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Results from a study on gene expression variability markers in early-stage human embryos shows that NFYA is a putative expression variability marker for the 3-day, 8-cell embryo stage.
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Our results identified for the first time one of the mechanisms responsible for NF-Y expression, which may be involved in the aberrant expression and activity observed in tumor cells and other pathological conditions.
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Suggest NF-YAs and lamin A expression levels as novel potential biomarkers useful to identify G1 endometrial carcinoma patients with risk of recurrence.
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increased expression of NF-YA may promote a malignant phenotype in OS cells via modulation of FASN expression.
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The findings indicate that overexpression of NF-YA contributes to tumor angiogenesis through EZH2-STAT3 signaling in human melanoma cells, highlighting NF-YA as a potential therapeutic target in human melanoma.
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Data indicate that specific cancer-driving nodes are generally under NF-YA/B control.
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Presence of NF-Y transcription factor plays a pivotal role in transcriptional regulation of ID genes in development.
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our results indicate that NF-YA alternative splicing is an influential muscle cell determinant, through direct regulation of selected cell cycle blocking genes, and, directly and indirectly, of muscle-specific transcription factors
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A direct non-transcriptional role of NF-Y in the overall efficiency of DNA replication, specifically in the DNA elongation process.
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enhanced CDCA8 promoter activities by NF-Y overexpression and reduced CDCA8 transcription by NF-Y knockdown further verified that NF-Y is a positive regulator of CDCA8 transcription.
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Data show that Zinc-fingers and homeoboxes 2 (ZHX2) represses nuclear transcription factor Y alpha (NF-Y)-mediated activation of multidrug resistance 1 (MDR1) transcription.
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NF-Y inhibits NT2/D1 cell growth in p53-independent manner and decreases SOX2 expression.
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Stimulation of the lymphocytes with phytohemagglutinin, restores normal OGG1 levels and repair rates. MAP kinase c-Jun N-terminal kinase (JNK) and the recruitment of the transcription factor NFYA to the promoter region of OGG1 are shown to be involved.
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Association of p21 with NF-YA suppresses the expression of PLK1 and prevents mitotic death in response to DNA damage.
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NF-YA binds directly over the CCAAT sequence.
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NF-Y recruits the developmentally regulated, erythroid transcription activator GATA-2 and general repressor BCL11A to modulate transcription of the gamma-globin gene.
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The crystal structure of NF-Y bound to a 25 bp CCAAT oligonucleotide shows that the histone-fold domains dimer binds to the DNA sugar-phosphate backbone, mimicking the nucleosome H2A/H2B-DNA assembly; NF-YA both binds to NF-YB/NF-YC and inserts an alpha helix deeply into the DNA minor groove, providing sequence-specific contacts to the CCAAT box.
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NFYA could be a target of mutant TBP in SCA17.
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This study unveils a new role for NF-Y in the regulation of human proteasome genes.
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Sp1, CREB, HNF-1, and NF-Y, known to be responsive to hormones and diet, regulate NAGS transcription
