Aperçu des produits pour anti-NFYA (NFYA) Anticorps

Human Nuclear Transcription Factor Y, alpha (NFYA) interaction partners

1. Curcumin ameliorates PRMT5-MEP50 arginine methyltransferase expression by decreasing the Sp1 and NF-YA transcription factors in the A549 and MCF-7 cells.

2. NFYA is a diffuse subtype- specific independent prognostic factor in gastric cancer.

3. 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.

4. 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.

5. Suggest NF-YAs and lamin A expression levels as novel potential biomarkers useful to identify G1 endometrial carcinoma patients with risk of recurrence.

6. increased expression of NF-YA may promote a malignant phenotype in OS cells via modulation of FASN expression.

7. 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.

8. Data indicate that specific cancer-driving nodes are generally under NF-YA/B control.

9. Presence of NF-Y transcription factor plays a pivotal role in transcriptional regulation of ID genes in development.

10. 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

11. A direct non-transcriptional role of NF-Y in the overall efficiency of DNA replication, specifically in the DNA elongation process.

12. 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.

13. 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.

14. NF-Y inhibits NT2/D1 cell growth in p53-independent manner and decreases SOX2 expression.

15. 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.

16. Association of p21 with NF-YA suppresses the expression of PLK1 and prevents mitotic death in response to DNA damage.

17. NF-YA binds directly over the CCAAT sequence.

18. NF-Y recruits the developmentally regulated, erythroid transcription activator GATA-2 and general repressor BCL11A to modulate transcription of the gamma-globin gene.

19. 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.

20. NFYA could be a target of mutant TBP in SCA17.

Cow (Bovine) Nuclear Transcription Factor Y, alpha (NFYA) interaction partners

1. 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.

Mouse (Murine) Nuclear Transcription Factor Y, alpha (NFYA) interaction partners

1. The results reveal a previously unrecognized physiological function of NFYA in controlling glucose metabolism by up-regulating the gluconeogenic genes Pck1 and G6pc.

2. 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.

3. 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.

4. 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.

5. these results indicate that the transcription factor NF-Y regulates the proximal promoter activity of mouse Col11a1 gene in chondrocytes

6. these results raise an exciting possibility that targeting CDK1 or NF-Y in the diseased heart may inhibit fibrosis and subsequently confer cardioprotection.

7. 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.

8. 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.

9. Sp1, CREB, HNF-1, and NF-Y, known to be responsive to hormones and diet, regulate NAGS transcription

10. 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.

11. Findings establish that NF-Y acts upstream of E2F1 in p53-mediated apoptosis.

12. Transcriptional regulation of myeloid differentiation primary response (MyD) genes during myeloid differentiation is mediated by nuclear factor Y.

13. NF-Y recruits RNAPII and general transcription factors onto various CCAAT box-containing promoters to permit strong transcriptional activation independently of histone modifications

14. NF-Y can stimulate or repress the FGF-4 promoter in an enhancer-dependent manner

15. 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

16. 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.

17. Sequestration of NF-YA component to mutant huntingtin aggregates in model mouse brain results in the reduction of HSP70 gene transcription.

18. These data indicate a role of NF-Y in modulating the structure and transcriptional competence of chromatin.

19. NF-Y is a fundamental switch at the heart of decision between gene activation and repression in CCAAT regulated genes.

20. 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