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Items: 30

1.

A noncanonical function of cGAMP in inflammasome priming and activation.

Swanson KV, Junkins RD, Kurkjian CJ, Holley-Guthrie E, Pendse AA, El Morabiti R, Petrucelli A, Barber GN, Benedict CA, Ting JP.

J Exp Med. 2017 Dec 4;214(12):3611-3626. doi: 10.1084/jem.20171749. Epub 2017 Oct 13.

2.

Porphyromonas gingivalis mediates inflammasome repression in polymicrobial cultures through a novel mechanism involving reduced endocytosis.

Taxman DJ, Swanson KV, Broglie PM, Wen H, Holley-Guthrie E, Huang MT, Callaway JB, Eitas TK, Duncan JA, Ting JP.

J Biol Chem. 2012 Sep 21;287(39):32791-9. Epub 2012 Jul 26.

3.

ASC-dependent RIP2 kinase regulates reduced PGE2 production in chronic periodontitis.

Taxman DJ, Lei Y, Zhang S, Holley-Guthrie E, Offenbacher S, Ting JP.

J Dent Res. 2012 Sep;91(9):877-82. doi: 10.1177/0022034512454541. Epub 2012 Jul 24.

4.

The NLR adaptor ASC/PYCARD regulates DUSP10, mitogen-activated protein kinase (MAPK), and chemokine induction independent of the inflammasome.

Taxman DJ, Holley-Guthrie EA, Huang MT, Moore CB, Bergstralh DT, Allen IC, Lei Y, Gris D, Ting JP.

J Biol Chem. 2011 Jun 3;286(22):19605-16. doi: 10.1074/jbc.M111.221077. Epub 2011 Apr 12.

5.

Critical role of apoptotic speck protein containing a caspase recruitment domain (ASC) and NLRP3 in causing necrosis and ASC speck formation induced by Porphyromonas gingivalis in human cells.

Huang MT, Taxman DJ, Holley-Guthrie EA, Moore CB, Willingham SB, Madden V, Parsons RK, Featherstone GL, Arnold RR, O'Connor BP, Ting JP.

J Immunol. 2009 Feb 15;182(4):2395-404. doi: 10.4049/jimmunol.0800909.

6.

Epstein-Barr virus lytic infection contributes to lymphoproliferative disease in a SCID mouse model.

Hong GK, Gulley ML, Feng WH, Delecluse HJ, Holley-Guthrie E, Kenney SC.

J Virol. 2005 Nov;79(22):13993-4003.

7.

The Epstein-Barr virus protein BMRF1 activates gastrin transcription.

Holley-Guthrie EA, Seaman WT, Bhende P, Merchant JL, Kenney SC.

J Virol. 2005 Jan;79(2):745-55.

8.

The Epstein-Barr virus polymerase accessory factor BMRF1 adopts a ring-shaped structure as visualized by electron microscopy.

Makhov AM, Subramanian D, Holley-Guthrie E, Kenney SC, Griffith JD.

J Biol Chem. 2004 Sep 24;279(39):40358-61. Epub 2004 Jul 30.

9.

The Epstein-Barr virus immediate-early protein BZLF1 induces expression of E2F-1 and other proteins involved in cell cycle progression in primary keratinocytes and gastric carcinoma cells.

Mauser A, Holley-Guthrie E, Zanation A, Yarborough W, Kaufmann W, Klingelhutz A, Seaman WT, Kenney S.

J Virol. 2002 Dec;76(24):12543-52.

10.

The Epstein-Barr virus immediate-early protein BZLF1 induces both a G(2) and a mitotic block.

Mauser A, Holley-Guthrie E, Simpson D, Kaufmann W, Kenney S.

J Virol. 2002 Oct;76(19):10030-7.

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Identification of transactivator and nuclear localization domains in the Epstein-Barr virus DNA polymerase accessory protein, BMRF1.

Zhang Q, Holley-Guthrie E, Dorsky D, Kenney S.

J Gen Virol. 1999 Jan;80 ( Pt 1):69-74.

PMID:
9934686
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Killing Epstein-Barr virus-positive B lymphocytes by gene therapy: comparing the efficacy of cytosine deaminase and herpes simplex virus thymidine kinase.

Rogers RP, Ge JQ, Holley-Guthrie E, Hoganson DK, Comstock KE, Olsen JC, Kenney S.

Hum Gene Ther. 1996 Dec 1;7(18):2235-45.

PMID:
8953314
18.

Epstein-Barr viral latency is disrupted by the immediate-early BRLF1 protein through a cell-specific mechanism.

Zalani S, Holley-Guthrie E, Kenney S.

Proc Natl Acad Sci U S A. 1996 Aug 20;93(17):9194-9.

19.

Functional and physical interactions between the Epstein-Barr virus (EBV) proteins BZLF1 and BMRF1: Effects on EBV transcription and lytic replication.

Zhang Q, Hong Y, Dorsky D, Holley-Guthrie E, Zalani S, Elshiekh NA, Kiehl A, Le T, Kenney S.

J Virol. 1996 Aug;70(8):5131-42.

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The bZIP transactivator of Epstein-Barr virus, BZLF1, functionally and physically interacts with the p65 subunit of NF-kappa B.

Gutsch DE, Holley-Guthrie EA, Zhang Q, Stein B, Blanar MA, Baldwin AS, Kenney SC.

Mol Cell Biol. 1994 Mar;14(3):1939-48.

22.

Direct BRLF1 binding is required for cooperative BZLF1/BRLF1 activation of the Epstein-Barr virus early promoter, BMRF1.

Quinlivan EB, Holley-Guthrie EA, Norris M, Gutsch D, Bachenheimer SL, Kenney SC.

Nucleic Acids Res. 1993 Jul 11;21(14):1999-2007.

23.

The Epstein-Barr virus immediate-early promoter BRLF1 can be activated by the cellular Sp1 transcription factor.

Zalani S, Holley-Guthrie EA, Gutsch DE, Kenney SC.

J Virol. 1992 Dec;66(12):7282-92.

24.

The cellular oncogene c-myb can interact synergistically with the Epstein-Barr virus BZLF1 transactivator in lymphoid cells.

Kenney SC, Holley-Guthrie E, Quinlivan EB, Gutsch D, Zhang Q, Bender T, Giot JF, Sergeant A.

Mol Cell Biol. 1992 Jan;12(1):136-46.

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The Epstein-Barr virus immediate-early gene product, BMLF1, acts in trans by a posttranscriptional mechanism which is reporter gene dependent.

Kenney S, Kamine J, Holley-Guthrie E, Mar EC, Lin JC, Markovitz D, Pagano J.

J Virol. 1989 Sep;63(9):3870-7.

29.

The Epstein-Barr virus (EBV) BZLF1 immediate-early gene product differentially affects latent versus productive EBV promoters.

Kenney S, Kamine J, Holley-Guthrie E, Lin JC, Mar EC, Pagano J.

J Virol. 1989 Apr;63(4):1729-36.

30.

Regulation of NAD metabolism in Salmonella typhimurium: genetic analysis and cloning of the nadR repressor locus.

Foster JW, Holley-Guthrie EA, Warren F.

Mol Gen Genet. 1987 Jun;208(1-2):279-87.

PMID:
3039308

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