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BCL9L dysfunction contributes to aneuploidy tolerance in both TP53 (zeige TP53 ELISA Kits)-WT and mutant cells by reducing basal caspase-2 (zeige CASP2 ELISA Kits) levels and preventing cleavage of MDM2 (zeige MDM2 ELISA Kits) and BID (zeige BID ELISA Kits).
The inhibition of the transcriptional activity of BCL9-2 by WWOX (zeige WWOX ELISA Kits) and HDAC3 (zeige HDAC3 ELISA Kits) constitutes a new molecular mechanism and provides new insight for a broad range of cancers.
BCL9-2 induces ER positive breast cancers in vivo, regulates ER expression by a novel ss-catenin independent mechanism in breast cancer cells.
Data show that beta-cat (zeige GCM1 ELISA Kits)enin/BCL9-Like (BCL9L)/T-cell factor 4 (TCF4) signalling directly targets the GCM1/syncytin pathway and thereby regulates the fusion of human choriocarcinoma cells.
BCL9-2 promotes early phases of intestinal tumor progression in humans and in transgenic mice. BCL9-2 increases the expression of a subset of canonical Wnt (zeige WNT2 ELISA Kits) target genes but also regulates genes that are required for early stages of tumor progression.
Pygo2 PHD (zeige PDC ELISA Kits) is the only known PHD (zeige PDC ELISA Kits) finger that is capable of interacting simultaneously with two functional ligands, B9L and BCL9 (zeige BCL9 ELISA Kits).
crystallographic analysis of how beta-catenin (zeige CTNNB1 ELISA Kits), BCL9 (zeige BCL9 ELISA Kits), BCL9-2 and Tcf4 (zeige TCF4 ELISA Kits) interact
Transcriptional cofactors Bcl9 (zeige BCL9 ELISA Kits), Bcl9l and Pygo1/2 act independently of beta-catenin (zeige CTNNB1 ELISA Kits) to ensure proper enamel formation.
Data show that the GCM1 (zeige GCM1 ELISA Kits)/syncytin-B pathway is significantly downregulated in the placenta of BCL9L-deficient mice and that the fusion and differentiation of ST-II cells are blocked.
We demonstrated that nuclear B9L expression was closely associated with the high nuclear grade cancer phenotype and the expression of ErbB2/HER-2 (zeige ERBB2 ELISA Kits) in breast cancers.
BCL9 is associated with B-cell acute lymphoblastic leukemia. It may be a target of translocation in B-cell malignancies with abnormalities of 1q21. Its function is unknown. The overexpression of BCL9 may be of pathogenic significance in B-cell malignancies.
B-cell CLL/lymphoma 9-like protein
, B-cell lymphoma 9-like protein
, BCL9-like protein
, nuclear co-factor of beta-catenin signalling
, protein BCL9-2
, BCL9-related beta-catenin-binding protein
, B-cell CLL/lymphoma 9-like
, b-cell CLL/lymphoma 9-like protein-like