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Symbol CCNB1 contributors: mct/npt/pgu - updated : 26-11-2013
HGNC name cyclin B1
HGNC id 1579
  • a cytoplasmic retention signal (CRS1)
  • a leucine-rich nuclear export signal (NES)
  • a N terminal cyclin domain
  • a C terminal cyclin domain
  • conjugated PhosphoP , Other
    interspecies homolog to rattus Ccnb1 (87 pc)
    homolog to murine Ccnb1 (86.7 pc)
  • cyclin family
  • Cyclin AB subfamily
  • CATEGORY regulatory
    SUBCELLULAR LOCALIZATION     intracellular
    text accumulating in the cytoplasm through S and G2 phases and translocating to the nucleus during prophase after phosphorylation by Polo-like kinase
    basic FUNCTION
  • regulating G2/M transition (checkpoint) of the cell cycle
  • nucleocytoplasmic shuttling protein
  • involved in positive regulation of ubiquitin-protein ligase activity during mitotic cell cycle
  • involved in proliferation, and aggressiveness of prolactin pituitary tumors
  • critical factor in proliferation and differentiation of endometrial cells, and progesterone may inhibit cell proliferation, mediate G2/M cell cycle arrest and induce apoptosis in endometrial cells via down-regulating CCNB1
  • CCNB1 and CCNB2 are particularly critical for the maintenance of the mitotic state
  • critical regulator of mitotic entry via its interaction with cyclin-dependent kinase 1
  • CELLULAR PROCESS cell cycle, division, mitosis
    cell cycle, checkpoint
    a component
  • complexing with CDC2 (M phase promoting factor (MPF) component), antagonized by PPP2CA
  • CDK1/CCNB1 activity shields cells against extrinsic death stimuli and unravel the molecular details of the crosstalk between cell cycle and extrinsic apoptotic pathways
    small molecule
  • interacting with the CDC2 protein kinase to form a serine/threonine kinase holoenzyme complex also known as maturation promoting factor (MPF)
  • binding to CCNB1IP1
  • CDK5 activation in cells that overexpress CCNG1 leads to MYC phosphorylation on Ser-62, which is responsible for CCNG1-mediated transcriptional activation of CCNB1
  • interacting with catalytically active RALBP1 and CDC2 during mitosis to form an endocytotic complex during interphase
  • overexpression of AURKA may stabilize CCNB1 through inhibiting its degradation
  • different levels of CCNB1-CDK1 kinase activity trigger different mitotic events, thus revealing how the remarkable reorganization of the cell is coordinated at mitotic entry
  • CCNA2 helps initiate mitosis, in part through its effects on CCNB1, and CCNB1 and CCNB2 are particularly critical for the maintenance of the mitotic state
  • CPEB1 is bound and represses cyclin B1 mRNA translation until a signal to proliferate phosphorylates CPEB1, resulting in an increase in cyclin B1 protein and progression into mitosis
  • TSC2 binds and regulates the G 2/M cyclin, cyclin B1
  • CDK1/CCNB1-dependent hyper-phosphorylation of BCL2L11 during prolonged mitotic arrest is an important cell death signal
  • SPARC induced G2/M cell cycle arrest was mediated through inhibition of the CCNB1-regulated signaling pathway involving CDKN1A and CDC2 expression
  • STOX1 promotes mitotic entry by binding to the CCNB1 promotor
  • CARM1 represses replicative senescence by methylating ELAVL1 and thereby enhancing ELAVL1 ability to regulate the turnover of CCNA1, CCNB1, FOS, SIRT1, and CDKN2A mRNAs (
  • cell & other
    repressed by AR (negative regulation of CCNB1 by AR is mediated through switching between E2F1 and E2F4 on the promoter of CCNB1
    Other phosphorylated by PLK and independently but perhaps synergically by MAPK (ERK2) at different sites in the CRS and translocated to the nucleus
    ubiquitinated by the SCF(NIPA) complex during interphase, leading to its destruction
    its expression is regulated by cytoplasmic polyadenylation element binding protein in astrocytes
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral     --over  
    overexpression of cyclins B could contribute to the chromosomal instability observed in cancer
    tumoral     --other  
    aberrantly expressed in non-small cell lung cancer and some precursor lesions
    Variant & Polymorphism
    Candidate gene
    Therapy target