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Human Polyclonal BCL9L Primary Antibody for WB - ABIN1881110
Miller, Rutherford, Johnson, Fiedler, Bienz: Allosteric remodelling of the histone H3 binding pocket in the Pygo2 PHD finger triggered by its binding to the B9L/BCL9 co-factor. in Journal of molecular biology 2010
Show all 5 Pubmed References
we identify BCL9L as a novel regulator of TGF-beta-induced EMT in pancreatic cancer.
BCL9L dysfunction contributes to aneuploidy tolerance in both TP53-WT and mutant cells by reducing basal caspase-2 levels and preventing cleavage of MDM2 and BID.
The inhibition of the transcriptional activity of BCL9-2 by WWOX and HDAC3 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-catenin/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 target genes but also regulates genes that are required for early stages of tumor progression.
Pygo2 PHD is the only known PHD finger that is capable of interacting simultaneously with two functional ligands, B9L and BCL9.
crystallographic analysis of how beta-catenin, BCL9, BCL9-2 and Tcf4 interact
Transcriptional cofactors Bcl9, Bcl9l and Pygo1/2 act independently of beta-catenin to ensure proper enamel formation.
Data show that the GCM1/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 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