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The Necdin expression was further associated with suppression of both cell proliferation and death in osteoblasts.
Data reveal that necdin promotes mitochondrial biogenesis through stabilization of endogenous PGC-1alpha (show PPARGC1A ELISA Kits) to exert neuroprotection against mitochondrial insults.
Our data suggest that necdin suppresses PIAS1 both by inhibiting SUMO E3 ligase activity and by promoting ubiquitin-dependent degradation.
Necdin is a candidate downstream effector for Galphao (show GNAO1 ELISA Kits).
Myc (show MYC ELISA Kits) overexpression in the cpk kidney results from the dysregulation of the cystin-necdin regulatory complex and c-Myc (show MYC ELISA Kits), in turn, contributes to cystogenesis in the cpk mouse.
Antagonistic interplay between necdin and Bmi1 (show BMI1 ELISA Kits) controls proliferation of neural precursor cells in the embryonic mouse neocortex.
using several mouse models, we reveal a competition between non-imprinted Ndn promoters which results in monoallelic (paternal or maternal) Ndn expression, suggesting that Ndn allelic exclusion occurs in the absence of imprinting regulation.
oxygen tension regulates the necdin protein level in NSCs through HIF-2alpha (show EPAS1 ELISA Kits)-mediated proteasomal
necdin exerts its pro-survival activity by counteracting the action of the pro-apoptotic protein Cell Cycle Apoptosis Regulatory Protein (show TGFB1 ELISA Kits) (CCAR1/CARP1 (show CCAR1 ELISA Kits))
Necdin-null adult hematopoietic stem cells are less quiescent and more proliferative than normal hematopoietic stem cells, demonstrating the similar role of necdin and p53 (show TP53 ELISA Kits) in promoting hematopoietic stem cells quiescence during steady-state conditions.
In the skeletal muscle of neonate pigs, both NECD and SNRPN (show SNRPN ELISA Kits) were maternally imprinted, while UBE3A (show ube3a ELISA Kits) was not imprinted.
Imprinting analysis showed that NDN and MAGEL2 (show MAGEL2 ELISA Kits) are paternally expressed in all tissues of pig where the genes were expressed as in human and mouse.
One candidate variant was located in an alpha helix of Necdin (NDN), phased to the paternally inherited allele. NDN is maternally imprinted within the 15q11.2 Prader-Willi Syndrome (PWS) region
NDN is an imprinted tumor suppressor gene which affects cancer cell motility, invasion and growth and that its loss of function in ovarian cancer can be caused by both genetic and epigenetic mechanisms.
Germline single nucleotide polymorphism in necdin gene is associated with breast cancer.
NDN and CD1A (show CD1A ELISA Kits) are novel prognostic methylation markers in patients with head and neck squamous carcinomas
Necdin expression declined during replicative aging of IMR90 primary human fibroblasts or after induction of premature senescence.Showed that in normal human cells, Necdin expression mimicked the effect of p53 (show TP53 ELISA Kits) inactivation by increasing radioresistance.
Hypermethylation and mutation of necdin is associated with neoplasms.
necdin exerts its pro-survival activity by counteracting the action of the pro-apoptotic protein Cell Cycle Apoptosis Regulatory Protein (CCAR1/CARP1 (show CCAR1 ELISA Kits))
necdin has multiple roles within protein complexes in different subcellular compartments, and indicate that it can utilize multiple karyopherin-dependent pathways to modulate its localization.
In pre-adipocytes, necdin over-expression inhibits adipogenesis, while reducing necdin levels enhances adipogenic differentiation in tissue culture cell
Necdin, a negative growth regulator,identified as a novel STAT3 (show STAT3 ELISA Kits) target gene, whose expression is down-regulated at the mRNA and protein levels when STAT3 (show STAT3 ELISA Kits) is constitutively active.
This intronless gene is located in the Prader-Willi syndrome deletion region. It is an imprinted gene and is expressed exclusively from the paternal allele. Studies in mouse suggest that the protein encoded by this gene may suppress growth in postmitotic neurons.
, Prader-Willi syndrome chromosome region
, necdin homolog