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)

Fertilization of metaphase II-arrested mouse eggs results in resumption of meiosis and a decrease in both cdc2/cyclin B kinase and MAP kinase activities; the decrease in cdc2/cyclin B kinase activity precedes the decrease in MAP kinase activity. Cycloheximide treatment of metaphase II-arrested mouse eggs also results in resumption of meiosis but bypasses the fertilization-induced Ca2+ transient. However, it is not known if cycloheximide treatment results in the same temporal changes in cdc2/cyclin B kinase and MAP kinase activities that are intimately associated with resumption of meiosis. We report that cycloheximide-treated mouse eggs manifest similar temporal changes in the decrease in both cdc2/cyclin B kinase and MAP kinase activities that occur following fertilization, although cortical granule exocytosis is not stimulated. The decrease in cdc2/cyclin B kinase activity, however, does not seem to be required for the decrease in MAP kinase activity, since the decrease in MAP kinase activity still occurs in cycloheximide-treated eggs that are also incubated in the presence of nocodazole, which inhibits cyclin B degradation and hence the decrease in cdc2/cyclin B kinase. Following removal of these drugs, cdc2/cyclin B kinase activity remains high, MAP kinase activity increases to levels similar to that in the metaphase II-arrested eggs, and a spindle(s) forms with the chromosomes aligned on a metaphase plate. Results of these experiments suggest that some other protein with a relatively short half-life, e.g. cmos, a known upstream activator of MAP kinase, may be responsible for events leading to the decrease in MAP kinase activity.
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PMID:Cycloheximide-induced activation of mouse eggs: effects on cdc2/cyclin B and MAP kinase activities. 871 65

7-hydroxystaurosporine (UCN-01) is a more selective protein kinase C inhibitor than staurosporine. UCN-01 exhibits antitumor activity in experimental tumor models and is presently in clinical trials. Our study reveals that human myeloblastic leukemia HL60 and K562 and colon carcinoma HT29 cells undergo internucleosomal DNA fragmentation and morphological changes characteristic of apoptosis after UCN-01 treatment. These three cell lines lack functional p53, and K562 and HT29 cells are usually resistant to apoptosis. DNA fragmentation in HT29 and K562 cells occurred after 1 day of treatment while it took less than 4 h in HL60 cells. Cycloheximide prevented UCN-01-induced DNA fragmentation in HT-29 cells, but not in HL60 and K562 cells, suggesting that macromolecular synthesis is selectively required for apoptotic DNA fragmentation in HT29 cells. UCN-01-induced DNA fragmentation was preceded by activation of cyclin B1/cdc2 kinase. Further studies in HL60 cells showed that UCN-01-induced apoptosis was associated with degradation of CPP32, PARP, and lamin B and that the inhibitor of caspases (ICE/CED-3 cysteine proteases), Z-VAD-FMK, and the serine protease inhibitor, DCI, protected HL60 cells from UCN-01-induced DNA fragmentation. However, only DCI and TPCK, but not Z-VAD-FMK, inhibited DNA fragmentation in the HL60 cell-free system, suggesting that serine protease(s) may play a role in the execution phase of apoptosis in HL60 cells treated with UCN-01. Z-VAD-FMK and DCI also inhibited apoptosis in HT29 cells. These data demonstrate that the protein kinase C inhibitor and antitumor agent, UCN-01 is a potent apoptosis inducer in cell lines that are usually resistant to apoptosis and lack p53 and that caspases and probably serine proteases are activated during UCN-01-induced apoptosis.
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PMID:7-Hydroxystaurosporine (UCN-01) induces apoptosis in human colon carcinoma and leukemia cells independently of p53. 926 Sep 9

The roles of auxin and cytokinin in cell cycle reactivation were studied during the first 48 h of culture of mesophyll protoplasts of Nicotiana tabacum. Using hormone delay and withdrawal studies we found that auxin was required by 0-4 h of culture, whereas cytokinin was not required until hour 10-12, which is 6-10 h before S phase. Cycloheximide blocks division, indicating that protein synthesis is required. In an effort to detect a molecular response to either hormone, we examined the expression of the cell cycle marker, cdc2. Cdc2 expression was detected by 12 h of culture, coincident with the timing of the cytokinin requirement and well before the entry into S. However, cdc2 was partially induced by either auxin or cytokinin alone, suggesting that cdc2 expression is not the primary target of either hormone. Our hormone delay experiments suggest that there are separate signal transduction pathways leading from auxin and from cytokinin to reactivation of the cell cycle and that these pathways converge before S. The underlying mechanisms for these distinct pathways remain to be elucidated. Key Words. Auxin-Cytokinin-Tobacco-Protoplast-Development-cdc2
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PMID:Hormonal Control of Gene Expression During Reactivation of the Cell Cycle in Tobacco Mesophyll Protoplasts. 989 45

17Alpha,20beta-dihydroxy-4-pregnen-3-one (17alpha,20beta-DP) was identified as maturation-inducing hormone (MIH) in several teleost fishes. In goldfish (Carassius auratus), 17alpha,20beta-DP induces oocyte maturation by stimulating the de novo synthesis of cyclin B, a regulatory subunit of maturation-promoting factor (MPF). In this study, we examined the control mechanisms of 17alpha,20beta-DP-induced de novo synthesis of cyclin B protein in oocytes, which is a prerequisite step for MPF activation during oocyte maturation in goldfish. Cycloheximide-treated oocytes failed to undergo meiotic maturation in response to 17alpha,20beta-DP; in this group neither cyclin B nor 34-kDa active cdc2 was detectable in oocytes. In contrast, oocytes exposed to actinomycin D plus 17alpha,20beta-DP or 17alpha,20beta-DP underwent maturation; in these groups both cyclin B and 34-kDa cdc2 were present. Northern blotting showed that cyclin B mRNA is present in both immature and mature oocytes. Sequence analysis revealed that goldfish cyclin B mRNA contains four copies of cytoplasmic polyadenylation element (CPE)-like motifs in the 3' noncoding region, suggesting that the initiation of cyclin B synthesis during oocyte maturation may be controlled by the elongation of poly (A) tail. We then examined the polyadenylation state of cyclin B mRNA during 17alpha,20beta-DP-induced oocyte maturation by means of a PCR poly (A) test, and found that cyclin B mRNA is polyadenylated during oocyte maturation. Polyadenylation of cyclin B mRNA occurred at the same time of germinal vesicle breakdown. Furthermore, cordycepin, an inhibitor of poly (A) addition of mRNA, prevented 17alpha,20beta-DP-induced oocyte maturation. These findings suggest that in goldfish oocytes, the synthesis of cyclin B protein is under translational control and that cytoplasmic 3' poly(A) elongation is involved in 17alpha,20beta-DP-induced translation of cyclin B mRNA.
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PMID:Translational regulation of cyclin B mRNA by 17alpha,20beta-dihydroxy-4-pregnen-3-one (maturation-inducing hormone) during oocyte maturation in a teleost fish, the goldfish (Carassius auratus). 1063 Apr 8