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抗Human NFYA 抗体:
抗Mouse (Murine) NFYA 抗体:
抗Rat (Rattus) NFYA 抗体:
Curcumin ameliorates PRMT5-MEP50 arginine methyltransferase expression by decreasing the Sp1 and NF-YA transcription factors in the A549 and MCF-7 cells.
NFYA is a diffuse subtype- specific independent prognostic factor in gastric cancer.
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.
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.
Suggest NF-YAs and lamin A expression levels as novel potential biomarkers useful to identify G1 endometrial carcinoma patients with risk of recurrence.
increased expression of NF-YA may promote a malignant phenotype in OS cells via modulation of FASN expression.
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.
Data indicate that specific cancer-driving nodes are generally under NF-YA/B control.
Presence of NF-Y transcription factor plays a pivotal role in transcriptional regulation of ID genes in development.
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
A direct non-transcriptional role of NF-Y in the overall efficiency of DNA replication, specifically in the DNA elongation process.
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.
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.
NF-Y inhibits NT2/D1 cell growth in p53-independent manner and decreases SOX2 expression.
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.
Association of p21 with NF-YA suppresses the expression of PLK1 and prevents mitotic death in response to DNA damage.
NF-YA binds directly over the CCAAT sequence.
NF-Y recruits the developmentally regulated, erythroid transcription activator GATA-2 and general repressor BCL11A to modulate transcription of the gamma-globin gene.
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.
NFYA could be a target of mutant TBP in SCA17.
Interaction of C/EBP-beta and NF-Y factors constrains activity levels of the nutritionally controlled promoter IA expressing the acetyl-CoA carboxylase-alpha gene in cattle.
The results reveal a previously unrecognized physiological function of NFYA in controlling glucose metabolism by up-regulating the gluconeogenic genes Pck1 and G6pc.
Data show that nuclear factor Y (NF-Y) binds to the inverted CCAAT element (ICE) in the Fatty acid synthase (Fasn) 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 are important for the basal transcription of Pcyt2 and that NF-Y is involved in the inhibitory effects of 25-HC on Pcyt2 transcription.
these results indicate that the transcription factor NF-Y regulates the proximal promoter activity of mouse Col11a1 gene in chondrocytes
these results raise an exciting possibility that targeting CDK1 or NF-Y in the diseased heart may inhibit fibrosis and subsequently confer cardioprotection.
NF-Ya is a functional activator of Bmal1 transcription and it cooperates with Sp1 and Rev-Erbalpha to generate the daily cycle of Bmal1 expression.
NF-Y belongs to the restricted circle of transcription factors that govern mouse embryonic stem cells, and that NF-YAs is the active isoform in these cells.
Sp1, CREB, HNF-1, and NF-Y, known to be responsive to hormones and diet, regulate NAGS 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 in p53-mediated apoptosis.
Transcriptional regulation of myeloid differentiation primary response (MyD) genes during myeloid differentiation is mediated by nuclear factor Y.
NF-Y recruits RNAPII and general transcription factors onto various CCAAT box-containing promoters to permit strong transcriptional activation independently of histone modifications
NF-Y can stimulate or repress the FGF-4 promoter in an enhancer-dependent manner
NF-Y activation by TGF-beta1 involves ERK1/2 and potentially an interplay between MAPK pathways, thereby opening the possibility for finely tuned transcriptional regulation
NF-Y binds to the promoter and/or within the coding region. NF-Y is embedded in positive & negative methyl histone marks, serving a dual function in transcriptional regulation, as an activator or as a repressor.
Sequestration of NF-YA component to mutant huntingtin aggregates in model mouse brain results in the reduction of HSP70 gene transcription.
These data indicate a role of NF-Y in modulating the structure and transcriptional competence of chromatin.
NF-Y is a fundamental switch at the heart of decision between gene activation and repression in CCAAT regulated genes.
results demonstrate that interaction of NF-Y at the CCAAT box is pivotal to FGFR2 gene transcription partly through the construction of a local open chromatin configuration across the promoter
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