MEG3 (maternally expressed 3) is a maternally expressed,
imprintedlong non-coding RNAgene.[3] At least 12 different isoforms of MEG3 are generated by
alternative splicing.[4] Expression of MEG3 is lost in cancer cells.[4][5] It acts as a growth suppressor in
tumour cells, and activates
p53.[5][6] A
pituitary transcript variant has been associated with inhibited
cell proliferation. Studies in
mouse and
sheep suggest that an upstream
intergenic differentially
methylated region (
IG-DMR) regulates imprinting of the region. The expression profile in mouse of the co-regulated Meg3 and
Dlk1 genes suggests a causative role in the pathologies found in
uniparental disomy animals, characterized by defects in
skeletal muscle maturation,
bone formation,
placenta size and organization and
prenatal lethality. The sheep
homolog is associated with the
callipyge mutation which in
heterozygous individuals affects a muscle-specific long-range control element located in the DLK1-GTL2 intergenic region and results in the callipyge muscular
hypertrophy. The non-
Mendelian inheritance pattern, known as
polar overdominance, likely results from the combination of the
cis-effect on the expression levels of genes in the DLK1-GTL2 imprinted domain, and
trans interaction between the products of reciprocally imprinted genes.[7] MEG3 is thought to play a role in the development of Alzheimer's disease by triggering
necroptosis.[8][9]
Zhao J, Zhang X, Zhou Y, Ansell PJ, Klibanski A (2006). "Cyclic AMP stimulates MEG3 gene expression in cells through a cAMP-response element (CRE) in the MEG3 proximal promoter region". The International Journal of Biochemistry & Cell Biology. 38 (10): 1808–20.
doi:
10.1016/j.biocel.2006.05.004.
PMID16793321.
MEG3 (maternally expressed 3) is a maternally expressed,
imprintedlong non-coding RNAgene.[3] At least 12 different isoforms of MEG3 are generated by
alternative splicing.[4] Expression of MEG3 is lost in cancer cells.[4][5] It acts as a growth suppressor in
tumour cells, and activates
p53.[5][6] A
pituitary transcript variant has been associated with inhibited
cell proliferation. Studies in
mouse and
sheep suggest that an upstream
intergenic differentially
methylated region (
IG-DMR) regulates imprinting of the region. The expression profile in mouse of the co-regulated Meg3 and
Dlk1 genes suggests a causative role in the pathologies found in
uniparental disomy animals, characterized by defects in
skeletal muscle maturation,
bone formation,
placenta size and organization and
prenatal lethality. The sheep
homolog is associated with the
callipyge mutation which in
heterozygous individuals affects a muscle-specific long-range control element located in the DLK1-GTL2 intergenic region and results in the callipyge muscular
hypertrophy. The non-
Mendelian inheritance pattern, known as
polar overdominance, likely results from the combination of the
cis-effect on the expression levels of genes in the DLK1-GTL2 imprinted domain, and
trans interaction between the products of reciprocally imprinted genes.[7] MEG3 is thought to play a role in the development of Alzheimer's disease by triggering
necroptosis.[8][9]
Zhao J, Zhang X, Zhou Y, Ansell PJ, Klibanski A (2006). "Cyclic AMP stimulates MEG3 gene expression in cells through a cAMP-response element (CRE) in the MEG3 proximal promoter region". The International Journal of Biochemistry & Cell Biology. 38 (10): 1808–20.
doi:
10.1016/j.biocel.2006.05.004.
PMID16793321.