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Intestinal ablation of CKIalpha highlights invasiveness control

ABSTRACT: Wnt signaling, which drives the rapid self-renewal of the gut epithelium is causally associated with intestinal neoplasia. Here we show that CKIalpha is a activation depends on p53 and p21Waf1/Cip1: CKIÎ± ablation provokes activation of p53 and p21, which assume a pivotal role in suppressing invasive cancer. Dual loss of CKIalpha and either p53 or p21 results in rapid, rampant malignant signature denoted p53supinv (p53-suppressed invasiveness) that is conditionally induction of invasiveness. Like invasiveness control, the transcriptional suppression of p53supinv genes is largely mediated by p21, independently of cell cycle control, representing a novel tumor suppressor function of wild-type p53. 13 arrays of mice entrocytes herto or homozygot for gut specific KO of CKI alpha. Crossed with p53 or p21 KO mice.

ORGANISM(S): Mus musculus

SUBMITTER: Zoltan Wiener

PROVIDER: E-GEOD-24760 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Intestinal ablation of CKIalpha highlights invasiveness control

Project description:Wnt signaling, which drives the rapid self-renewal of the gut epithelium is causally associated with intestinal neoplasia. Here we show that CKIalpha is a activation depends on p53 and p21Waf1/Cip1: CKIα ablation provokes activation of p53 and p21, which assume a pivotal role in suppressing invasive cancer. Dual loss of CKIalpha and either p53 or p21 results in rapid, rampant malignant signature denoted p53supinv (p53-suppressed invasiveness) that is conditionally induction of invasiveness. Like invasiveness control, the transcriptional suppression of p53supinv genes is largely mediated by p21, independently of cell cycle control, representing a novel tumor suppressor function of wild-type p53.

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2011-09-16 | E-GEOD-23957 | biostudies-arrayexpress

Gene expression profiles of E14 ESCs treated with low levels of HDAC inhibitors for 16 hrs

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2011-09-16 | E-GEOD-23958 | biostudies-arrayexpress

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Project description:A genetic study of the PRF1 gene has shown association of several polymorphisms with multiple sclerosis (MS). Haplotype analysis identified risk haplotypes strongly associated with male patients having the primary-progressive form of MS (PPMS). Gene expression microarrays were performed in 10 male PPMS patients carrying the risk (n=6) and protective haplotypes (n=4) in order to identify pathways associated with the risk haplotypes. Pathway analysis revealed overrepresentation of the cell killing gene ontology category among down-regulated genes in patients carrying risk haplotypes compared with patients carrying protective haplotypes. Number of samples analyzed: 10 Protective haplotype samples: UOM982, EMA1473, MMC-998, CDP1842 Risk haplotype samples: UUS1554, RAU1550, RPS1011, AGS1013, PFB1530, MGA1014

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