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Epstein-Barr virus nuclear antigen 3...

Cooper, Andrew Christian.

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Epstein-Barr virus nuclear antigen 3A (EBNA-3A) can inhibit c-myc expression and lymphoblastoid cell growth.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Epstein-Barr virus nuclear antigen 3A (EBNA-3A) can inhibit c-myc expression and lymphoblastoid cell growth./
作者:	Cooper, Andrew Christian.
面頁冊數:	141 p.
附註:	Adviser: Elliott D. Kieff.
Contained By:	Dissertation Abstracts International63-04B.
標題:	Biology, Microbiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3051136
ISBN:	0493656448

Epstein-Barr virus nuclear antigen 3A (EBNA-3A) can inhibit c-myc expression and lymphoblastoid cell growth.
Cooper, Andrew Christian.

Epstein-Barr virus nuclear antigen 3A (EBNA-3A) can inhibit c-myc expression and lymphoblastoid cell growth. - 141 p.

Adviser: Elliott D. Kieff.

Thesis (Ph.D.)--Harvard University, 2002.

EBNA-3A is an EBV encoded nuclear protein that is essential for EBV primary B lymphocyte growth transformation into lymphoblastoid cell lines (LCLs). EBNA-3A, -3B, and -3C interact with the cellular transcription factor RBP-Jκ and in transient assays repress RBP-Jκ dependent transactivation by EBNA-2. We now find that conditional three-fold over-expression of EBNA-3A in the 1B4 LCL, but not in EBV negative Burkitt's lymphoma cells, results in a G0/G1 growth arrest. EBNA-3A over-expression increased EBNA-3A association with RBP-Jκ, decreased EBNA-2 association with RBP-Jκ, and down-regulated <italic>c-myc</italic> mRNA and protein; EBNA and LMP-1 expression were unaffected. Co-expression of a conditional <italic>c-myc</italic> partially restored S phase entry, resulting in apoptotic cell death. Thus, EBNA-3A is nearly at a level in LCLs where it can inhibit EBNA-2 association with RBP-Jκ and down-regulate <italic>c-myc</italic> transcription.

ISBN: 0493656448Subjects--Topical Terms:

1017734
Biology, Microbiology.

Epstein-Barr virus nuclear antigen 3A (EBNA-3A) can inhibit c-myc expression and lymphoblastoid cell growth.
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245 1 0 $a Epstein-Barr virus nuclear antigen 3A (EBNA-3A) can inhibit c-myc expression and lymphoblastoid cell growth.
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500 $a Source: Dissertation Abstracts International, Volume: 63-04, Section: B, page: 1695.
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520 $a EBNA-3A is an EBV encoded nuclear protein that is essential for EBV primary B lymphocyte growth transformation into lymphoblastoid cell lines (LCLs). EBNA-3A, -3B, and -3C interact with the cellular transcription factor RBP-Jκ and in transient assays repress RBP-Jκ dependent transactivation by EBNA-2. We now find that conditional three-fold over-expression of EBNA-3A in the 1B4 LCL, but not in EBV negative Burkitt's lymphoma cells, results in a G0/G1 growth arrest. EBNA-3A over-expression increased EBNA-3A association with RBP-Jκ, decreased EBNA-2 association with RBP-Jκ, and down-regulated <italic>c-myc</italic> mRNA and protein; EBNA and LMP-1 expression were unaffected. Co-expression of a conditional <italic>c-myc</italic> partially restored S phase entry, resulting in apoptotic cell death. Thus, EBNA-3A is nearly at a level in LCLs where it can inhibit EBNA-2 association with RBP-Jκ and down-regulate <italic>c-myc</italic> transcription.
520 $a EBNA-3A mutational analyses showed that interaction with RBP-Jκ and dissociation of EBNA-2 from RBP-Jκ are required for <italic>c-myc </italic> down-regulation and growth arrest. Although the amino terminal 277 amino acids of EBNA-3A, including a domain homologous to EBNA-3B and -3C (homology domain, HD), can bind RBP-Jκ <italic>in vitro</italic>, these residues are not sufficient for high level RBP-Jκ association, repression of EBNA-2 transactivation of a multimerized RBP-Jκ binding site reporter, down-regulation of <italic>c-myc</italic>, or inhibition of IB4 cell growth. However, the amino-terminal 523 amino acids of EBNA-3A were similar to wild-type EBNA-3A in all effects on EBNA-2 activity. Most importantly, alanine substitutions for three of five adjacent amino acids within the HD abrogated EBNA-3A repression in transient assays, decreased displacement of EBNA-2 from RBP-Jκ, prevented <italic> c-myc</italic> down-regulation, and did not inhibit LCL growth. Thus, strong EBNA-3A association with RBP-Jκ is required for competitive inhibition of the EBNA-2 association with RBP-Jκ, for down-regulation of <italic> c-myc</italic> expression, and for inhibition of LCL proliferation. These data implicate RBP-Jκ in mediating EBNA-2 effects at the <italic>c-myc </italic> promoter and support the hypothesis that RBP-Jκ can mediate <italic> c-myc</italic> promoter activation.
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