Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.22.36 (caspase-1)
 6,285 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Cultured cerebellar granule neurons maintained in medium containing 26 mM potassium (high K+ or HK+) undergo cell death when switched to medium with 5 mM potassium (low K+ or LK+). This low K(+)-induced cell death has typical features of apoptosis. The intracellular signaling pathway of low K(+)-induced apoptosis has been investigated. 2. Cerebellar granule neurons become committed to undergo apoptosis between 2 and 5 h after K+ deprivation, judging from the inability of high K+ to rescue them after this time. Although the levels of most mRNAs decrease markedly concomitant with commitment, expression of c-jun mRNA increases 2-3 h after K+ deprivation. Among the family of caspases, a caspase-3-like protease is activated within 4 h of lowering the K+ concentration. A caspase-1-like protease is also activated within 2 h of K+ deprivation. 3. Inhibition of phosphatidylinositol 3-kinase (PI3-K) activity by LY294002 or wortmannin also induces apoptosis in cerebellar granule neurons. The intracellular signaling pathway of LY294002-induced apoptosis has been investigated. The activity of c-Jun N-terminal kinase (JNK) increases 8 h after addition of LY294002 to high K+ medium or low K+ medium containing BDNF. Expression of c-Jun protein also increases almost simultaneously. 4. The low K(+)-induced apoptosis of cerebellar granule neurons is prevented by high K+ (membrane depolarization by high K+), BDNF, IGF-1, bFGF or cAMP. The intracellular signaling pathways by which these agents prevent low K(+)-induced apoptosis have been investigated. Agents other than cAMP prevent apoptosis through PI3-K and a Ser/Thr kinase, Akt/PKB. The survival-promoting effect of cAMP does not depend on the PI3-K-Akt pathway.
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PMID:[Apoptosis-inducing and -preventing signal transduction pathways in cultured cerebellar granule neurons]. 1008 75

By using flow-cytometric analysis, we examined the involvement of p53, c-Myc, Bcl-2 and Bax in the glutamate-induced cell death in cultured cortical neurons. The activities of caspase-1-like and caspase-3-like proteases were also measured after the glutamate treatment. The apoptosis rate of the cells increased after 12 h and 24 h treatment with glutamate. The temporal profile of p53, c-Myc, Bcl-2, Bax expression and caspases activation after glutamate treatment suggest that Bcl-2, c-Myc and caspase-3 play important roles in the excitotoxic neuronal cell death. The down-regulation of Bcl-2 may be an important early stage event, which may cause the activation of caspase-3. c-Myc is also involved in the process of apoptosis though its precise role remains elusive. bFGF exhibited the capability to antagonize the neuronal apoptosis caused by glutamate. The antiapoptotic potential of bFGF may result from its attenuating effect on the down-regulation of Bcl-2 induced by glutamate and, subsequently, blockade of apoptosis cascade. This may provide a possible explanation for its neuroprotective effect against ischemic cell death.
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PMID:Roles of p53, c-Myc, Bcl-2, Bax and caspases in glutamate-induced neuronal apoptosis and the possible neuroprotective mechanism of basic fibroblast growth factor. 1052 75

It is the purpose of this paper to assess the expression, cellular localization, and hormonal regulation of rat ovarian interleukin (IL)-1beta converting enzyme (ICE), a putative apoptotic marker. In agreement with previous observations ICE transcripts were noted in relatively increased abundance in the thymus, lung, spleen and small intestine. Although ICE transcripts were barely expressed in the untreated, immature rat ovary, they were apparent throughout a simulated estrous cycle. The in vivo expression of ovarian ICE rose gradually from 6 h after ovulation triggering to a peak (1.74-fold increase versus control, P < 0.05) 24 h after human chorionic gonadotropin administration, a marked and significant decrease to baseline being noted 24 h later. To examine the effect of in vitro culture on ovarian ICE gene expression, whole ovarian dispersates from immature rats were cultured without treatment for 72 h. ICE gene expression significantly (P < 0.01) increased to a maximum 24 h post plating (2.55-fold increase as compared with time zero). Treatment with IL-1beta was associated with a small but statistically insignificant increase in ovarian ICE gene expression. Similarly, provision of IL-RA resulted in a modest, albeit statistically insignificant, decrease in ovarian ICE gene expression. Treatment with GnRH (but not FSH, LH or PMSG) significantly (P < 0.05) increased ovarian ICE gene expression (41.5% increase versus control). Treatment with dexamethasone (but not diethylstilbestrol, R5020 or R1881) produced a significant (P < 0.05) 42.3% decrease in ovarian ICE gene expression as compared with untreated controls. Treatment with TNF alpha (but not ET-1, TGF alpha, TGF beta, IGF-I or bFGF) produced a significant (P < 0.01) 2.5-fold increase in ovarian ICE gene expression as compared with untreated controls. Taken together, our present findings: (1) reaffirm the ovarian expression of the ICE gene, (2) document a periovulatory increase in ovarian ICE gene expression, (3) show the inhibitory effect of glucocorticoids in this regard, and (4) establish TNF alpha as an upregulator. Taken together, these findings suggest a role for ovarian ICE either in the context of apoptosis/atresia or in the context of the ovulatory process.
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PMID:Expression and hormonal regulation of rat ovarian interleukin-1beta converting enzyme, a putative apoptotic marker: endocrine- and paracrine-dependence. 1066 Feb 63