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anti-Mouse (Murine) BCL9 Anticorps:
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Both XBcl9 and XPygo2 are required to induce supernumerary axis and dorsal gene activation in Xenopus embryos.
Transcriptional cofactors Bcl9, Bcl9l and Pygo1/2 act independently of beta-catenin to ensure proper enamel formation.
ARX positively regulates Wnt/ beta-catenin signaling and the C-terminal domain of ARX interacts with the armadillo repeats in beta-catenin to promote Wnt/beta-catenin signaling. In addition, we found BCL9 and P300 also interact with ARX to modulate Wnt/beta-catenin signaling.
Study demonstrates that the Golgi resident protein GM130 activates the spindle assembly factor TPX2 to nucleate microtubules around the Golgi and further captures them to couple mitotic membranes to the spindle.
Pax6, the master regulator of eye development, directly activates Bcl9/9l transcription.
These results suggest a critical role of BCL9/9-2 in the Wnt-mediated regulation of adult, as opposed to embryonic, myogenic progenitors.
miR-30a acts as a tumor suppressor by double-targeting COX-2 and BCL9, and significantly affects the development of H. pylori-induced gastric cancer, shedding new light on the mechanisms underlying H. pylori-associated gastric cancer.
We found that miR-532 was significantly upregulated in patients with intervertebral disc degeneration and plays a pro-apoptotic role in human intervertebral disc nucleus pulposus cells. Further, Bcl-9 was confirmed to be a direct target of miR-532 and might be a potential target for disc degeneration therapy.
Specific regulation of BCL9 expression by HIF-1alpha may prove to be an underlying crosstalk between Wnt/beta-catenin signaling and hypoxia signaling pathways.
Results find that BCL9 is upregulated in osteosarcoma (OS) tissues and promotes OS proliferation, migration and invasion. BCL9 is a downstream target of miR-1301 in OS cells. In addition, BCL9 restoration could reversed the functional effects of miR-1301 overexpression on OS cell proliferation, migration and invasion. These results revealed the important role of BCL9 in OS tumor progression.
High BCL9 expression is associated with cisplatin-resistance in non-small cell lung cancer.
miR-1301 inhibits hepatocellular carcinoma cell migration, invasion, and angiogenesis by decreasing Wnt/beta-catenin signaling through targeting BCL9.
results from this study demonstrated that hypoxia induced BCL-9 expression in human CRC cells mainly through HIF-1alpha, which could be an important underlying mechanism for increased BCL-9 expression in CRC.
SOX7 inhibits oncogenic beta-catenin-mediated transcription by disrupting the beta-catenin/BCL9 interaction.
The authors used CRISPR/Cas9 genome engineering of Drosophila legless (lgs) and human BCL9 and B9L to show that the C-terminus downstream of their adaptor elements is crucial for Wnt responses.
MEF2D-BCL9-positive patients had B-cell precursor immunophenotype and were characterized as being older in age, being resistant to chemotherapy, having very early relapse, and having leukemic blasts that mimic morphologically mature B-cell leukemia with markedly high expression of HDAC9.
it was demonstrated that miR218 modulated a novel molecular target and the present study provided novel insights into potential mechanisms of RCC oncogenesis.
findings indicate that BCL9 most likely does not harbor a common genetic variant that can increase the risk for schizophrenia in the Japanese population
BCL9/9L-beta-catenin Signaling is Associated With Poor Outcome in Colorectal Cancer
BCL9 is a molecular driver of DCIS invasive progression.
PCDH10 antagonized MM cell proliferation via the downregulation of Wnt/beta-catenin/BCL-9 signaling, whereas PCDH10 repressed the expression of AKT to promote the expression of GSK3beta and then to restrain the activation of beta-catenin
By beta-catenin's association with LEF1 and BCL9-2/B9L.
MiR-30-5p downregulation occurs as a result of interaction between multiple myeloma cells and bone marrow stromal cells, which in turn enhances expression of BCL9.
we detected five SNPs in the first two genes/loci - BCL9 and C9orf5 - strongly associated with negative symptoms of schizophrenia
Inhibition of the BCL9-beta-catenin interaction and selectively suppresses oncogenic Wnt transcription.
growth factor induced proliferation mediates a neutralizing response by significantly increasing miR-30c-2* which reduces BCL9 expression and cell proliferation in SKOV-3 and OVCAR-3 cells
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
, B-cell lymphoma 9
, B-cell CLL/lymphoma 9 protein-like
, b-cell CLL/lymphoma 9 protein-like
, B-cell CLL/lymphoma 9 protein
, B-cell lymphoma 9 protein
, nuclear co-factor of beta-catenin signalling
, protein legless homolog