The Role of CDKs and CDKIs in Murine Development

Abstract

Cyclin-dependent kinases (CDKs) and their inhibitors (CDKIs) play pivotal roles in the regulation of the cell cycle. As a result of these functions, it may be extrapolated that they are essential for appropriate embryonic development. The twenty known mouse CDKs and eight CDKIs have been studied to varying degrees in the developing mouse, but only a handful of CDKs and a single CDKI have been shown to be absolutely required for murine embryonic development. What has become apparent, as more studies have shone light on these family members, is that in addition to their primary functional role in regulating the cell cycle, many of these genes are also controlling specific cell fates by directing differentiation in various tissues. Here we review the extensive mouse models that have been generated to study the functions of CDKs and CDKIs, and discuss their varying roles in murine embryonic development, with a particular focus on the brain, pancreas and fertility.

The RNA methyltransferase NSUN6 suppresses pancreatic cancer development by regulating cell proliferation

“…Cyclins, cyclin-dependent kinases (CDKs) and cyclin-dependent kinase inhibitors (CDKNs) are well-known markers of cell proliferation [25] . The association between NSUN6 levels and cellular proliferation markers including 26 Cyclins, 20 CDKs and 8 CDKNs were analyzed based on our PC gene microarray data.…”

Study on The Effect of Different Type of Sugar on Lipid Deposition in Goose Fatty Liver

“…Cyclin Dependent Kinase (CDKs) is the core of the entire cell cycle regulatory protein. CDKs can only be activated to perform their functions after combining with the corresponding cell cycle regulatory protein to form a CDKs-cyclin complex [25]. In this experiment, the gene expression of CDK1 was signi cantly increased in the overfeeding group, especially the glucose overfeeding group, indicating that glucose promoted the mitosis of hepatocytes and induced the proliferation and meristem of hepatocytes.…”

Oncogenic dysregulation of pre‐mRNA processing by protein kinases: challenges and therapeutic opportunities

“…CDK9 also mediates the phosphorylation of the RNPII CTD at Ser2 [ 108 ]. Loss of CDK9 expression in vivo causes embryonic lethality [ 119 ] and its activity was shown to contribute to developmental and tissue‐specific differentiation programme types, such as myogenic and lymphoid differentiation [ 120 , 121 ]. Together with its partner Cyclin T1, CDK9 is a key component of the P‐TEFb complex involved in transcription elongation.…”