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抗Human NFYA 抗体:
抗Mouse (Murine) NFYA 抗体:
抗Rat (Rattus) NFYA 抗体:
increased expression of NF-YA may promote a malignant phenotype in OS cells via modulation of FASN (显示 FASN 抗体) expression.
The findings indicate that overexpression of NF-YA contributes to tumor angiogenesis through EZH2 (显示 EZH2 抗体)-STAT3 (显示 STAT3 抗体) signaling in human melanoma cells, highlighting NF-YA as a potential therapeutic target in human melanoma.
Data indicate that specific cancer-driving nodes are generally under NF-YA/B control.
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 (显示 EIF3K 抗体) transcription factors
enhanced CDCA8 (显示 CDCA8 抗体) promoter activities by NF-Y overexpression and reduced CDCA8 (显示 CDCA8 抗体) transcription by NF-Y knockdown further verified that NF-Y is a positive regulator of CDCA8 (显示 CDCA8 抗体) transcription.
Data show that Zinc-fingers and homeoboxes 2 (ZHX2 (显示 ZHX2 抗体)) represses nuclear transcription factor Y alpha (NF-Y)-mediated activation of multidrug resistance 1 (MDR1 (显示 TBC1D9 抗体)) transcription.
NF-Y inhibits NT2/D1 cell growth in p53 (显示 TP53 抗体)-independent manner and decreases SOX2 (显示 SOX2 抗体) expression.
Stimulation of the lymphocytes with phytohemagglutinin, restores normal OGG1 (显示 OGG1 抗体) levels and repair rates. MAP kinase (显示 MAPK1 抗体) c-Jun N-terminal kinase (JNK) and the recruitment of the transcription factor NFYA to the promoter region of OGG1 (显示 OGG1 抗体) are shown to be involved.
Association of p21 (显示 CDKN1A 抗体) with NF-YA suppresses the expression of PLK1 (显示 PLK1 抗体) and prevents mitotic death in response to DNA damage.
NF-YA binds directly over the CCAAT sequence.
Interaction of C/EBP-beta (显示 CEBPB 抗体) and NF-Y factors constrains activity levels of the nutritionally controlled promoter IA expressing the acetyl-CoA carboxylase-alpha (显示 ACACA 抗体) gene in cattle.
Data show that nuclear factor Y (NF-Y) binds to the inverted CCAAT element (ICE) in the Fatty acid synthase (Fasn (显示 FASN 抗体)) promoter specifically in refeeding states.
findings may point to a possible role of NF-YA in stress conditions that occur in chronic obesity, ER stress might be involved in the pathogenesis of obesity through NF-YA depletion.
we conclude that NF-Y and YY1 (显示 YY1 抗体) are important for the basal transcription of Pcyt2 (显示 PCYT2 抗体) and that NF-Y is involved in the inhibitory effects of 25-HC on Pcyt2 (显示 PCYT2 抗体) transcription.
these results indicate that the transcription factor NF-Y regulates the proximal promoter activity of mouse Col11a1 (显示 COL11A1 抗体) gene in chondrocytes
these results raise an exciting possibility that targeting CDK1 (显示 CDK1 抗体) or NF-Y in the diseased heart may inhibit fibrosis and subsequently confer cardioprotection.
NF-Ya is a functional activator of Bmal1 (显示 ARNTL 抗体) transcription and it cooperates with Sp1 (显示 SP1 抗体) and Rev-Erbalpha (显示 NR1D1 抗体) to generate the daily cycle of Bmal1 (显示 ARNTL 抗体) expression.
Sp1 (显示 SP1 抗体), CREB (显示 CREB1 抗体), HNF-1 (显示 HNF1A 抗体), and NF-Y, known to be responsive to hormones and diet, regulate NAGS (显示 NAGS 抗体) transcription
results indicate nuclear transcription factor NF-Y as a pivotal upstream participant in a regulatory network necessary for the preservation of cycling hematopoietic stem cell.
Findings establish that NF-Y acts upstream of E2F1 (显示 E2F1 抗体) in p53 (显示 TP53 抗体)-mediated apoptosis.
Transcriptional regulation of myeloid differentiation primary response (MyD) genes during myeloid differentiation is mediated by nuclear factor Y.
The protein encoded by this gene is one subunit of a trimeric complex, forming a highly conserved transcription factor that binds to CCAAT motifs in the promoter regions in a variety of genes. Subunit A associates with a tight dimer composed of the B and C subunits, resulting in a trimer that binds to DNA with high specificity and affinity. The sequence specific interactions of the complex are made by the A subunit, suggesting a role as the regulatory subunit. In addition, there is evidence of post-transcriptional regulation in this gene product, either by protein degradation or control of translation. Further regulation is represented by alternative splicing in the glutamine-rich activation domain, with clear tissue-specific preferences for the two isoforms.
, nuclear transcription factor Y, alpha
, CAAT box DNA-binding protein subunit A
, CAAT-box DNA binding protein subunit A
, CCAAT-binding transcription factor subunit B
, HAP2 CCAAT-binding protein
, Transcription factor NF-Y, A subunit
, nuclear transcription factor Y subunit A
, nuclear transcription factor Y subunit alpha
, CAAT-box DNA-binding protein subunit A
, NF-Y protein chain A
, nuclear transcription factor-Y alpha