Area:
Cell Biology, Genetics
We are testing a new system for linking grants to scientists.
The funding information displayed below comes from the
NIH Research Portfolio Online Reporting Tools and the
NSF Award Database.
The grant data on this page is limited to grants awarded in the United States and is thus partial. It can nonetheless be used to understand how funding patterns influence mentorship networks and vice-versa, which has deep implications on how research is done.
You can help! If you notice any innacuracies, please
sign in and mark grants as correct or incorrect matches.
Sign in to see low-probability grants and correct any errors in linkage between grants and researchers.
High-probability grants
According to our matching algorithm, Andrew W. Tai is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2008 |
Tai, Andrew Wen-Yuan |
F32Activity Code Description: To provide postdoctoral research training to individuals to broaden their scientific background and extend their potential for research in specified health-related areas. |
Whole-Genome Sirna Screen For Host Genes Supporting Hepatitis C Virus Replication @ Massachusetts General Hospital
[unreadable] DESCRIPTION (provided by applicant): Project Summary: Chronic hepatitis C virus (HCV) infection affects about 3 percent of the world's population and HCV cirrhosis is now the leading indication for liver transplantation in the United States. The best current therapy for chronic HCV infection (combination peginterferon and ribavirin) leads to sustained virologic responses in only about half of all treated individuals. However, there are subgroups that have much lower rates of treatment response, such as African Americans and people with HIV coinfection. There is therefore a great need for novel HCV therapies. Small molecule inhibitors of HCV proteins are promising, but it is clear that viral resistance develops quickly to such agents. We propose to identify host genes that serve as viral replication cofactors, with the rationale that cellular cofactors may be targets for HCV therapy. For example, cyclophilin B is a host protein that has been shown to be involved in HCV replication, and small molecule inhibitors of cyclophilin B are potent inhibitors of HCV replication both in vitro and in vivo. In this application, we will screen a whole human genome siRNA library against a HCV replicon cell line that encodes a luciferase reporter gene. siRNA downregulation of essential cellular cofactors is expected to block HCV replication and luciferase activity in this system. Preliminary studies show that high-throughput siRNA transfection of a HCV replicon cell line is feasible. We discuss methods of hit selection, as well as secondary screening steps designed to minimize the number of false positive results. Public Health Relevance Hepatitis C virus infection can cause serious liver disease, including cirrhosis and liver cancer. The best current therapy for HCV only works in about half of all treated people, and also can cause serious side effects. This project hopes to discover the human proteins that the virus needs to reproduce inside cells, as these might turn out to be possible targets for new HCV therapies. [unreadable] [unreadable] [unreadable]
|
0.906 |
2020 — 2021 |
Kidd, Jeffrey M (co-PI) [⬀] Tai, Andrew W. Telesnitsky, Alice [⬀] |
R21Activity Code Description: To encourage the development of new research activities in categorical program areas. (Support generally is restricted in level of support and in time.) |
Hiv-1 Genomic Rna Integrity @ University of Michigan At Ann Arbor
HIV-1 genomic RNA integrity Retroviruses are the only viruses that encapsidate two copies of their genetic material. One possible reason for this is that retroviral RNA appears to be damaged prior to reverse transcription; therefore, the presence of two copies of viral genomic RNA allows for successful reverse transcription through template switching. When virion RNA is examined on non-denaturing northern blots, it runs as a single dimer band. However, when heat- denatured to disrupt the dimer linkage, virion RNA includes a monomer band of reduced intensity compared to the dimer and also a smear of more rapidly-migrating RNAs, suggesting encapsidated RNA is extensively fragmented. Our central hypothesis is that this fragmentation of HIV-1 genomic RNA is due to the action of one or more host enzymes, the absence of which would lead to virions with more intact genomic RNAs and higher infectious titers. The objective of this proposal is to identify cellular genes that are associated with HIV- 1 RNA nicking using unbiased genetic screens and to test if these represent a new class of restriction factors. The proposed work combines Telesnitsky lab expertise in retroviral RNA with Tai lab expertise in whole- genome genetic screens for cellular factors that modulate viral infection plus Kidd lab expertise in specialized library preparation and bioinformatics, and consists of two aims: In Aim 1: we will seek to identify cellular genes that are required for observed damage to encapsidated HIV-1 RNAs using a whole-genome CRISPR library encoded in a lentiviral vector, and will validate candidate genes by using genetic depletion and rescue experiments. In Aim 2: we will assess properties of virion RNA fragmentation and examine its ramifications for viral replication. If successful, this project may reveal a new class of cellular restriction factors, may help illuminate novel cellular RNA processing pathways if the identified genes have not previously been shown to participate in RNA quality control, and may provide new insight into virion RNA structures and accessibility.
|
0.901 |