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anti-Human BCR Antibodies:
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Human Polyclonal BCR Primary Antibody for IF, WB - ABIN197420
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
Show all 4 references for ABIN197420
Human Polyclonal BCR Primary Antibody for IHC (p), WB - ABIN196938
Million, Harakawa, Roumiantsev, Varticovski, Van Etten: A direct binding site for Grb2 contributes to transformation and leukemogenesis by the Tel-Abl (ETV6-Abl) tyrosine kinase. in Molecular and cellular biology 2004
Show all 4 references for ABIN196938
Human Polyclonal BCR Primary Antibody for IF, WB - ABIN362836
Li, Couvillon, Brasher, Van Etten: Tyrosine phosphorylation of Grb2 by Bcr/Abl and epidermal growth factor receptor: a novel regulatory mechanism for tyrosine kinase signaling. in The EMBO journal 2001
Show all 3 references for ABIN362836
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 Antibodies)-positive acute myeloid leukemia (show BCL11A Antibodies) (BCR-ABL (show ABL1 Antibodies)+ AML (show RUNX1 Antibodies)) seems to depend on the cytogenetic and/or molecular background rather than on BCR-ABL (show ABL1 Antibodies) itself.
demonstrated that depletion of endogenous MAPK15 (show MAPK15 Antibodies) expression inhibited BCR-ABL1 (show ABL1 Antibodies)-dependent cell proliferation
Identify a novel BCR-ABL (show ABL1 Antibodies)/IkappaBalpha (show NFKBIA Antibodies)/p53 (show TP53 Antibodies) network, whereby BCR-ABL (show ABL1 Antibodies) functionally inactivates a key tumor suppressor in chronic myeloid leukemia (show BCL11A Antibodies).
Blockade of the interaction between Bcr-Abl (show ABL1 Antibodies) and PTB1B by small molecule SBF-1 (show SBF1 Antibodies) to overcomes imatinib-resistance of K562 cells.
BCR-ABL1 transcript types found in Syria were similar to that of Indian Far-Eastern, African or European populations. The M-BCR rearrangement types were not dependent on white blood count, platelet count, hemoglobin level or gender of the patients.
Data suggest elevated interleukin-1beta secretion from tyrosine kinase (show TXK Antibodies) inhibitor- (TKI-)resistant chronic myeloid leukemia (show BCL11A Antibodies) (CML) cells contributes to TKI/imatinib resistance via promotion of cell viability/migration; cells used lack BCR-ABL (show ABL1 Antibodies) mutation.
Higher incidence of BCR-ABL and lower incidence of TEL-AML1 are associated with acute lymphoblastic leukemia.
Suggest that AIC-47 in combination with imatinib strengthened the attack on cancer energy metabolism in BCR-ABL (show ABL1 Antibodies)-harboring leukemic cells.
Molecular rearrangements and the minimal residual disease follow-up for 5 chronic myeloid leukaemia patients; 3 resulted from new rearrangements between the BCR and ABL1 (show ABL1 Antibodies) sequences (the breakpoints being located within BCR exon 13 in 2 cases and within BCR exon 18 in one case). The other 2 cases revealed a complex e8-[ins (show INS Antibodies)]-a2 fusion transcript involving a 3rd partner gene.
BCR signaling elicits maximal cell death through upregulation of multiple BH3-only (show BBC3 Antibodies) proteins; namely Bim (show BCL2L11 Antibodies), Bik (show BIK Antibodies), and Noxa (show PMAIP1 Antibodies).
The resistance in BCR-ABL1 (show ABL1 Antibodies) cells resulted either from the Y253H mutation in the BCR-ABL1 (show ABL1 Antibodies) gene or incubation in increasing concentrations of imatinib.
PDZK1 (show PDZK1 Antibodies) has novel SR-BI (show SCARB1 Antibodies)-independent function in VSM that affords protection from neointima formation, and this involves PDZK1 (show PDZK1 Antibodies) suppression of VSM cell proliferation via an inhibitory interaction with Bcr
Hap1 (show HAP1 Antibodies) interacts with Bcr on microtubules to regulate neuronal differentiation.
Grb10 (show GRB10 Antibodies) is involved in BCR-ABL (show ABL1 Antibodies)-positive leukemia in mice.
Bcr is an integral member of the Par (show AFG3L2 Antibodies)-Tiam1 (show TIAM1 Antibodies) complex that controls polarized cell migration by locally restricting both Rac1 and PKCzeta (show PRKCZ Antibodies) 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 Antibodies) and overcome imatinib resistance in patients with chronic myeloid leukemia (show BCL11A Antibodies).
IRF8 (show IRF8 Antibodies)-rescued BCR-ABL (show ABL1 Antibodies)-expressing dendritic cells were capable of inducing CTLs more efficiently than control dendritic cells.
study provided evidence for a novel, BCR-ABL (show ABL1 Antibodies)-mediated antiapoptotic mechanism, which results from the increased acetylation of p53 (show TP53 Antibodies) at the K317/K320 residue, thus preventing the nuclear export of p53 (show TP53 Antibodies) 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