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Cloning and functional analysis of the bim gene.
sequestration of Bim by Mcl-1 (show MCL1 Proteins) is a mechanism of intrinsic ABT-199 resistance and supports the clinical development of ABT-199 in combination with cytarabine or daunorubicin for the treatment of AML (show RUNX1 Proteins).
Knock down of VDR (show CYP27B1 Proteins) and BIM reduces the enhancement of cell death treated with Cytarabine (AraC) followed by the addition of Doxercalciferol together with Carnosic acid (CA).
UMI-77 enhances TRAIL-induced apoptosis by unsequestering Bim and Bak (show BAK1 Proteins), which provides a novel therapeutic strategy for the treatment of gliomas.
Conversion of Bim-BH3 from Activator to Inhibitor of Bak (show BAK1 Proteins) through Structure-Based Design.
in FOXO3 (show FOXO3 Proteins)-death-resistant cells no point mutations in the TP53 (show TP53 Proteins)-DBD were found-in these cells FOXO3 (show FOXO3 Proteins)-TP53 (show TP53 Proteins) complexes are formed and FOXO3 (show FOXO3 Proteins)-binding to the BIM-promoter, but not the induction of the detoxifying protein SESN3 (show SESN3 Proteins), were prevented, which in turn increased chemo-protection in this type of high-stage-derived neuroblastoma (show ARHGEF16 Proteins) cells
At BCL2L11, the authors identify a haematopoietic enhancer hub that is inactivated by the Epstein-Barr virus repressors EBNA3A and EBNA3C through recruitment of the H3K27 methyltransferase EZH2 (show EZH2 Proteins).
observations suggest that an association of a deletion polymorphism of BIM and the response to induction therapy in B-cell precursor acute lymphoblastic leukemia may be clinically minimal
expression of Bim is mediated by FoxO1 (show FOXO1 Proteins) and indirectly downregulated by thyroid hormone/thyroid hormone (show PTH Proteins) receptor (show THRA Proteins), leading to chemotherapy resistance and doxorubicin-promoted metastasis of hepatoma cells.
BIM is associated with favorable prognostic markers for prediction of disease-free survival and overall survival in cervical cancer.
this study shows that BIM deletion polymorphisms are associated with a poor clinical response to erlotinib and represents an independent prognostic factor for patients with EGFR (show EGFR Proteins) positive non-small-cell lung cancer
Bcl2l11 as the direct target of miR (show MLXIP Proteins)-9 and manipulation of miR (show MLXIP Proteins)-9 induces the corresponding changing of Bcl2l11 protein level.
these data suggest that the Bim may be a novel therapeutic target in the treatment of systemic lupus erythematosus.
Data show that the induction of BIM in the MYC (show MYC Proteins)- and RAS-driven leukemia is mediated by the downregulation of miR-17-92, and suggest that induction of BIM-mediated apoptosis may be a therapeutic approach for acute lymphoblastic leukemia (ALL).
Myt3 suppression sensitizes islet cells to high glucose-induced cell death via Bim induction.
understanding the cell autonomous role Bim plays in the retinal vascular homeostasis will give us new insight into how to modulate pathological retinal neovascularization and vessel regression to preserve vision
The central role of Bim-dependent apoptosis in Buruli Ulcer pathogenesis
we found a temporal and tissue-specific role for Bim in limiting thymic agonist selection of CD8alphaalpha precursors and their TCRbeta repertoire, but not in the maintenance of CD8alphaalpha intraepithelial lymphocytes in the intestine.
loss of the BH3-only (show BBC3 Proteins) protein BIM accelerated lymphoma development in p53 (show TP53 Proteins)-deficient mice. This process was negated by concomitant loss of RAG1 (show RAG1 Proteins)/2-mediated antigen receptor gene rearrangement.
Overexpression of miR (show MLXIP Proteins)-29 or miR (show MLXIP Proteins)-24 is sufficient to inhibit the induction of Bim and Puma (show BBC3 Proteins) in young sympathetic neurons.
Pseudorabies virus glycoprotein gE-mediated ERK 1 (show MAPK3 Proteins)/2 phosphorylation also occurs in epithelial cells and in these cells, gE-mediated ERK 1 (show MAPK3 Proteins)/2 signaling is associated with degradation of the pro-apoptotic protein Bim.
BIMEL expression is regulated in porcine cumulus cells by oocyte secreted factor GDF9 (show GDF9 Proteins).
It was concluded that apoptotic cumulus cells, in which BIM(EL) up-regulation was involved, accelerated oocyte aging and degeneration in vitro via a paracrine action.
The protein encoded by this gene belongs to the BCL-2 protein family. BCL-2 family members form hetero- or homodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. The protein encoded by this gene contains a Bcl-2 homology domain 3 (BH3). It has been shown to interact with other members of the BCL-2 protein family, including BCL2, BCL2L1/BCL-X(L), and MCL1, and to act as an apoptotic activator. The expression of this gene can be induced by nerve growth factor (NGF), as well as by the forkhead transcription factor FKHR-L1, which suggests a role of this gene in neuronal and lymphocyte apoptosis. Transgenic studies of the mouse counterpart suggested that this gene functions as an essential initiator of apoptosis in thymocyte-negative selection. Several alternatively spliced transcript variants of this gene have been identified.
, Bcl-2 interacting mediator of cell death
, bcl-2 interacting mediator of cell death
, bcl-2 interacting protein Bim
, bcl-2-like protein 11
, bcl-2-related ovarian death agonist
, Bcl2 interacting mediator of cell death
, bcl2-interacting mediator of cell death
, Bcl-2 related apoptotic gene product BimL
, bcl-2-related ovarian death protein