoxicity and accumulation of CML in mice. in British journal of cancer 2007
Show all 5 Pubmed References
Human BCR Primary Antibody for IHC - ABIN965655
Sattler, Verma, Byrne, Shrikhande, Winkler, Algate, Rohrschneider, Griffin: BCR/ABL directly inhibits expression of SHIP, an SH2-containing polyinositol-5-phosphatase involved in the regulation of hematopoiesis. in Molecular and cellular biology 1999
Data indicate the Sp1 (显示 PSG1 抗体) oncogene (显示 RAB1A 抗体) functions as a positive regulator for BCR/ABL (显示 ABL1 抗体) expression.
dehydrocostus lactone significantly inhibits the phosphorylation expression of Bcr/Abl (显示 ABL1 抗体), STAT5 (显示 STAT5A 抗体), JAK2 (显示 JAK2 抗体), and STAT3 (显示 STAT3 抗体) and downstream molecules including p-CrkL (显示 CRKL 抗体), Mcl-1 (显示 MCL1 抗体), Bcl-XL (显示 BCL2L1 抗体), and Bcl-2 (显示 BCL2 抗体) proteins in K562 cells.
H19 (显示 NCKAP1 抗体) overexpression, a frequent event in chronic myeloid leukemia (显示 BCL11A 抗体), was associated with higher BCR-ABL (显示 ABL1 抗体) transcript and disease progression. H19 (显示 NCKAP1 抗体) DMR (显示 WDR20 抗体)/ICR hypomethylation in CML may be one of the mechanisms mediating H19 (显示 NCKAP1 抗体) overexpression.
Frequent molecular monitoring and intervention are required for patients who do not show a reduction in BCR-ABL1 (显示 ABL1 抗体) 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 抗体) associated with BCR
the e13a2 BCR-ABL1 (显示 ABL1 抗体) 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 抗体) cells and can be regulated by BCR/ABL (显示 ABL1 抗体) signal transduction through downstream phosphoinositide 3-kinase/Akt (显示 AKT1 抗体) and Janus kinase/signal transducer and activator of transcription (显示 STAT1 抗体) pathways, suggesting cell division cycle protein 6 as a potential therapeutic target in chronic myeloid leukemia (显示 BCL11A 抗体).
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 抗体), and the 3D structures of SH2 domains of CrkL (显示 CRKL 抗体) and Bcr-Abl (显示 ABL1 抗体), were performed.
The present study screened for the presence of bcr-abl (显示 ABL1 抗体) transcripts in the blood of a group of healthy individuals.
BCR signaling elicits maximal cell death through upregulation of multiple BH3-only (显示 BBC3 抗体) proteins; namely Bim (显示 BCL2L11 抗体), Bik (显示 BIK 抗体), and Noxa (显示 PMAIP1 抗体).
The resistance in BCR-ABL1 (显示 ABL1 抗体) cells resulted either from the Y253H mutation in the BCR-ABL1 (显示 ABL1 抗体) gene or incubation in increasing concentrations of imatinib.
PDZK1 (显示 PDZK1 抗体) has novel SR-BI (显示 SCARB1 抗体)-independent function in VSM that affords protection from neointima formation, and this involves PDZK1 (显示 PDZK1 抗体) suppression of VSM cell proliferation via an inhibitory interaction with Bcr
Hap1 (显示 HAP1 抗体) interacts with Bcr on microtubules to regulate neuronal differentiation.
Grb10 (显示 GRB10 抗体) is involved in BCR-ABL (显示 ABL1 抗体)-positive leukemia in mice.
Bcr is an integral member of the Par (显示 AFG3L2 抗体)-Tiam1 (显示 TIAM1 抗体) complex that controls polarized cell migration by locally restricting both Rac1 and PKCzeta (显示 PRKCZ 抗体) 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 抗体) and overcome imatinib resistance in patients with chronic myeloid leukemia (显示 BCL11A 抗体).
IRF8 (显示 IRF8 抗体)-rescued BCR-ABL (显示 ABL1 抗体)-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 抗体)-mediated antiapoptotic mechanism, which results from the increased acetylation of p53 (显示 TP53 抗体) at the K317/K320 residue, thus preventing the nuclear export of p53 (显示 TP53 抗体) 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