Selected-GenAtlas references SOURCE GeneCards NCBI Gene Swiss-Prot Ensembl
HGNC UniGene Nucleotide OMIM UCSC
Home Page
FLASH GENE
Symbol NFYB contributors: mct - updated : 18-03-2015
HGNC name nuclear transcription factor Y, beta
HGNC id 7805
RNA
TRANSCRIPTS type messenger
EXPRESSION
Type widely
constitutive of
   expressed in (based on citations)
organ(s)
cell lineage
cell lines
fluid/secretion
at STAGE
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
a N terminal A domain,a highly conserved central B domain involved in DNA binding,a C terminal C domain rich in glutamine and acidic residues involved in protein-protein interactions
HOMOLOGY
intraspecies homolog to H2B
Homologene
FAMILY cbf-a subfamily
CATEGORY transcription factor
SUBCELLULAR LOCALIZATION     intracellular
intracellular,nucleus
basic FUNCTION
  • essential for expression of the proapoptotic BCL2L11 gene in sympathetic neurons
    • CELLULAR PROCESS nucleotide, transcription
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component forming a trimeric complex with NFYB and NFYC
    INTERACTION
    DNA binding to the CCAAT and the inverted CCAT-box,Y-box (ATGG) motifs in a variety of promoters
    RNA
    small molecule
    protein
  • interacting with SARS2 (NFYA, NFYB, NFYC influences directionality of transcription from the bidirectional MRPS12/SARS2 promoter)
  • NFYA, NFYB, NFYC, cooperates with FOXO3 to recruit EP300 to the BCL2L11 promoter to form a stable multi-protein/DNA complex that activates BCL2L11 transcription after survival factor withdrawal
  • NFYA, NFYB, NFYC can act as a transcriptional activator of ABCB4
  • NFYA, NFYB, NFYC and YY1 are important for the basal transcription of PCYT2 and NFY is involved in the inhibitory effects of 25-HC on PCYT2 transcription
    • cell & other
    REGULATION
    activated by ATF6
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional       loss of function
    impaired cells from exiting G2/M, but did not interfere with S-phase progression (
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    ANIMAL & CELL MODELS