Pub. Date : 2003 Dec
PMID : 14675202
8 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | 17beta-estradiol inhibits oxidative stress-induced apoptosis in keratinocytes by promoting Bcl-2 expression. | Estradiol | BCL2 apoptosis regulator | Homo sapiens |
| 2 | H2O2 decreased, whereas 17beta-estradiol increased Bcl-2 protein and mRNA levels in keratinocytes, and H2O2 plus 17beta-estradiol led to basal levels. | Estradiol | BCL2 apoptosis regulator | Homo sapiens |
| 3 | H2O2 suppressed, whereas 17beta-estradiol enhanced bcl-2 promoter activity, and H2O2 plus 17beta-estradiol led to basal activity. | Estradiol | BCL2 apoptosis regulator | Homo sapiens |
| 4 | Cyclic adenosine monophosphate (cAMP) response element on bcl-2 promoter was responsible for the effects of 17beta-estradiol and H2O2. | Estradiol | BCL2 apoptosis regulator | Homo sapiens |
| 5 | Bcl-2 expression was enhanced by membrane-impermeable bovine serum albumin-conjugated 17beta-estradiol, indicating the effects via membrane 17beta-estradiol-binding sites. | Estradiol | BCL2 apoptosis regulator | Homo sapiens |
| 6 | Bcl-2 expression was enhanced by membrane-impermeable bovine serum albumin-conjugated 17beta-estradiol, indicating the effects via membrane 17beta-estradiol-binding sites. | Estradiol | BCL2 apoptosis regulator | Homo sapiens |
| 7 | H-89, an inhibitor of cAMP-dependent protein kinase A, suppressed basal and 17beta-estradiol-induced cAMP response element-binding protein phosphorylation, cAMP response element-dependent transcriptional activity, Bcl-2 expression, and apoptosis resistance. | Estradiol | BCL2 apoptosis regulator | Homo sapiens |
| 8 | These results suggest that 17beta-estradiol may enhance Bcl-2 expression and prevent H2O2-induced apoptosis by phosphorylating cAMP response element-binding protein via cAMP/protein kinase A pathway in keratinocytes. | Estradiol | BCL2 apoptosis regulator | Homo sapiens |