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FLASH GENE

Symbol

CCNB1

contributors: mct/npt/pgu - updated : 26-11-2013

HGNC name	cyclin B1
HGNC id	1579

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

EXPRESSION

Type

widely

expressed in	(based on citations)
organ(s)	System Organ level 1 Organ level 2 Organ level 3 Organ level 4 Level Pubmed Species Stage Rna symbol Digestive esophagus       highly   liver       moderately   salivary gland       moderately Reproductive female system uterus cervix   highly   female system placenta     highly Skin/Tegument skin       highly

tissue

System Tissue Tissue level 1 Tissue level 2 Level Pubmed Species Stage Rna symbol Blood / Hematopoietic bone marrow       Connective bone     moderately Muscular striatum skeletal   highly

cell lineage
cell lines
fluid/secretion	predominantly in lymph

at STAGE

cell cycle

cell cycle, checkpoint, G2M

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains	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

HOMOLOGY

interspecies	homolog to rattus Ccnb1 (87 pc)
	homolog to murine Ccnb1 (86.7 pc)

Homologene

FAMILY	cyclin family
	Cyclin AB subfamily

CATEGORY

regulatory

SUBCELLULAR LOCALIZATION	intracellular
	intracellular,cytoplasm,cytoskeleton,microtubule,centrosome
	intracellular,nucleus,nucleoplasm
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

PHYSIOLOGICAL PROCESS

PATHWAY

metabolism

signaling

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

INTERACTION

DNA

RNA

small molecule

protein	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

REGULATION

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

ASSOCIATED DISORDERS

corresponding disease(s)

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein 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

Susceptibility

Variant & Polymorphism

Candidate gene

Marker

Therapy target

ANIMAL & CELL MODELS