HCA induces epithelial reversion at nanomolar concentrations by s

HCA induces epithelial reversion at nanomolar concentrations by suppressing Snail via the nuclear translocalization of GSK-3 beta, which results in the transcriptional upregulation

NCT-501 cell line of E-cadherin. HCA also activates the transcription factor KLF17, which suppresses Id-1, indicating that HCA inhibits EMT by multiple transcriptional programs. Further, HCA treatment significantly inhibits lung metastasis in a mouse orthotopic breast cancer model. This study demonstrates the anti-metastatic effect of the non-toxic natural compound HCA through attenuation of EMT in a breast cancer model.”
“The alternative sigma factor ComX is a key regulator of natural transformation in members of the genus Streptococcus. ComX controls expression of the late competence genes, which are essential for DNA binding, uptake and recombination. In Streptococcus pneumoniae, it has been demonstrated that ComX is degraded by ClpEP at the end of the competence period. In the present study we show that a different FaraA Clp protease complex, CIpCP, contributes to ComX degradation in Streptococcus thermophilus. Mutant strains lacking the CIpC chaperone displayed significantly increased transformability compared with the wild-type strain under conditions where ComX was expressed at relatively low levels. At higher expression levels,

CIpCP appears to become saturated and unable to prevent the accumulation of ComX. Together, our results suggest that the role of CIpC is to mediate degradation of ComX when the sigma factor is produced in low amounts, i.e. when the environmental stimulus promoting competence development is weak. This would prevent S. thermophilus from developing the competent

state at an inappropriate time and/or place.”
“Juxtanodin (JN) is a cytoskeleton-related oligodendrocyte-specific gene, and its underlying mechanism still needs detailed exploration. In this study, we tested whether a 1.9 kb fragment from the 5′-flanking region of JN is sufficient to specifically deliver the gene expression in oligodendrocytes. By reporter assay, we found that the 1.9 kb fragment specifically activated in C6 cells, which is further upregulated by ATRA-induced oligodendrocyte lineage differentiation. Bioinformatics ASK inhibitor study revealed that Nkx2.2 might be a transcription factor involved in the process. qPCR results showed that ATRA upregulated endogenous expression of Nkx2.2 in C6 cells. Further study revealed that Nkx2.2 could bind JN promoter and its overexpression increase the promoter activity of JN. In summary, our study here suggests that Nkx2.2 is one of the essential transcription factors delivering the specificity of JN promoter in oligodendrocytes.”
“Since its discovery as the first human tumor virus, Epstein-Barr virus (EBV) has been implicated in the development of a wide range of B-cell lymphoproliferative disorders, the first being Burkitt lymphoma.

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