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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Cyclin-dependent kinase inhibitor 1C

p57, Cyclin-Dependent Kinase Inhibitor p57, KIP2, p57KIP2, CDKN1C, TFII-I
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. [provided by RefSeq, Oct 2010] (from NCBI)
Top mentioned proteins: PCNA, p27, p21, CAN, HAD
Papers using p57 antibodies
p57KIP2 immunohistochemistry in early molar pregnancies: emphasis on its complementary role in the differential diagnosis of hydropic abortuses.
Blagosklonny Mikhail V., In PLoS ONE, 2004
... Induction of SMARCB1 and CDKN1C in transformed cell lines was achieved by the addition of 1 µM 4-hydroxytamoxifen (4HT: Sigma Aldrich Castle Hill Australia) ...
Papers on p57
TGF-β/β2-spectrin/CTCF-regulated tumor suppression in human stem cell disorder Beckwith-Wiedemann syndrome.
Mishra et al., In J Clin Invest, Feb 2016
Imprinting of the IGF2/H19 locus and the CDKN1C/KCNQ1 locus on chromosome 11p15.5 is mediated by CTCF, and this regulation is lost in BWS, leading to aberrant overexpression of growth-promoting genes.
Histologic and Molecular Profile of Pediatric Insulinomas: Evidence of a Paternal Parent-of-Origin Effect.
Stanley et al., Philadelphia, United States. In J Clin Endocrinol Metab, Feb 2016
Immunohistochemical analysis revealed nuclear loss of p57 staining consistent with loss of the maternal 11p15 allele in 11 of the 12 insulinomas, including all 5 MEN1-associated tumors.
Self-Renewal and High Proliferative Colony Forming Capacity of Late-Outgrowth Endothelial Progenitors is Regulated by Cyclin-Dependent Kinase Inhibitors Driven by Notch Signaling.
Khosrotehrani et al., Australia. In Stem Cells, Feb 2016
Transcriptomic analysis identified cyclin-dependent kinase (CDK) cell cycle inhibiting genes (p16, p21, and p57), the Notch signaling pathway (dll1, dll4, hes1, and hey1), and the endothelial cytokine il33 as highly expressed in CD34 + ECFC.
Cbx4 maintains the epithelial lineage identity and cell proliferation in the developing stratified epithelium.
Botchkarev et al., Shanghai, China. In J Cell Biol, Feb 2016
Cbx4 ablation in mice results in a marked decrease of the epidermal thickness and keratinocyte (KC) proliferation associated with activation of numerous neuronal genes and genes encoding cyclin-dependent kinase inhibitors (p16/p19 and p57).
Combined inhibition of BET family proteins and histone deacetylases as a potential epigenetics-based therapy for pancreatic ductal adenocarcinoma.
Siveke et al., Stanford, United States. In Nat Med, Oct 2015
Finally, using a CRISPR-Cas9-based method for gene editing directly in the mouse adult pancreas, we show that de-repression of p57 (also known as KIP2 or CDKN1C) upon combined BET and HDAC inhibition is required for the induction of combination therapy-induced cell death in PDAC.
G-Protein-Coupled Receptors: Next Generation Therapeutic Targets in Head and Neck Cancer?
Carey et al., Japan. In Toxins (basel), Aug 2015
GALR1 inhibits proliferation of HNSCC cells though ERK1/2-mediated effects on cell cycle control proteins such as p27, p57, and cyclin D1, whereas GALR2 inhibits cell proliferation and induces apoptosis in HNSCC cells.
The clinical course of an overgrowth syndrome, from diagnosis in infancy through adulthood: the case of Beckwith-Wiedemann syndrome.
Pappas, New York City, United States. In Curr Probl Pediatr Adolesc Health Care, Apr 2015
Beckwith-Wiedemann syndrome (BWS) is the most common genetic overgrowth syndrome, and it is frequently clinically recognizable because of characteristic features.
