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NF-YC was significantly increased in gliomas. Knockdown of NF-YC reduced brain tumor size in vivo. NF-YC played as an independent predictor of patient survival.
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p53 negatively regulates the expression of the PRR11-SKA2 bidirectional transcription unit through NF-Y, suggesting that the inability to repress the PRR11-SKA2 bidirectional transcription unit after loss of p53 might contribute to tumorigenesis.
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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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TAF12 and NFYC are transcription factors that regulate the epigenome, whereas RAD54L plays a central role in DNA repair
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the expression of the adipogenic differentiation genes fatty acid binding protein-4, adiponectin, and leptin and the formation of fat droplets were impaired.
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NFY-C expression was elevated in colorectal adenocarcinomas; moreover, NFY-C mRNA levels correlated with time to disease progression, while NFY-C protein expression was significantly higher in metastatic disease
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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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Sp1, NF-Y and FOXO transcription factors are involved in the regulation of LKB1 transcription.
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NF-YC functions as a new corepressor of agonist-bound mineralocorticoid receptor via alteration of aldosterone-induced MR conformation
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role in repressing Smad2 and Smad3 transactivating activity
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The NF-YB/NF-YC structure gives insight into DNA binding and transcription regulation by CCAAT factor NF-Y.
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p300 binds to multiple NF-Y trimers to regulate cyclin B2 promoter function
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Histone deacetylase inhibitors can induce Gadd45 through its promoter without the need for functional p53, and both Oct-1 and NF-Y concertedly participate in trichostatin A-induced activation of the gadd45 promoter.
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C/EBPbeta contributes to the induction of hepatocyte replication in response to HGF in rodents, which is likely due to post-translational modifications.
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Expression levels of NF-Y target genes changed by CDKN1B correlate with clinical prognosis in multiple neoplasms.
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NF-YC complexity is generated by dual promoters and alternative splicing
