CDKN1C Recombinant Monoclonal Antibody

1. HOXD-AS1 could interact with EZH2, and then repress p57 expression, to aggravate osteosarcoma oncogenesis. PMID: 30119259
2. review provides an appraisal of the published data on the p57Kip2 protein; mainly focused on the regulation of CDKN1C (the p57Kip2 encoding gene) expression and its relevance in human diseases, including overgrowth and undergrowth syndromes PMID: 29614816
3. If, as expected, the consequences of the deregulation of the CDKN1C-E2F1-TP53 axis were the same as those experimentally demonstrated in mouse models, the disruption of this axis might be useful to predict tumor aggressiveness, and to provide the basis towards the development of potential therapeutic strategies in human Precursor T-cell lymphoblastic lymphomas PMID: 29661169
4. Data suggest that expression of CDKN1C and IGF2 is significantly up-regulated in placenta after assisted reproductive technology; DNA methylation was significantly down-regulated in DMR of CDKN1C and up-regulated in DMR of IGF2. (CDKN1C = cyclin-dependent kinase inhibitor-1C; IGF2 = insulin like growth factor 2; DMR = differential methylation regions) PMID: 29277274
5. The expression of SH3PXD2A-AS1 was inversely correlated with the expression of P57 and KLF2 in Colorectal Cancer tissue samples. PMID: 29734178
6. expression of the nearby cyclindependent kinase inhibitor 1C (CDKN1C) gene was revealed to be upregulated after SP3 knockdown in cells that possessed non-risk alleles. This suggests that CDKN1C is potentially one of the functional targets of SNP rs163184, which modulates the binding activity of the locus for Sp3 and Lsd1/Kdm1a PMID: 29207083
7. SNHG17 exerted oncogenic effects partly through epigenetically silencing P57 expression through interaction with EZH2. PMID: 28933484
8. Studies indicate that misregulation of p57(kip2) expression has been associated, to growth disorders and the onset of several types of cancers [Review]. PMID: 28930539
9. conclusion, our data suggested an essential role of CDKN1C in the tumorgenesis of breast cancer. Targeting CDKN1C may be a promising strategy for anticancer therapeutics. PMID: 29428729
10. This study showed that negative p57KIP2 immunostaining reliably identified complete mole (CM)and could be used in association with the histological findings to distinguish CM from its mimics. PMID: 28574027
11. findings showed that pathogenesis of selective intrauterine growth restriction may be related to the co-effect of the up-regulated protein expression of CDKN1C and down-regulated mRNA expression of KCNQ1OT1 in the placenta. PMID: 28803575
12. Gain-of-function mutations in the PCNA domain of CDKN1C have been reported as the genetic basis of various growth-retarded syndromes including IMAGe syndrome, Russell Silver syndrome as well as a novel undergrowth syndrome that additionally exhibited early adulthood onset diabetes. {review] PMID: 28508599
13. The mean Beckwith-Wiedemann syndrome (BWS)score was 5.6 for 19 subjects with "IC2 hypomethylation"(KCNQ1OT1-associated ), compared with 3.8 for 2 subjects with pUPD. The BWS score of one subject with CDKN1C mutation and one with IC1( H19-associated imprinting center) hypermethylation was 6 and 7, respectively PMID: 27436784
14. Data provide evidence that SLC22A18 and/or CDKN1C are tumor modifier genes involved in the tumorigenesis of SDHD-mutated paraganglioma. PMID: 27402879
15. The differences in p18(INK4c)and p57(Kip2)activities in chronic myeloid leukemia and normal stem cells suggest a different cell cycle regulation. PMID: 26985855
16. 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, 11p15.5 paternal uniparental disomy, and CDKN1C mutation. PMID: 26857110
17. 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-dependent induction of the gene does not involve just their methylation status but, rather, the differential H3 lysine 9 dimethylation at KvDMR1. PMID: 27611768
18. CDKN1C protein expression in the BM of newly diagnosed, treatment-naive MDS and secondary AML patients was identified as a prognostic factor for poor survival in patients treated with antiproliferative chemotherapy. PMID: 27170453
19. Low P57KIP2 Expression is associated with Hydatidiform Moles. PMID: 27221896
20. These results indicate that the inhibitory effect of rapamycin may be due mainly to increased p14, p15, and p57 expression via promoter demethylation and decreased mTOR and p70S6K expression in ALL cell lines. PMID: 26362858
21. Jab1/Csn5 expression with concurrent low p57 expression associated with poor overall survival in hepatocellular carcinoma PMID: 26606000
22. Using human placental samples, we show that the expression of the imprinted gene CDKN1C associates with birth weight PMID: 26091021
23. Our data indicated that reduced cytoplasmic p57 expression is associated with hepatocellular carcinoma invasion. PMID: 26271467
