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anti-Mouse (Murine) BCL9 Antikörper:
anti-Human BCL9 Antikörper:
anti-Rat (Rattus) BCL9 Antikörper:
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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 (zeige BCL9L Antikörper) and Pygo1 (zeige PYGO1 Antikörper)/2 act independently of beta-catenin (zeige CTNNB1 Antikörper) to ensure proper enamel formation.
ARX positively regulates Wnt (zeige WNT2 Antikörper)/ beta-catenin (zeige CTNNB1 Antikörper) signaling and the C-terminal domain of ARX interacts with the armadillo (zeige PKP1 Antikörper) repeats in beta-catenin (zeige CTNNB1 Antikörper) to promote Wnt (zeige WNT2 Antikörper)/beta-catenin (zeige CTNNB1 Antikörper) signaling. In addition, we found BCL9 and P300 (zeige NOTCH1 Antikörper) also interact with ARX to modulate Wnt (zeige WNT2 Antikörper)/beta-catenin (zeige CTNNB1 Antikörper) signaling.
Study demonstrates that the Golgi resident protein GM130 (zeige GOLGA2 Antikörper) activates the spindle assembly factor TPX2 (zeige DAZL Antikörper) to nucleate microtubules around the Golgi and further captures them to couple mitotic membranes to the spindle.
Pax6 (zeige PAX6 Antikörper), the master regulator of eye development, directly activates Bcl9/9l transcription.
These results suggest a critical role of BCL9/9-2 in the Wnt (zeige WNT2 Antikörper)-mediated regulation of adult, as opposed to embryonic, myogenic progenitors.
results from this study demonstrated that hypoxia induced BCL-9 expression in human CRC (zeige CALR Antikörper) cells mainly through HIF-1alpha (zeige HIF1A Antikörper), which could be an important underlying mechanism for increased BCL-9 expression in CRC (zeige CALR Antikörper).
SOX7 (zeige SOX7 Antikörper) inhibits oncogenic beta-catenin (zeige CTNNB1 Antikörper)-mediated transcription by disrupting the beta-catenin (zeige CTNNB1 Antikörper)/BCL9 interaction.
The authors used CRISPR/Cas9 genome engineering of Drosophila legless (lgs) and human BCL9 and B9L (zeige BCL9L Antikörper) to show that the C-terminus downstream of their adaptor elements is crucial for Wnt (zeige WNT2 Antikörper) responses.
MEF2D (zeige MEF2D Antikörper)-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 (zeige HDAC9 Antikörper).
it was demonstrated that miR218 modulated a novel molecular target and the present study provided novel insights into potential mechanisms of RCC (zeige XRCC1 Antikörper) 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 (zeige CTNNB1 Antikörper) Signaling is Associated With Poor Outcome in Colorectal Cancer
BCL9 is a molecular driver of DCIS invasive progression.
PCDH10 (zeige PCDH10 Antikörper) antagonized MM cell proliferation via the downregulation of Wnt (zeige WNT2 Antikörper)/beta-catenin (zeige CTNNB1 Antikörper)/BCL-9 signaling, whereas PCDH10 (zeige PCDH10 Antikörper) repressed the expression of AKT (zeige AKT1 Antikörper) to promote the expression of GSK3beta and then to restrain the activation of beta-catenin (zeige CTNNB1 Antikörper)
By beta-catenin's association with LEF1 (zeige LEF1 Antikörper) and BCL9-2/B9L (zeige BCL9L Antikörper).
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 , bcl-9 , nuclear co-factor of beta-catenin signalling , protein legless homolog