PDF DatasheetAntibody (Suitable for clinical applications)
| Specification | Recommendation |
|---|---|
| Recommended Dilution (Conc) | 1:25-1:50 |
| Pretreatment | Citrate Buffer pH 6.0 |
| Incubation Parameters | 30 min at Room Temperature |
Prior to use, inspect vial for the presence of any precipitate or other unusual physical properties. These can indicate that the antibody has degraded and is no longer suitable for patient samples. Please run positive and negative controls simultaneously with all patient samples to account and control for errors in laboratory procedure. Use of methods or materials not recommended by enQuire Bio including change to dilution range and detection system should be routinely validated by the user.
p57Kip2 Information for Pathologists
Summary:
Also called CDKN1C. First described in 1995 (Genes Dev 1995;9:650). Strongly paternally imprinted gene on 11p15.5, expressed predominantly from the maternal allele in most tissues. Pathophysiology Genetic imprinting: differential DNA methylation of maternal and paternal alleles leading to allele specific expression.
Common Uses By Pathologists:
Differentiate complete hydatidiform mole (no nuclear DNA of maternal origin ? p57kip2 underexpressed) vs. partial hydatidiform mole or spontaneous abortion (p57+, Am J Surg Pathol 2001;25:1225, Am J Clin Pathol 2010;133:196), but molecular genotyping may be helpful because complete moles are rarely p57+ (Am J Surg Pathol 2009;33:1409) and partial moles are rarely p57- (Am J Surg Pathol 2011;35:1586, Am J Surg Pathol 2009;33:805). Identifies maternal 11p15 loss (p57-) with paternal K(ATP) mutation as predominant causative mechanism of focal hyperinsulinism (Mod Pathol 2006;19:122). Microscopic (histologic) images Images hosted on other servers:. Missing Image.
| p57Kip2 General Information | |
|---|---|
| Alternate Names | |
| Molecular Weight | |
| 32.2 kDa | |
| Chromosomal Location | |
| p15.4 [chr: 11] [chr_start: 2883213] [chr_end: 2885773] [strand: -1]; [chr: CHR_HSCHR11_1_CTG7] [chr_start: 2883205] [chr_end: 2885904] [strand: -1] | |
| Curated Database and Bioinformatic Data | |
| Gene Symbol | CDKN1C |
| Entrez Gene ID | 1028 |
| RefSeq Protein Accession(s) | NP_001116102; NP_000067; NP_001116103; XP_016872577 |
| RefSeq mRNA Accession(s) | NM_001362474; NM_001362475; NM_000076; NM_001122630; NM_001122631 |
| RefSeq Genomic Accession(s) | NT_187585; NG_008022; NC_000011 |
| UniProt ID(s) | P49918 |
| PharmGKB ID(s) | PA26320 |
| KEGG Gene ID(s) | hsa:1028 |
| Associated Diseases (KEGG IDs) | Beckwith-Wiedemann syndrome (BWS) [MIM:130650]: A disorder characterized by anterior abdominal wall defects including exomphalos (omphalocele), pre- and postnatal overgrowth, and macroglossia. Additional less frequent complications include specific developmental defects and a predisposition to embryonal tumors. {ECO:0000269|PubMed:10424811, ECO:0000269|PubMed:26077438}. The disease is caused by mutations affecting the gene represented in this entry.; Intrauterine growth retardation, metaphyseal dysplasia, adrenal hypoplasia congenita, and genital anomalies (IMAGE) [MIM:614732]: A rare condition characterized by intrauterine growth restriction, metaphyseal dysplasia, congenital adrenal hypoplasia, and genital anomalies. Patients with this condition may present shortly after birth with severe adrenal insufficiency, which can be life-threatening if not recognized early and commenced on steroid replacement therapy. Other reported features in this condition include, hypercalciuria and/or hypercalcemia, craniosynostosis, cleft palate, and scoliosis. {ECO:0000269|PubMed:22634751}. The disease is caused by mutations affecting the gene represented in this entry. |
| General Description of p57Kip2 . | |
| This antibody is specific to a protein of 57 kDa known as p57Kip2 a cell cycle regulatory mitotic inhibitor. This antibody does not cross-react with p27Kip1. p57Kip2 is a potent tight-binding inhibitor of several G1 cyclin complexes and a negative regulator of cell proliferation. | |
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