24. CDKN1C sequencing should be performed for BWS patients presenting with abdominal wall defects or cleft palate without 11p15 methylation defects or body asymmetry, or in familial cases of BWS. PMID: 26077438
25. This report shows that p57(Kip2) is a novel target of miR-21 in prostate cancer and revealing a novel oncogenic function of this microRNA. PMID: 25216674
26. Data show the presence of maternally derived extra copies of the distal chromosome 11p involving the wild-type cyclin-dependent kinase inhibitor 1C protein (CDKN1C). PMID: 25427884
27. downregulation of CDKN1 by siRNA blocked the activity of miR-25 on promoting glioma cell proliferation. PMID: 25960208
28. Polymer-based immunohistochemical staining of p57(kip2) (paternally imprinted gene, expressed from maternal allele) is a very effective method that can be used to differentiate androgenetic complete mole from partial mole and hydropic abortion. PMID: 26161420
29. Up-regulation of miR-199a-5p in ADPKD tissues might promote cell proliferation through suppressing CDKN1C PMID: 25588980
30. p57Kip2 has a role in DNA damage response, suppresses tumorigenesis and causes chemoresistance. PMID: 25195859
31. opposed functional mutations in CDKN1C cause opposite clinical features; loss-of-function mutations cause overgrowth; gain-of-function mutations in the PCNA domain result in growth restriction; only maternally inherited mutations in CDKN1C are associated with disturbed growth [review] PMID: 25262539
32. The gene expression pattern of CDKN1C, H19, IGF2, KCNQ1 and PHLDA2 genes was evaluated using RT-PCR. PMID: 24986528
33. Staining intensities of cell cycle inhibitors p27 and p57 significantly increased in all parts of preeclamptic placentas compared to control PMID: 24852133
34. We report a novel CDKN1C mutation associated with features of IMAGe syndrome, but without adrenal insufficiency or metaphyseal dysplasia, and characterized by early-adulthood-onset diabetes. PMID: 25057881
35. p57 expression is highly correlated with genotyping, serves as a reliable marker for diagnosis of complete hydatidiform moles PMID: 23887308
36. A report of a novel mutation of CDKN1C affecting the PCNA-binding domain in a family with a history of Russell Silver syndrome. PMID: 24065356
37. p57 regulates T-cell development and prevents lymphomagenesis by balancing p53 activity and pre-TCR signaling. PMID: 24652995
38. In conclusion, combined p57 immunostaining and FISH with a set of 3 CEP probes for chromosomes X, Y, and 17 could be useful in the classification of hydatidiform moles. PMID: 24613849
39. Increased protein stability of CDKN1C causes a gain-of-function phenotype in patients with IMAGe syndrome. PMID: 24098681
40. This study indicates that the abnormal expression of p57 and RhoA contributes to progression of hepatocellular carcinoma and poor survival of patients. PMID: 23842948
41. p57kip2 appears to be widely expressed in the human oligodendroglial lineage, and potential beneficial effects on remyelination in the mulltiple sclerosis brain are not based on subcellular p57kip2 localization shifts. PMID: 23828667
42. p15(INK4b) and p57(KIP2) may be involved in the progression of vulvar carcinomas and the combined p14(ARF)/p15(INK4b)/p16(INK4a) status was a statistically independent prognostic factor. PMID: 23580324
43. These data suggest that HER2/Akt is an important negative regulator of p57 (Kip2), and that p57 restoration in HER2-overexpressing cells can reduce breast tumor growth. PMID: 23421998
44. A novel mutation in CDKN1C was found in a family with Beckwith-Wiedemann syndrome and cleft palate, sensorineural hearing loss, and supernumerary flexion creases. PMID: 23197429
45. Data suggest that CSN6 is an important negative regulator of p57 (Kip2) , and that overexpression of CSN6 in many types of cancer could lead to decreased expression of p57 (Kip2) and result in promoted cancer cell growth. PMID: 23187808
46. High p57 KIP2 is asociated with breast cancer. PMID: 23244105
47. miR-221 inhibits CDKN1C/P57 expression by post-transcriptional gene silencing to promote colorectal carcinoma development and progression. PMID: 21538272
48. Downregulation of CDKN1C is associated with poor disease outcome in patients with cutaneous T-cell lymphoma, while upregulation of AHI1 shows a weak association with aggressive disease course. PMID: 23171462
49. MIR221 can interact with the target site on the 3'-UTR of CDKN1C/p57 mRNA to inhibit CDKN1C/p57 expression by post-transcriptional gene silencing to promote colon carcinoma cell proliferation. PMID: 22126772
50. Cdkn1c (p57/KIP2) is a novel regulator of early epidermal differentiation and controls proliferation in primary keratinocytes and HaCaT cells. PMID: 23008285

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HGNC: 1786

OMIM: 130650

KEGG: hsa:1028

STRING: 9606.ENSP00000411552

UniGene: Hs.106070