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Data provide evidence that SLC22A18 and/or CDKN1C are tumor modifier genes involved in the tumorigenesis of SDHD (show SDHD ELISA Kits)-mutated paraganglioma.
The differences in p18(INK4c (show CDKN2C ELISA Kits))and p57(Kip2)activities in chronic myeloid leukemia (show BCL11A ELISA Kits) and normal stem cells suggest a different cell cycle regulation.
The data has been provided on fetal growth patterns and on the molecular subtypes of Beckwith-Wiedemann syndrome, including gain or loss of DNA methylation (show HELLS ELISA Kits), 11p15.5 paternal uniparental disomy, and CDKN1C mutation.
Analysis of the chromatin status of Cdkn1c promoter and KvDMR1 in unresponsive compared to responsive cell types showed that their differential responsiveness to the MyoD (show MYOD1 ELISA Kits)-dependent induction of the gene does not involve just their methylation status but, rather, the differential H3 lysine 9 dimethylation at KvDMR1.
CDKN1C protein expression in the BM of newly diagnosed, treatment-naive MDS (show PAFAH1B1 ELISA Kits) and secondary AML (show RUNX1 ELISA Kits) patients was identified as a prognostic factor for poor survival in patients treated with antiproliferative chemotherapy.
Low P57KIP2 Expression is associated with Hydatidiform Moles.
These results indicate that the inhibitory effect of rapamycin may be due mainly to increased p14 (show S100A9 ELISA Kits), p15 (show CDKN2B ELISA Kits), and p57 expression via promoter demethylation and decreased mTOR (show FRAP1 ELISA Kits) and p70S6K (show RPS6KB1 ELISA Kits) expression in ALL cell lines.
Jab1/Csn5 (show COPS5 ELISA Kits) expression with concurrent low p57 expression associated with poor overall survival in hepatocellular carcinoma
Using human placental samples, we show that the expression of the imprinted gene CDKN1C associates with birth weight
Our data indicated that reduced cytoplasmic p57 expression is associated with hepatocellular carcinoma invasion.
Myod (show MYOD1 ELISA Kits) in turn up-regulates cdkn1c, thereby providing a positive feedback loop that switches myogenic cells to terminal differentiation
p57Kip2 is both necessary and sufficient to mediate Shh (show SHH ELISA Kits)-induced cell-cycle exit in the deveoping zebrafish retina.
during late embryogenesis, neural cells that have low but functional levels of Cdkn1c, regulated by Notch (show NOTCH1 ELISA Kits) activity, are specified for oligodendrocyte fate
this study identifies E2A (show TCF3 ELISA Kits) target genes in embryonic neural stem cells and demonstrates that E47 (show TCF3 ELISA Kits) regulates neuronal differentiation via p57(KIP2).
This is the first report linking elevated Cdkn1c to altered behaviour in mice. Importantly, the findings from our study may have relevance for Silver Russell Syndrome and highlight a potentially underreported aspect of this disorder.
Dnmt3a (show DNMT3A ELISA Kits)-cKO muscles exhibit fewer Pax7 (show PAX7 ELISA Kits)+ SCs (show TWIST1 ELISA Kits), which show increased expression of p57Kip2 protein
indicate that the effects of insulin-like growth factor 2 (IGF2 (show IGF2 ELISA Kits)) are mediated by direct upregulation of the cyclin-dependent kinase inhibitor p57 (p57).
Data show that transforming growth factor beta (TGFbeta (show TGFB1 ELISA Kits))-induced changes in Gata2 transcription factor (show GATA2 ELISA Kits) and cyclin-dependent kinase inhibitor 1C (P57) expression in hematopoietic progenitors are conveyed through Smad (show SMAD1 ELISA Kits) signaling via Smad4 protein (show SMAD4 ELISA Kits).
This study reveals a key requirement for Cdkn1c in the early development of the brown adipose lineages.
Lhx6 (show LHX6 ELISA Kits) and Lhx8 (show LHX8 ELISA Kits) promote palate development through negative regulation of a cell cycle inhibitor gene, p57Kip2
hepatoblasts in p57(Kip2)-/- mice were highly proliferative and had deficient maturation compared with those in wild-type (WT) mice.
Data indicate that cyclin-dependent kinase inhibitor 1C (P57 was post-transcriptionally regulated by microRNA miR (show MLXIP ELISA Kits)-221 in embryonic stem (ES) cells.
Data show that disruption of potassium voltage-gated channel, KQT-like subfamily Q, member1 (KCNQ1 (show KCNQ1 ELISA Kits)) results in increased expression of cyclin-dependent kinase inhibitor 1C (Cdkn1c) only when the mutation is on the paternal allele.
Methylation of KvDMR1 involved in regulating the imprinting of CDKN1C
proper expression levels of the imprinted genes CDKN1C and PHLDA2 (show PHLDA2 ELISA Kits) are critical for embryo development
This gene is imprinted, with preferential expression of the maternal allele. The encoded protein is a tight-binding, strong inhibitor of several G1 cyclin/Cdk complexes and a negative regulator of cell proliferation. Mutations in this gene are implicated in sporadic cancers and Beckwith-Wiedemann syndorome, suggesting that this gene is a tumor suppressor candidate. Three transcript variants encoding two different isoforms have been found for this gene.
cyclin-dependent kinase inhibitor 1C
, cyclin-dependent kinase inhibitor p57
, cyclin-dependent kinase inhibitor 1C (p57, Kip2)
, cyclin-dependent kinase inhibitor 1C, p57
, p57KIP2 A3sh