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1 ced in activated HSCs, is a direct target of necdin.
2 m23-H1 as well as the biological function of Necdin.
3 ic and antiproliferative effects mediated by Necdin.
4  confirmed by overexpression of ectopic Flag-necdin.
5 n via interaction with the tumor suppressor, necdin.
6 inted expression and methylation patterns of necdin, a gene outside the deletion region, indicate tha
7                                              Necdin, a melanoma antigen family protein, promotes neur
8 d method, we found that pre-IL-1 alpha binds necdin, a nuclear protein with growth suppressor activit
9               Furthermore, overexpression of necdin activates GnRH transcription through cis elements
10           These data suggest that changes in necdin and E2F4 expression after rosiglitazone exposure
11 ition of Myc expression via interaction with necdin and maintenance of FPC as functional component of
12  whereas the transcriptionally inactive loci necdin and MyoD1 contained very little H3-meK79.
13 rmal HSCs, demonstrating the similar role of necdin and p53 in promoting HSC quiescence during steady
14 own in activated HSCs, causes suppression of necdin and Wnt, epigenetic derepression of Ppargamma, an
15 roduction of SSc fibroblasts through binding necdin, and by counteracting its effects on cell growth
16  brain development (e.g., Dlk1, Peg3, Ube3a, necdin, and Grb10).
17 matopoietic stem cells (HSCs) and identified necdin as a candidate p53 target gene.
18                             Here we identify necdin as a potent PGC-1alpha stabilizer that promotes m
19 could change the subcellular localization of Necdin as well as rescue cells from the antiangiogenic a
20 the region of pre-IL-1 alpha responsible for necdin binding and found it to be localized near the N t
21 nRH transcription through these elements and necdin co-immunoprecipitates with Msx from GnRH neuronal
22                                              Necdin controls the HSC response to genotoxic stress via
23                                          The Necdin-deficient mouse is the only model that reproduces
24                         Here, we report that Necdin deletion disturbs the migration of serotonin (5-H
25                            We also show that Necdin directly interacts with Nm23-H1, resulting in mod
26 ogether, these results indicate that lack of necdin during development likely contributes to the hypo
27                         Forced expression of necdin enhances mitochondrial function in primary cortic
28 promoter of the GnRH gene, and knock-down of necdin expression reduces GnRH gene expression.
29 tes with rosiglitazone did not alter E2F4 or necdin, expression of both genes was significantly alter
30                             We conclude that necdin functions as a molecular switch in adult hematopo
31                           Adult mice lacking necdin have reduced numbers of gonadotropin-releasing ho
32              To define the intrinsic role of necdin in adult hematopoiesis, in the present study, we
33 A3C can modulate the biological functions of Necdin in the context of EBV infection and transformatio
34 nstrated that pre-IL-1 alpha associates with necdin in the nuclei of mammalian cell lines and regulat
35             These studies suggest a role for Necdin in the regulation of downstream cellular targets
36                  Moreover, overexpression of necdin in the substantia nigra in vivo of adult mice pro
37                                 Furthermore, Necdin is a cellular protein which is highly induced in
38                                              Necdin is a growth-suppressing protein and the gene enco
39                                     Finally, necdin is necessary for generation of the full complemen
40               Herein, we show that, although necdin is not expressed in an immature, migratory GnRH n
41          The present study demonstrates that necdin is selectively expressed in HSCs among different
42 ctivity is sufficient to cause the apneas in Necdin-KO pups, and that fluoxetine may offer therapeuti
43                                           In Necdin-KO pups, the genetic deletion of Slc6a4 or treatm
44 d transcript (H19) ([Formula: see text]) and necdin, MAGE family member (NDN) ([Formula: see text]) a
45  NDN gene, encoding the MAGE family protein, necdin, maps to the PWS chromosome region and is highly
46 sx from GnRH neuronal cells, indicating that necdin may activate GnRH gene expression by preventing r
47  endothelial growth factor promoter but also Necdin-mediated growth suppression and antiangiogenic ef
48 A3C and Nm23-H1 were able to rescue not only Necdin-mediated transcriptional repression of the downst
49  overexpression-based screening and identify Necdin (Ndn) as a driver gene for paternal Dup15q result
50                                 We show that necdin-null adult HSCs are less quiescent and more proli
51 specific proteins decreases significantly in necdin-null cortical neurons, where mitochondrial functi
52 iesis, in the present study, we transplanted necdin-null fetal liver cells into lethally irradiated r
53 wever, wild-type recipients repopulated with necdin-null hematopoietic stem/progenitor cells show enh
54                                    Moreover, necdin overexpression potently inhibited adipocyte diffe
55                       These data reveal that necdin promotes mitochondrial biogenesis through stabili
56 rapamycin, mitogen-activated protein kinase, necdin, reactive oxygen species, and sphingolipids.
57 d NDN (which encodes the DNA-binding protein necdin; refs 7,8,9,10).
58                   In fact, overexpression of Necdin relieves Msx repression of GnRH transcription thr
59                                              Necdin silencing abrogates three epigenetic signatures i
60                                              Necdin strongly stabilizes PGC-1alpha by inhibiting its
61 ld in muscle and 2.5-fold in adipose tissue; necdin was identified in adipose tissue only and increas
62                                The levels of Necdin were consistently lower in EBV-positive cells, an
63 nscription factors E2F4 and the MAGE protein necdin were similarly altered in all subjects after rosi
64 ed through amino acid residues 191 to 222 of Necdin, which are also known to be important for nuclear
65 urotrophin receptor-dependent apoptosis, and necdin, which is a strong suppressor of cell proliferati
66 h suppressors, such as the Prader-Willi gene NECDIN, whose function was confirmed by overexpression o
67                                 Silencing of necdin with adenovirally expressed shRNA, reverses activ
68  dedifferentiation of adipocytes as such the necdin-Wnt pathway causes epigenetic repression of the m
69              Our results demonstrate a novel necdin-Wnt pathway, which serves to mediate antiadipogen