Abstract

The Protein Expression Facility will provide investigators a common source of highly purified proteins and the technical knowledge for use of these proteins to meet the experimental objectives of this Program Project. The Protein Expression Facility will consolidate the efforts of five laboratories into one facility, eliminating unnecessary duplication of technical expertise and decreasing expenses for technical staff, while providing quality control for critical reagents. The Facility will provide functional fragments of TNF receptor and related receptors and their signaling molecules using baculovirus and bacterial expression systems. A formalized procedure for establishing priority reagent requests among the investigators is described. The Facility will be located at UC Riverside.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Program Projects (P01)
Project #
5P01CA069381-03
Application #
6103187
Study Section
Project Start
1998-07-01
Project End
1999-06-30
Budget Start
Budget End
Support Year
3
Fiscal Year
1998
Total Cost
Indirect Cost

  Institution

Name
Sanford-Burnham Medical Research Institute
Department
Type
DUNS #
009214214
City
La Jolla
State
CA
Country
United States
Zip Code
92037

  Publications

Xu, X-P; Zhai, D; Kim, E et al. (2013) Three-dimensional structure of Bax-mediated pores in membrane bilayers. Cell Death Dis 4:e683
Chipuk, Jerry E; McStay, Gavin P; Bharti, Archana et al. (2012) Sphingolipid metabolism cooperates with BAK and BAX to promote the mitochondrial pathway of apoptosis. Cell 148:988-1000
Fujikura, D; Ito, M; Chiba, S et al. (2012) CLIPR-59 regulates TNF-?-induced apoptosis by controlling ubiquitination of RIP1. Cell Death Dis 3:e264
Oberst, Andrew; Dillon, Christopher P; Weinlich, Ricardo et al. (2011) Catalytic activity of the caspase-8-FLIP(L) complex inhibits RIPK3-dependent necrosis. Nature 471:363-7
Leverrier, S; Salvesen, G S; Walsh, C M (2011) Enzymatically active single chain caspase-8 maintains T-cell survival during clonal expansion. Cell Death Differ 18:90-8
Krajewska, Maryla; You, Zerong; Rong, Juan et al. (2011) Neuronal deletion of caspase 8 protects against brain injury in mouse models of controlled cortical impact and kainic acid-induced excitotoxicity. PLoS One 6:e24341
Akpan, Nsikan; Serrano-Saiz, Esther; Zacharia, Brad E et al. (2011) Intranasal delivery of caspase-9 inhibitor reduces caspase-6-dependent axon/neuron loss and improves neurological function after stroke. J Neurosci 31:8894-904
Zervoudi, Efthalia; Papakyriakou, Athanasios; Georgiadou, Dimitra et al. (2011) Probing the S1 specificity pocket of the aminopeptidases that generate antigenic peptides. Biochem J 435:411-20
Pop, Cristina; Oberst, Andrew; Drag, Marcin et al. (2011) FLIP(L) induces caspase 8 activity in the absence of interdomain caspase 8 cleavage and alters substrate specificity. Biochem J 433:447-457
Cheung, Timothy C; Ware, Carl F (2011) The canonical and unconventional ligands of the herpesvirus entry mediator. Adv Exp Med Biol 691:353-62

Showing the most recent 10 out of 192 publications