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The role of p38 mitogen activated pr...

Khatri, Jitender.

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The role of p38 mitogen activated protein kinase in post-transcriptional regulation of cyclooxygenase-2 in intleukin-1beta and tumor necrosis factor-alpha stimulated prostate cancer cell lines.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	The role of p38 mitogen activated protein kinase in post-transcriptional regulation of cyclooxygenase-2 in intleukin-1beta and tumor necrosis factor-alpha stimulated prostate cancer cell lines./
作者:	Khatri, Jitender.
面頁冊數:	67 p.
附註:	Source: Dissertation Abstracts International, Volume: 72-08, Section: B, page: .
Contained By:	Dissertation Abstracts International72-08B.
標題:	Biology, Molecular. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3459190
ISBN:	9781124693804

The role of p38 mitogen activated protein kinase in post-transcriptional regulation of cyclooxygenase-2 in intleukin-1beta and tumor necrosis factor-alpha stimulated prostate cancer cell lines.
Khatri, Jitender.

The role of p38 mitogen activated protein kinase in post-transcriptional regulation of cyclooxygenase-2 in intleukin-1beta and tumor necrosis factor-alpha stimulated prostate cancer cell lines. - 67 p.

Source: Dissertation Abstracts International, Volume: 72-08, Section: B, page: .

Thesis (Ph.D.)--University of Massachusetts Lowell, 2011.

Cyclooxygenase (COX) the rate-limiting enzyme in prostaglandin (PG) synthesis exists in two principle isoforms, COX-1 and COX-2. A considerable body of evidence implicates COX-2 (and hence PG) up-regulation as a major factor in carcinogenesis in many tissues. In previous work, we have determined that the half-life of COX-2 mRNA is significantly increased in cytokine-stimulated human and rat cells. The objective of this work was to determine the putative molecular mechanisms that operate in human COX-2 mRNA stabilization by p38 mitogen activated protein kinase (MAPK) in normal and prostate cancer cell lines. I show that COX-2 up-regulation in human prostate cancer cells is, in part, induced by the stabilization of the COX-2 mRNA transcript by p38 MAPK.

ISBN: 9781124693804Subjects--Topical Terms:

1017719
Biology, Molecular.

The role of p38 mitogen activated protein kinase in post-transcriptional regulation of cyclooxygenase-2 in intleukin-1beta and tumor necrosis factor-alpha stimulated prostate cancer cell lines.
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245 1 4 $a The role of p38 mitogen activated protein kinase in post-transcriptional regulation of cyclooxygenase-2 in intleukin-1beta and tumor necrosis factor-alpha stimulated prostate cancer cell lines.
300 $a 67 p.
500 $a Source: Dissertation Abstracts International, Volume: 72-08, Section: B, page: .
500 $a Adviser: Bruce Jackson.
502 $a Thesis (Ph.D.)--University of Massachusetts Lowell, 2011.
520 $a Cyclooxygenase (COX) the rate-limiting enzyme in prostaglandin (PG) synthesis exists in two principle isoforms, COX-1 and COX-2. A considerable body of evidence implicates COX-2 (and hence PG) up-regulation as a major factor in carcinogenesis in many tissues. In previous work, we have determined that the half-life of COX-2 mRNA is significantly increased in cytokine-stimulated human and rat cells. The objective of this work was to determine the putative molecular mechanisms that operate in human COX-2 mRNA stabilization by p38 mitogen activated protein kinase (MAPK) in normal and prostate cancer cell lines. I show that COX-2 up-regulation in human prostate cancer cells is, in part, induced by the stabilization of the COX-2 mRNA transcript by p38 MAPK.
520 $a The human prostate cancer cell lines DU145 and PC3 were utilized in this study. I have determined that MAPK inhibitors down-regulate COX-2 mRNA levels in stimulated DU145 and PC-3 human prostate cancer cells but not in the normal prostate cell line, CRL2221. I found that DU145 cells treated with the specific p38 MAPK inhibitor, SB203580, showed significant decreases in COX-2 mRNA levels relative to the identically treated CRL2221 cells. In the present study, I also provide evidence that p38 MAPK pathway regulates stability of COX-2 mRNA and hence PG production in DU145 and PC3 cells. This inhibitory effect, however, is significantly less in CRL221 cells.
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