Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 오세관 | * |
dc.date.accessioned | 2018-05-02T08:15:17Z | - |
dc.date.available | 2018-05-02T08:15:17Z | - |
dc.date.issued | 2004 | * |
dc.identifier.issn | 1528-7394 | * |
dc.identifier.other | OAK-2456 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/242640 | - |
dc.description.abstract | Fumonisin B 1, a specific inhibitor of ceramide synthase, and ISP1 (Myriocin), a serine palmitoyl-transferase inhibitor, modulate the de novo sphingolipid biosynthesis pathway. This study was conducted to determine whether serum deprivation-induced cell death is regulated by de novo sphingolipid biosynthesis in pig kidney LLC-PK1 cells. Serum withdrawal from the culture medium produced cell death in LLC-PK1 cells. Fumonisin B 1 at concentrations ranging from 5 M to 30 M delayed until 48 h this cell death resulting from the absence of fetal bovine serum (FBS) in cell culture. Pretreatment of cultured cells with fumonisin B 1 in the presence of serum for 24 h increased by approximately 70% this cytoprotective activity of fumonisin B 1 against serum deprivation-induced cell death. Serum deprivation increased sphingolipid biosynthesis threefold compared to 5% serum-enriched culture. Fumonisin B 1 at 5-30 M lowered the content of total complex sphingolipids to levels of 50% and 77% of the content in serum-enriched culture, although the concentration of intracellular free sphinganine was elevated. ISP1 alone at greater than 1 nM concentration reduced total complex sphingolipid content to values in LLC-PK1 cells grown in the presence of 5% FBS. The results suggest that the de novo complex sphingolipid biosynthesis modulated by either fumonisin B 1 or ISP1 may regulate serum deprivation-induced cell death in LLC-PK1 cells. | * |
dc.language | English | * |
dc.title | Altered de novo sphingolipid biosynthesis is involved in the serum deprivation-induced cell death in LLC-PK1 cells | * |
dc.type | Conference Paper | * |
dc.relation.issue | 23-24 | * |
dc.relation.volume | 67 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 2085 | * |
dc.relation.lastpage | 2094 | * |
dc.relation.journaltitle | Journal of Toxicology and Environmental Health - Part A | * |
dc.identifier.doi | 10.1080/15287390490515065 | * |
dc.identifier.wosid | WOS:000225105900015 | * |
dc.identifier.scopusid | 2-s2.0-8444242541 | * |
dc.author.google | Yu M.U. | * |
dc.author.google | Jae M.Y. | * |
dc.author.google | Youn S.L. | * |
dc.author.google | Yong M.L. | * |
dc.author.google | Jin T.H. | * |
dc.author.google | Ki W.O. | * |
dc.author.google | Song S. | * |
dc.author.google | Yeo P.Y. | * |
dc.author.google | Hwan S.Y. | * |
dc.author.google | Oh S. | * |
dc.contributor.scopusid | 오세관(7404103757) | * |
dc.date.modifydate | 20240118133340 | * |