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FLASH GENE

Symbol

XIST

contributors: mct - updated : 07-05-2016

HGNC name	X (inactive)-specific transcript
HGNC id	12810

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

HOMOLOGY

Homologene

FAMILY

CATEGORY

regulatory

SUBCELLULAR LOCALIZATION	intracellular
	intracellular,nucleus
text	non chromatin nuclear structure

basic FUNCTION	associating with inactive X and involved in chromatin packaging
	involved in the overexpression of H2A1M in inactivated X
	implicated in recognizing the number of X chromosomes and initiating a silencing signal on cis
	delayed reprogramming of XIST/reactivation of inactive X chromosome after cell fusion was accelerated by DNA methylation and histone deacetylation of XIST, which follow upregulation of DNMT3A and TSIX
	reprogramming of X-chromosome inactivation during the acquisition of pluripotency is accompanied by the repression of XIST, the trigger of X-inactivation, and the upregulation of its antisense counterpart TSIX (

CELLULAR PROCESS

PHYSIOLOGICAL PROCESS

PATHWAY

metabolism

signaling

a component

possible constituent of non chromatin nuclear structure

INTERACTION

DNA

RNA	binding to XIST RNA with the hot spot of H3lys9

small molecule

protein	YY1 interacts with XIST RNA through Repeat C
	SPEN is required for gene repression by XIST
	CIZ1 has likely an essential role in anchoring XIST to the nuclear matrix in specific somatic lineages
	SPEN acts as a molecular integrator for the initiation of X-chromosome inactivation (XCI), bridging XIST RNA with the transcription machinery-as well as with nucleosome remodellers and histone deacetylases-at active enhancers and promoters

cell & other

REGULATION

inhibited by	trichostatin A, which normally activates gene expression, but results in downregulation of XIST

repressed by	TSIX, its transcription is negatively regulated by its antisense partner TSIX, whose disruption results in nonrandom X-chromosome inactivation in females

Other	replication regulated (replicated before its expressed allele)
	methylation is the initial event in the spread of the inactivation signal
	maintenance of XIST methylation is controlled differently than global genomic methylation and in the absence of both DNMT1 and DNMT3B
	regulated by a balance of multiple XIST activators and repressors, and levels of POU5F1 and TSIX are crucial toward achieving this balance

ASSOCIATED DISORDERS

corresponding disease(s)

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function constitutional germinal mutation       promoter mutated in skewed X inactivation and the choice of X chromosome inactivation reflects stabilization of a higher order chromatin conformation impinging on the CTCF-XIST promoter complex tumoral     --other   aberrantly demethylated in testicular germ cell tumor and in male-derived plasma tumoral     --over   by demethylation in aggressive prostate cancer

Susceptibility

Variant & Polymorphism

Candidate gene

Marker

Therapy target

ANIMAL & CELL MODELS