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anti-Human NFYA Anticorps:
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Human Polyclonal NFYA Primary Antibody pour ICC, IF - ABIN4339382
Jin, Yang, Li, Yang, Ma, Zhang: p53-targeted lincRNA-p21 acts as a tumor suppressor by inhibiting JAK2/STAT3 signaling pathways in head and neck squamous cell carcinoma. dans Molecular cancer 2019
The internalized NF-YA is capable of trimerization with the HFD subunits and binding to the target CCAAT box. Functionality is further suggested by protein transfection in C2C12 cells, leading to inhibition of differentiation to myotubes. In conclusion, NF-YA contains CPPs, hinting at novel -and unexpected- properties of this subunit.
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.
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.
Through genome-wide studies in mouse embryonic stem cells study finds that NF-Y is essential for the maintenance of the nucleosome-depleted region at gene promoters. Depletion of the NF-YA protein leads to the accumulation of ectopic nucleosomes over the transcription start site, reducing promoter accessibility.
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.
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