Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.22 (cdc2)
 8,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin A deficiency in male rats arrests spermatogenesis and leads to the loss of advanced germ cells. Retinol treatment of these rats seems to result in a synchronous spermatogenesis initiated from the remaining type A1 spermatogonia. To determine at a molecular level the onset of the M phase of the cell cycle occurring in the retinol-treated germ cells, the H1 histone kinase activity associated with the cdc2 kinase/cyclin B complex was measured. This kinase activity is an excellent molecular indicator of mitosis (M phase) since it is known to be high only for approximately 2 h between the G2/M phase transition of the cell cycle and the metaphase of mitosis. This activity was low in vitamin A-deficient testis, increased by 4 h after retinol treatment, and reached a 15.6-fold level at 12 h. These results suggest that the germ cells of vitamin A-deficient testis begin to enter the M phase around 4 h after retinol injection, with the highest percentage of cells entering at 12 h. These results are consistent with placing the origin of synchronous spermatogenesis in regenerated seminiferous tubules at the end of the S phase of the cell cycle.
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PMID:Vitamin A-deficient testis germ cells are arrested at the end of S phase of the cell cycle: a molecular study of the origin of synchronous spermatogenesis in regenerated seminiferous tubules. 838 46

Retinoids, including retinol and retinoic acid (RA) derivatives, have been shown to be involved in the processes of lung development as well as of lung repair after injury. Recently, we have provided evidence that RA could stimulate proliferation of lung alveolar type 2 epithelial cells (E. Nabeyrat, V. Besnard, S. Corroyer, V. Cazals, and A. Clement. Am. J. Physiol. Lung Cell. Mol. Physiol. 275: L71-L79, 1998). To gain some insight into the mechanisms involved in the mitogenic action of RA, we focused in the present study on the effects of RA on the expression of G(1) phase cyclins and their cell cycle-dependent kinases (Cdks). Experiments were performed with serum-deprived cells cultured in the absence and presence of RA. The results showed no effects of RA on the expression of either cyclins or Cdks. In contrast, RA treatment was found to prevent the decrease in cyclin E-Cdk2 activity observed when cells were growth arrested by serum deprivation. The observation that changes in cyclin E-Cdk2 activity were not associated with modifications in the amount of complexes formed led to the suggestion that the Cdk inhibitory protein (CKI) was involved. Study of the CKI p21(CIP1) revealed marked differences in its expression in the absence and presence of RA, with a dramatic downregulation observed in RA-treated cells. Interestingly, immunoprecipitation experiments provided evidence that the decreased levels of p21(CIP1) were associated with a reduced interaction of this CKI with cyclin E-Cdk2 complexes. These data together with previous results obtained in various situations of type 2 cell growth arrest emphasize the role of p21(CIP1) in the control of lung alveolar epithelial cell proliferation.
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PMID:Retinoic acid-induced proliferation of lung alveolar epithelial cells is linked to p21(CIP1) downregulation. 1064 89