In today's world, NFYB has taken a crucial role in society. His influence extends to all areas of life, from politics to popular culture. Day by day, NFYB becomes more relevant and its impact is felt everywhere. In this article, we will explore in detail the role NFYB plays in different aspects of society and how it has evolved over time. From its origins to its current state, NFYB has generated unprecedented interest, awakening debates and reflections in all types of audiences. Therefore, it is essential to closely examine the various angles surrounding NFYB, in order to understand its importance and know how to adapt to its constant changes.
Nuclear transcription factor Y subunit beta is a protein that in humans is encoded by the NFYBgene.[5][6]
Function
The protein encoded by this gene is one subunit of a trimeric complex, forming a highly conserved transcription factor that binds with high specificity to CCAAT motifs in the promoter regions in a variety of genes. This gene product, subunit B, forms a tight dimer with the C subunit, a prerequisite for subunit A association. The resulting trimer binds to DNA with high specificity and affinity. Subunits B and C each contain a histone-like motif. Observation of the histone nature of these subunits is supported by two types of evidence; protein sequence alignments and experiments with mutants.[7]
^"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^"Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^Li XY, Mattei MG, Zaleska-Rutczynska Z, Hooft van Huijsduijnen R, Figueroa F, Nadeau J, Benoist C, Mathis D (Mar 1992). "One subunit of the transcription factor NF-Y maps close to the major histocompatibility complex in murine and human chromosomes". Genomics. 11 (3): 630–4. doi:10.1016/0888-7543(91)90070-U. PMID1774067.
^Maity SN, de Crombrugghe B (Jun 1998). "Role of the CCAAT-binding protein CBF/NF-Y in transcription". Trends Biochem Sci. 23 (5): 174–8. doi:10.1016/S0968-0004(98)01201-8. PMID9612081.
^Izumi H, Molander C, Penn LZ, Ishisaki A, Kohno K, Funa K (Apr 2001). "Mechanism for the transcriptional repression by c-Myc on PDGF beta-receptor". J. Cell Sci. 114 (Pt 8): 1533–44. doi:10.1242/jcs.114.8.1533. PMID11282029.
Lloberas J, Soler C, Celada A (1998). "Repression mechanisms of the I-A beta gene of the major histocompatibility complex". Immunobiology. 198 (1–3): 249–63. doi:10.1016/s0171-2985(97)80045-9. PMID9442396.
Izumi H, Molander C, Penn LZ, Ishisaki A, Kohno K, Funa K (2001). "Mechanism for the transcriptional repression by c-Myc on PDGF beta-receptor". J. Cell Sci. 114 (Pt 8): 1533–44. doi:10.1242/jcs.114.8.1533. PMID11282029.