Format
Sort by
Items per page

Send to

Choose Destination

Links from PubMed

Items: 1 to 20 of 210

1.

The Rela(p65) subunit of NF-kappaB is essential for inhibiting double-stranded RNA-induced cytotoxicity.

Li M, Shillinglaw W, Henzel WJ, Beg AA.

J Biol Chem. 2001 Jan 12;276(2):1185-94.

2.

Lack of essential role of NF-kappa B p50, RelA, and cRel subunits in virus-induced type 1 IFN expression.

Wang X, Hussain S, Wang EJ, Wang X, Li MO, García-Sastre A, Beg AA.

J Immunol. 2007 Jun 1;178(11):6770-6.

5.

Genetic deletion of PKR abrogates TNF-induced activation of IkappaBalpha kinase, JNK, Akt and cell proliferation but potentiates p44/p42 MAPK and p38 MAPK activation.

Takada Y, Ichikawa H, Pataer A, Swisher S, Aggarwal BB.

Oncogene. 2007 Feb 22;26(8):1201-12. Epub 2006 Aug 21.

PMID:
16924232
6.

Protein kinase R, IkappaB kinase-beta and NF-kappaB are required for human rhinovirus induced pro-inflammatory cytokine production in bronchial epithelial cells.

Edwards MR, Hewson CA, Laza-Stanca V, Lau HT, Mukaida N, Hershenson MB, Johnston SL.

Mol Immunol. 2007 Mar;44(7):1587-97. Epub 2006 Sep 20.

PMID:
16989899
7.
8.

IFN-alpha sensitizes human umbilical vein endothelial cells to apoptosis induced by double-stranded RNA.

Kaiser WJ, Kaufman JL, Offermann MK.

J Immunol. 2004 Feb 1;172(3):1699-710.

9.
11.
12.

The double-stranded RNA-activated protein kinase mediates radiation resistance in mouse embryo fibroblasts through nuclear factor kappaB and Akt activation.

von Holzen U, Pataer A, Raju U, Bocangel D, Vorburger SA, Liu Y, Lu X, Roth JA, Aggarwal BB, Barber GN, Keyomarsi K, Hunt KK, Swisher SG.

Clin Cancer Res. 2007 Oct 15;13(20):6032-9.

13.

Anti-apoptotic signalling by the Dot/Icm secretion system of L. pneumophila.

Abu-Zant A, Jones S, Asare R, Suttles J, Price C, Graham J, Kwaik YA.

Cell Microbiol. 2007 Jan;9(1):246-64. Epub 2006 Aug 15.

PMID:
16911566
16.

Caspase-mediated p65 cleavage promotes TRAIL-induced apoptosis.

Kim HS, Chang I, Kim JY, Choi KH, Lee MS.

Cancer Res. 2005 Jul 15;65(14):6111-9.

17.
18.
20.

Supplemental Content

Support Center