The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

Links

 

Gene Review

Nfya  -  nuclear transcription factor-Y alpha

Mus musculus

Synonyms: AA407810, CAAT box DNA-binding protein subunit A, Cbf-b, NF-YA, Nuclear transcription factor Y subunit A, ...
 
 
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.
 

Disease relevance of Nfya

 

High impact information on Nfya

  • These reagents are highly specific for either of the A or B subunits; we have mapped the epitopes recognized by the monoclonal antibodies to the glutamine-rich activation domain of NF-YA [2].
  • A dominant-negative form of NF-YA, ectopically expressed in M1 cells, blocked NF-Y binding to the -65/-52 IL-6RE and reduced induction of JunB by IL-6 [3].
  • This induced binding can be attributed to the observed induction of NF-YA protein expression and may reflect the molecular mechanism that couples proliferation to terminal differentiation of normal myeloblasts [3].
  • To understand the physiological function of the mammalian heterotrimeric CCAAT binding factor CBF, also known as NF-Y, we have generated a conditional Cbf-b mouse mutant by introducing loxP sites in the murine Cbf-b/Nf-ya gene [4].
  • NF-Y is composed of three subunits, NF-YA, NF-YB, and NF-YC, all required for DNA binding [5].
 

Biological context of Nfya

  • Importantly, we demonstrate that expression of a dominant-negative NF-YA mutant protein reduces the expression of FGF-4 promoter/reporter gene constructs in F9 EC cells [6].
  • On the other hand, the N-terminal parts of SMNF-YA and mouse NF-YA were shown to mediate transactivation; the integrity of a large 160 amino acid glutamine-rich domain of NF-YA was required for this function and an adjacent serine- and threonine-rich domain was necessary for full activity in HepG2, but redundant in other cell types [7].
  • This study provides direct evidence of the identification of NF-YA and NF-YB as the previously described factors A and B. Moreover, these results strongly implicate NF-Y in the expression of the MHC class II gene I-A beta [8].
  • These results suggest that the active binding protein is NF-YA in factor A extracts and NF-YB in factor B extracts [8].
  • Interestingly, the kinetics of NF-YA relocalization differs between epithelial cells and fibroblasts [9].
 

Anatomical context of Nfya

 

Associations of Nfya with chemical compounds

  • Mutation of the variant Asp at position 99 of the HFM alpha2-helix into a conserved serine recovers the capacity to interact with NF-YA, but not with DNA [10].
  • Specifically, we show that the binding of the transcription factor NF-YA, which binds to a critical CCAAT box, and the binding of a high mobility group (HMG) protein(s), which binds to a critical HMG motif, are not affected by diamide or N-ethylmaleimide [11].
 

Regulatory relationships of Nfya

  • The CCAAT-binding transcription factor, nuclear factor Y (NF-Y), activated the JunB promoter and a dominant negative NF-YA construct inhibited TAK1 activation of JunB [12].
  • Here, we show that TGF-beta induces nuclear translocation of the NF-YA subunit of the transcription factor NF-Y by a process that requires activation of the ERK cascade [9].
 

Other interactions of Nfya

  • Overexpression of NF-YA increased GnRHR promoter activity, whereas expression of a dominant negative NF-YA mutant decreased activity, further supporting a role of NF-Y in regulation of mGnRHR gene transcription [13].
  • OsNF-YB1 is capable of heterodimerizing with NF-YC, but not trimerizing with NF-YA, thus precluding CCAAT binding [10].
  • Serum stimulation of NIH3T3 cells gradually decreased the amount of endogenous NF-Y binding to the PDGF beta-receptor promoter, whereas NF-YA expression in the nuclear extracts remains unchanged [14].
  • NIH3T3 fibroblasts show an elevated basal level of phosphorylated p38 and delayed nuclear accumulation of NF-YA after TGF-beta treatment [9].
  • Furthermore, expression of a dominant-negative NF-YA mutant protein, which prevents DNA binding by NF-Y, enhances TbetaR-II promoter expression [15].
 

Analytical, diagnostic and therapeutic context of Nfya

  • On luciferase and electrophoretic mobility shift assays, Runx2-I was less active than Runx2-II in the absence of Cbfb, but the two Runx2 isoforms had similar activity levels in the presence of Cbfb [1].
  • Immunoprecipitation of whole cell extracts with anti-ERalpha antibody reveals an in vivo association between the two transcription factors, which is abolished by deletion of the NF-YA carboxyl-terminus [16].

