• However, as shown in our study, p19 INK4d played important roles independent of cell cycle regulation, and the lack of cell cycle change was probably due to the compensatory up-regulation of p18 INK4c following p19 INK4d knockdown. (biomedcentral.com)
  • Although carcinogenic roles for the INK4B, INK4C, INK4D, CIP1, KIP1, and KIP2 genes appear to be limited, INK4A is among the most commonly mutated genes in human tumors. (medscape.com)
  • The tumor suppressors Ink4c and p53 collaborate independently with Patched to suppress medulloblastoma formation. (childrensmercy.org)
  • Using cDNA microarray with double dots of 4096 human genes, P18 INK4C , a member of CKI, was found down-regulated in a gastric adenocarcinoma metastatic cell line (RF-48), compared with the corresponding primary cancer cell line (RF-1), which implied that P18 INK4C might be involved in cell invasion and metastatic progression of human gastric adenocarcinoma. (psu.edu)
  • These results implied that P18 INK4C might play a pivotal role in regulating cell invasion, rather than regulating cell cycle and proliferation in the progression of human gastric adenocarcinoma as expected before. (psu.edu)
  • Although carcinogenic roles for the INK4B, INK4C, INK4D, CIP1, KIP1, and KIP2 genes appear to be limited, INK4A is among the most commonly mutated genes in human tumors. (medscape.com)
  • In mechanistic studies, silibinin (50-75 microM) modulated the protein levels of cyclin-dependent kinases (CDKs) (4, 6, and 2), cyclins (D1, D3, and E), CDKIs (p18/INK4C, p21/Cip1, and p27/Kip1) in a differential manner in these three cell lines. (nih.gov)
  • Growth arrest was not associated with upregulation of the CDK inhibitors p21(Waf1/Cip1), p18(ink4c) or p16(ink4a), but was associated with a decrease in reactive oxygen species (ROS). (nih.gov)
  • CDK activity is modulated by the CDKIs p27 kip1 , p57 kip2 , p16 ink4A , p15 ink4B , p18 ink4C , and p19 ink4D . (medscape.com)
  • Be that as it may, announcement of the cubicle cycle inhibitor p18(INK4c) was paradoxically enhanced after SE induced by way of pilocarpine and coincided with the apex of Cdk1 and Nestin expression at hour 3 post-SE (Okamoto et al. (ozdifferent.sk)