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Overall, these results demonstrate that an increase of SERT activity is sufficient to cause the apneas in Necdin-knockout pups.
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 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.
Myc overexpression in the cpk kidney results from the dysregulation of the cystin-necdin regulatory complex and c-Myc, in turn, contributes to cystogenesis in the cpk mouse.
Antagonistic interplay between necdin and Bmi1 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-mediated proteasomal
necdin exerts its pro-survival activity by counteracting the action of the pro-apoptotic protein Cell Cycle Apoptosis Regulatory Protein (CCAR1/CARP1)
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 in promoting hematopoietic stem cells quiescence during steady-state conditions.
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.
These results suggest that necdin regulates Foxo1 acetylation and neuropeptide gene expression in the arcuate neurons to modulate the hypothalamic-pituitary-thyroid axis during development.
Necdin prevents excessive preadipocyte proliferation induced by adipogenic stimulation to control white adipocyte number during adipose tissue development.
Necdin is a binding partner of dysbindin-1. Dysbindin-1 recruits necdin to the cytoplasm, thereby attenuating the repressive effects of necdin on p53 transcriptional activity.
Necdin is implicated through the TNF-receptor 1 pathway in the developmental death of motoneuron
demonstrated that CREB and FoxO1 are recruited to the necdin promoter, likely interacting with specific consensus sequences in the proximal region
The necdin gene is imprinted, with preferential expression from the paternal allele in human and mouse.
necdin mediates the terminal differentiation and survival of NGF-dependent dorsal root ganglion neuron and that necdin-deficient nascent neurons are destined to caspase-3-dependent apoptosis.
Necdin promotes differentiation and survival of neurons through its antagonistic interactions with E2F1.
In the skeletal muscle of neonate pigs, both NECD and SNRPN were maternally imprinted, while UBE3A was not imprinted.
Imprinting analysis showed that NDN and MAGEL2 are paternally expressed in all tissues of pig where the genes were expressed as in human and mouse.
We focused on three important regulatory DNA elements which are all differentially methylated regions (DMRs), methylated on the maternal allele: the PWS imprinting center (PWS-IC), which is a germline DMR and the somatic NDN and MKRN3 DMRs, hierarchically controlled by PWS-IC.
the single-nucleotide polymorphism rs850807, which is putatively functional and linked with MAGEL2 and NDN Genetic variation in rs850807 was strongly and exclusively associated with the ideas of reference subscale of the schizophrenia spectrum, which is best typified as paranoia
this study shows that hypermethylation of NDN promotes cell proliferation by activating the Wnt signaling pathway in colorectal cancer
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 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 inactivation by increasing radioresistance.
Hypermethylation and mutation of necdin is associated with neoplasms.
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 target gene, whose expression is down-regulated at the mRNA and protein levels when STAT3 is constitutively active.
rare variant of necdin (p.V318A) was described in a family with Kallmann syndrome Familial segregation and in vitro analysis suggested that this non-synonymous variant did not have a direct causative role in hypogonadism phenotype.
Data suggest that the effects of necdin deletion on the developing nervous system may depend on the relative expression of p75NTR and TrkA in the cells of particular regions of the nervous system.
Necdin is a key protein regulating polarization of the cytoskeleton and myosin activation during development.
the constitutively up-regulated expression of pre-IL-1 alpha in the nuclei of systemic sclerosis (SSc) fibroblasts up-regulates proliferation and matrix production of SSC fibroblasts through binding necdin
Tissue-specific gene expression regulation and imprinted epigenetic modifications of the human NDN gene.
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