IndraLab

Statements


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"Moreover, siRNA mediated depletion of beta-catenin reduced the association of FOXG1 and LEF-1, indicating that the association of FOXG1 with LEF-1 is mediated by beta-catenin."

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"N-cadherin cytoplasmic domain sequesters β-catenin and reduces its ability to induce lymphocyte enhancer-binding factor 1 (LEF-1)-responsive transactivation in Chinese hamster ovary cells. xref In cultured porcine and juvenile human NP cells, N-cadherin appears to promote cell clustering and NP-like morphology, correlating with β-catenin nuclear translocation. xref It would be interesting to examine if β-catenin inhibits the constitutive LEF-1 responsive transactivation xref in the NP cells."

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"By expressing a truncated form of β-catenin that inhibits Lef1, hair genes were ectopically expressed in epidermal cells that normally do not express them, resulting in epitheliod cysts resembling hai[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"(53) Crucially, it has been shown that constitutive beta-catenin mediated activation of LEF-1 represses the osteoblast transcriptional regulator, Runx2, and subsequent maturation of osteoblasts."

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"In fact, in human CD34 + hematopoietic progenitor cells, inhibition of LEF1 but not of beta-catenin, impaired proliferation and apoptosis mechanisms of this cell population, supporting the hypothesis of a beta-catenin-independent function of LEF1 in early human myelopoiesis [XREF_BIBR]."

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"A constitutively active beta-catenin enhanced LEF1 dependent repression of Runx2."

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"The results showed that Nek2B increased LEF-1 promoter activity, which was reversed by suppression of β-catenin (Fig. 10g)."

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"Beta-catenin relieves I-mfa-mediated suppression of LEF-1 in mammalian cells."

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"CTNNB1 is negatively regulated by APC, transducing wingless signals and interacting with components of the LEF1 and TCF4 transcription complexes, urokinase, and PSEN1."

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"A constitutively active beta-catenin enhanced Lef1 dependent repression of Runx2 [30]."

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"The loss of E-cadherin results in the translocation of beta-catenin to the nucleus, where it activates beta-catenin-TCF and LEF -1 target genes and promotes the proliferation and metastasis of cancer."

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"The disruption through gene mutation of these key beta-catenin degradation components is known to increase the protein levels of beta-catenin which then translocates to the nucleus and activates LEF-1 and TCF transcription factors and gene networks that promote CRC development."