The HLA-B*35 allele modulates ER stress, inflammation and proliferation in PBMCs from Limited Cutaneous Systemic Sclerosis patients.
Trojanowska et al., Boston, United States. In Arthritis Res Ther, 2014
Furthermore, HLA-B*35 correlated with decreased expression of cyclin inhibitors (p21, p57) and pro-apoptotic genes (Bax, Gadd45) in lcSSc B35 subjects.
Cellular Response upon Stress: p57 Contribution to the Final Outcome.
Antonangeli et al., Roma, Italy. In Mediators Inflamm, 2014
p57 is a cyclin-dependent kinase inhibitor belonging to the CIP/KIP family and is a well-known regulator of the cell cycle during embryogenesis and tissue differentiation.
CDKN1C mutations: two sides of the same coin.
Begemann et al., Aachen, Germany. In Trends Mol Med, 2014
Cyclin-dependent kinase (CDK)-inhibitor 1C (CDKN1C) negatively regulates cellular proliferation and it has been shown that loss-of-function mutations in the imprinted CDKN1C gene (11p15.5)
Imprinting genes associated with endometriosis.
Kobayashi, Nara, Japan. In Excli J, 2013
From the genomic imprinting database, we picked 10 genes that were highly associated with female reproduction; prominent among them were paternally expressed genes (DIRAS3, BMP8B, CYP1B1, ZFAT, IGF2, MIMT1, or MIR296) and maternally expressed genes (DVL1, FGFRL1, or CDKN1C).
p57kip2 regulates glial fate decision in adult neural stem cells.
Küry et al., Düsseldorf, Germany. In Development, 2012
Short-hairpin RNA-mediated suppression of p57kip2 in cultured adult neural stem cells was found to strongly reduce astroglial characteristics, while oligodendroglial precursor features were increased.
Mutations in the PCNA-binding domain of CDKN1C cause IMAGe syndrome.
Vilain et al., Los Angeles, United States. In Nat Genet, 2012
All IMAGe-associated mutations clustered in the PCNA-binding domain of CDKN1C and resulted in loss of PCNA binding.
Duplication of GTF2I results in separation anxiety in mice and humans.
Osborne et al., Louisville, United States. In Am J Hum Genet, 2012
GTF2I duplication results in separation anxiety in mice and humans
The contribution of CLIP2 haploinsufficiency to the clinical manifestations of the Williams-Beuren syndrome.
Kooy et al., Edegem, Belgium. In Am J Hum Genet, 2012
CLIP2 haploinsufficiency by itself does not lead to the physical or cognitive characteristics of the Williams-Beuren syndrome; GTF2IRD1 and GTF2I are the main genes causing the cognitive defects
p57(KIP2) control of actin cytoskeleton dynamics is responsible for its mitochondrial pro-apoptotic effect.
Joseph et al., Stockholm, Sweden. In Cell Death Dis, 2011
The p57(KIP2-)mediated stabilization of the actin cytoskeleton was associated with the displacement of hexokinase-1 from the mitochondria, providing a possible mechanism for the promotion of the mitochondrial apoptotic cell death pathway.
Lung stem cell self-renewal relies on BMI1-dependent control of expression at imprinted loci.
Kim et al., Boston, United States. In Cell Stem Cell, 2011
Many imprinted genes were derepressed in Bmi1 knockout mice, and knockdown of Cdkn1c (p57) and other imprinted genes partially rescued the self-renewal defect of Bmi1 mutant lung cells.
p57(Kip2) and p27(Kip1) cooperate to maintain hematopoietic stem cell quiescence through interactions with Hsc70.
Suda et al., Tokyo, Japan. In Cell Stem Cell, 2011
cooperates with p27(Kip1)to maintain hematopoietic stem cell quiescence through interactions with Hsc70
p57 is required for quiescence and maintenance of adult hematopoietic stem cells.
Nakayama et al., Fukuoka, Japan. In Cell Stem Cell, 2011
required for quiescence and maintenance of adult hematopoietic stem cells
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