The HARC Center has engaged in a significant number of collaborations, both with members of the existing CHEETAH and PCHPI Centers and with members of the broader HIV and structure communities. Our systems-to-structure approach has lent itself naturally to extensive interactions, with particular excitement over the global HIV proteomic results. For example, Wes Sundquist and collaborators in CHEETAH have analyzed the set of Gag interacting proteins, which is not a focus of the HARC Center biology, and have uncovered several exciting viral phenotypes, established biochemical interactions, and solved the crystal structure of one interacting domain. Our goal is to emulate this paradigm to the greatest extent possible, by engaging even more of the HIV community, as well as those studying areas of host cell biology that pertain to possible connections to HIV. We propose three mechanisms to accomplish this: First we will continue outreach efforts with known investigators working in areas related to the Center projects on the viral accessory and regulatory proteins, or on technology development. The current panel of collaborations is described below. Second, we will establish a Collaborative Opportunity Fund, with an emphasis on encouraging new or non-HIV investigators to apply for funding with ideas relevant to the Center, as detailed below. Third, if Center funding is renewed, we propose to mobilize the other HIV Structure Centers to host a joint international symposium at UCSF focused broadly on HIV-host interactions. In that context, we hope to define any new emerging areas relevant to the structural biology of the interactions, with a wide net cast that might lead to extended collaborative efforts, perhaps in the broader contexts of host-pathogen interactions or drug design and possibly with other NIH-funded Center initiatives.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Specialized Center (P50)
Project #
5P50GM082250-09
Application #
8927013
Study Section
Special Emphasis Panel (ZRG1-AARR-K)
Project Start
Project End
2016-08-31
Budget Start
2015-09-01
Budget End
2016-08-31
Support Year
9
Fiscal Year
2015
Total Cost
$490,516
Indirect Cost
$159,875
Name
University of California San Francisco
Department
Type
DUNS #
094878337
City
San Francisco
State
CA
Country
United States
Zip Code
94143
Palovcak, Eugene; Wang, Feng; Zheng, Shawn Q et al. (2018) A simple and robust procedure for preparing graphene-oxide cryo-EM grids. J Struct Biol 204:80-84
Tambe, Akshay; East-Seletsky, Alexandra; Knott, Gavin J et al. (2018) RNA Binding and HEPN-Nuclease Activation Are Decoupled in CRISPR-Cas13a. Cell Rep 24:1025-1036
Paulo, Esther; Wu, Dongmei; Wang, Yangmeng et al. (2018) Sympathetic inputs regulate adaptive thermogenesis in brown adipose tissue through cAMP-Salt inducible kinase axis. Sci Rep 8:11001
Faust, Tyler B; Li, Yang; Bacon, Curtis W et al. (2018) The HIV-1 Tat protein recruits a ubiquitin ligase to reorganize the 7SK snRNP for transcriptional activation. Elife 7:
Eckhardt, Manon; Zhang, Wei; Gross, Andrew M et al. (2018) Multiple Routes to Oncogenesis Are Promoted by the Human Papillomavirus-Host Protein Network. Cancer Discov 8:1474-1489
Masand, Ruchi; Paulo, Esther; Wu, Dongmei et al. (2018) Proteome Imbalance of Mitochondrial Electron Transport Chain in Brown Adipocytes Leads to Metabolic Benefits. Cell Metab 27:616-629.e4
Binning, Jennifer M; Smith, Amber M; Hultquist, Judd F et al. (2018) Fab-based inhibitors reveal ubiquitin independent functions for HIV Vif neutralization of APOBEC3 restriction factors. PLoS Pathog 14:e1006830
Morris, Kyle L; Buffalo, Cosmo Z; Stürzel, Christina M et al. (2018) HIV-1 Nefs Are Cargo-Sensitive AP-1 Trimerization Switches in Tetherin Downregulation. Cell 174:659-671.e14
Chen, Si-Han; Jang, Gwendolyn M; Hüttenhain, Ruth et al. (2018) CRL4AMBRA1 targets Elongin C for ubiquitination and degradation to modulate CRL5 signaling. EMBO J 37:
Leoz, Marie; Kukanja, Petra; Luo, Zeping et al. (2018) HEXIM1-Tat chimera inhibits HIV-1 replication. PLoS Pathog 14:e1007402

Showing the most recent 10 out of 199 publications