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Cloning and functional analysis of the bim gene.
long non-coding RNA Morrbid regulates Bim and short-lived myeloid cell lifespan
BIM deletion polymorphism does not account for intrinsic resistance to EGFR (show EGFR ELISA Kits)-TKI in Patients With Lung Adenocarcinoma
Mechanistically, G-Rg1 (show PPP1R3A ELISA Kits) promoted the phosphorylation of Akt (show AKT1 ELISA Kits) and FoxO3a (show FOXO3 ELISA Kits) and led to the cytoplasmic translocation of FoxO3a (show FOXO3 ELISA Kits), which in turn suppressed FoxO3a (show FOXO3 ELISA Kits)-modulated expression of proapoptotic Bim and elevated the ratio of Bcl-2 (show BCL2 ELISA Kits) to Bax (show BAX ELISA Kits).
Dnd1 (show DND1 ELISA Kits) facilitates apoptosis by increasing the expression of Bim via its competitive combining with miR (show MLXIP ELISA Kits)-221 in Bim-3'UTR (show UTS2R ELISA Kits).
patients with BIM-g had significantly shorter progression-free survival than those without BIM-gamma (median: 304 vs. 732 days; p=0.023). CONCLUSION: Expression of BIM-gamma mRNA and BIM deletion polymorphism were strongly associated. BIM-gamma overexpression may have a role in apoptosis related to EGFR (show EGFR ELISA Kits)-tyrosine kinase (show TXK ELISA Kits) inhibitor
MicroRNA-301b directly targets the expression of Bim, a well-known pro-apoptotic protein.
FOXO4 (show FOXO4 ELISA Kits) has an inhibitory effect in clearcell renal carcinoma (show TSC2 ELISA Kits) cells, at least in part through inducing apoptosis via upregulation of Bim in the mitochondria-dependent pathway.
Results indicate that upregulation of miR (show MLXIP ELISA Kits)-124 could regulate apoptosis and impaired autophagy process in the MPTP (show PTPN2 ELISA Kits) model of Parkinson's disease, thus reducing the loss of dopaminergic neurons
the Bim activated by doxorubicin-induced DNA damage might directly interrupt the interaction of Bcl-xl (show BCL2L1 ELISA Kits) with pro-apoptotic proteins, Bak (show BAK1 ELISA Kits)/Bax (show BAX ELISA Kits), to activate mitochondriadriven apoptosis.
the BIM deletion polymorphism enhanced the emergence of populations with complete imatinib resistance, mimicking the situation in patients.
Rapid activation of AMPK (show PRKAA1 ELISA Kits) was detected after exposure of cortical neuronal cultures to zinc, which was induced by LKB1 (show STK11 ELISA Kits) activation but not increased intracellular AMP (show TMPRSS5 ELISA Kits) levels or CaMKKbeta activation.
Fluorizoline bind to prohibitin (show PHB ELISA Kits), inducing mitochondrial apoptotic pathway through NOXA (show PMAIP1 ELISA Kits) and BIM upregulation.
Consistent with a contribution of BCL2 (show BCL2 ELISA Kits) family proteins to the second wave of cell death during involution, loss of Bim reduced the number of apoptotic cells in this irreversible phase
The current study demonstrated that the BH3-only (show BBC3 ELISA Kits) protein, Bim, might regulate a subset of inflammatory cells in the gastric mucosa during H. pylori-mediated gastritis.
Bcl2 interacting mediator of cell death (Bim) and Bcl2 modifying factor (Bmf (show BMF ELISA Kits)), mediate apoptosis in the context of TACI (show TNFRSF13B ELISA Kits)-Ig overexpression that effectively neutralizes BAFF (show TNFSF13B ELISA Kits) as well as APRIL.
these results indicate that 1alpha,25(OH)2D3 and TX 527 trigger apoptosis by Bim protein increase which turns into the activation of caspase-3 (show CASP3 ELISA Kits) in SVEC and vGPCR cells
miR (show MLXIP ELISA Kits)-155 regulates the delicate balance between PAK1 (show PAK1 ELISA Kits)-mediated proliferation and apoptosis in T cells impacting lymphoid organ size and function.
The findings reveal an essential role for TRIM33 (show TRIM33 ELISA Kits) in preventing apoptosis in B lymphoblastic leukemia by interfering with enhancer-mediated Bim activation.
Pseudorabies virus glycoprotein gE-mediated ERK 1 (show MAPK3 ELISA Kits)/2 phosphorylation also occurs in epithelial cells and in these cells, gE-mediated ERK 1 (show MAPK3 ELISA Kits)/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 ELISA Kits).
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