References

  1. Cbf beta regulates Runx2 function isoform-dependently in postnatal bone development. Kanatani, N., Fujita, T., Fukuyama, R., Liu, W., Yoshida, C.A., Moriishi, T., Yamana, K., Miyazaki, T., Toyosawa, S., Komori, T. Dev. Biol. (2006) [Pubmed]
  2. Monoclonal antibodies to NF-Y define its function in MHC class II and albumin gene transcription. Mantovani, R., Pessara, U., Tronche, F., Li, X.Y., Knapp, A.M., Pasquali, J.L., Benoist, C., Mathis, D. EMBO J. (1992) [Pubmed]
  3. Transcriptional regulation of myeloid differentiation primary response (MyD) genes during myeloid differentiation is mediated by nuclear factor Y. Sjin, R.M., Krishnaraju, K., Hoffman, B., Liebermann, D.A. Blood (2002) [Pubmed]
  4. The B subunit of the CCAAT box binding transcription factor complex (CBF/NF-Y) is essential for early mouse development and cell proliferation. Bhattacharya, A., Deng, J.M., Zhang, Z., Behringer, R., de Crombrugghe, B., Maity, S.N. Cancer Res. (2003) [Pubmed]
  5. Requirement for down-regulation of the CCAAT-binding activity of the NF-Y transcription factor during skeletal muscle differentiation. Gurtner, A., Manni, I., Fuschi, P., Mantovani, R., Guadagni, F., Sacchi, A., Piaggio, G. Mol. Biol. Cell (2003) [Pubmed]
  6. NF-Y binds to the CCAAT box motif of the FGF-4 gene and promotes FGF-4 expression in embryonal carcinoma cells. Lamb, K.A., Johnson, L.R., Rizzino, A. Mol. Reprod. Dev. (1997) [Pubmed]
  7. Conservation and divergence of NF-Y transcriptional activation function. Serra, E., Zemzoumi, K., di Silvio, A., Mantovani, R., Lardans, V., Dissous, C. Nucleic Acids Res. (1998) [Pubmed]
  8. Identification of the transcription factors NF-YA and NF-YB as factors A and B that bound to the promoter of the major histocompatibility complex class II gene I-A beta. Celada, A., McKercher, S.R., Maki, R.A. Biochem. J. (1996) [Pubmed]
  9. Cell type-dependent control of NF-Y activity by TGF-beta. Alabert, C., Rogers, L., Kahn, L., Niellez, S., Fafet, P., Cerulis, S., Blanchard, J.M., Hipskind, R.A., Vignais, M.L. Oncogene (2006) [Pubmed]
  10. Ternary complex formation between MADS-box transcription factors and the histone fold protein NF-YB. Masiero, S., Imbriano, C., Ravasio, F., Favaro, R., Pelucchi, N., Gorla, M.S., Mantovani, R., Colombo, L., Kater, M.M. J. Biol. Chem. (2002) [Pubmed]
  11. Effects of oxidation and reduction on the binding of transcription factors to cis-regulatory elements located in the FGF-4 gene. Lickteig, K., Lamb, K., Brigman, K., Rizzino, A. Mol. Reprod. Dev. (1996) [Pubmed]
  12. TAK1 activation of the mouse JunB promoter is mediated through a CCAAT box and NF-Y. Eggen, B.J., Benus, G.F., Folkertsma, S., Jonk, L.J., Kruijer, W. FEBS Lett. (2001) [Pubmed]
  13. Oct-1 and nuclear factor Y bind to the SURG-1 element to direct basal and gonadotropin-releasing hormone (GnRH)-stimulated mouse GnRH receptor gene transcription. Kam, K.Y., Jeong, K.H., Norwitz, E.R., Jorgensen, E.M., Kaiser, U.B. Mol. Endocrinol. (2005) [Pubmed]
  14. p73 independent of c-Myc represses transcription of platelet-derived growth factor beta-receptor through interaction with NF-Y. Hackzell, A., Uramoto, H., Izumi, H., Kohno, K., Funa, K. J. Biol. Chem. (2002) [Pubmed]
  15. Transcriptional activation of the type II transforming growth factor-beta receptor gene upon differentiation of embryonal carcinoma cells. Kelly, D., Kim, S.J., Rizzino, A. J. Biol. Chem. (1998) [Pubmed]
  16. Inhibition of ERalpha-mediated trans-activation of human coagulation factor XII gene by heteromeric transcription factor NF-Y. Farsetti, A., Narducci, M., Moretti, F., Nanni, S., Mantovani, R., Sacchi, A., Pontecorvi, A. Endocrinology (2001) [Pubmed]
 
WikiGenes - Universities