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, Jin Wang is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2016 — 2020 |
Wang, Jin |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Molecular Regulation of Immunity to Viral Infections @ Methodist Hospital Research Institute
? DESCRIPTION (provided by applicant): Vaccination has been the most widely used strategy to protect against viral infections. The establishment of immunological memory is critical for the success of vaccines against future infections. However, the molecular mechanisms underlying the persistence of immunological memory cells in response to vaccines remain to be elucidated. We have found that autophagy plays a critical role in the long-term survival of memory B cells against influenza virus infection in mice. Compared to naïve B cells and germinal center B cells, memory B cells display elevated levels of basal autophagy with increased expression of genes that regulate autophagy initiation or autophagosome maturation. Mice with deficiency of autophagy in B cells show accelerated cell death in memory B cells after immunization with influenza, and fail to generate protective secondary antibody responses when re-challenged with the virus, resulting in high viral loads, widespread lung destruction and increased fatality. This suggests that autophagy is required for the survival of virus-specific memory B cells. Experiments are proposed to test the hypothesis that promoting autophagy can enhance the efficacy of vaccination against viral infections through the protection of memory B cells. The following studies are proposed: 1) To determine the mechanisms for active autophagy in memory B cells induced by influenza vaccination; 2) To investigate the mechanisms for autophagy in the protection of memory B cells induced by vaccination against influenza viruses; and 3) To determine whether induction of autophagy can boost immunological memory to influenza vaccination. In the long term, the knowledge gained from the study will be employed to develop novel strategies for boosting the efficacy of vaccination against viral pathogens by promoting the generation and maintenance of immunological memory cells in humans.
|
0.918 |
2016 — 2020 |
Wang, Jin |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Molecular Regulation of Long-Term Immune Memory @ Methodist Hospital Research Institute
? DESCRIPTION (provided by applicant): Effective generation and long-term maintenance of immune memory cells are critical for the success of vaccines against pathogens. Mice with autophagy deficiency in B cells show a severe defect in the maintenance of memory B cells after immunization, and succumb to viral infections due to failure to generate protective secondary antibody responses. Autophagy is required for the long-term persistence of memory B cells to protect against viral infections. Similarly, it has been shown that autophagy is also required for the protection of memory T cells. However, the precise mechanisms for autophagy in the protection of memory B cells remain to be defined. We have found that Nix and Bnip3, two Bcl-2 family members important for mitochondrial autophagy, are required for the generation of antigen-specific memory B cells. We hypothesize that autophagy is essential for the protection of mitochondrial functions to protect the survival and functions of memory B cells. We will perform the following experiments to test this hypothesis: 1) To determine the molecular mechanisms by which Nix and Bnip3- dependent mitochondrial autophagy protects antigen-specific memory B cells. Whether defective mitochondrial autophagy in Nix- and Bnip3-deficient memory B cells leads to aberrant metabolic functions will be determined; 2) To test the hypothesis that mitochondrial autophagy protects against cell death in memory B cells. Whether disruption of mitochondrial integrity leads to the release of mitochondrial ptoteins or DNA in the induction of cell death in memory B cells; and 3) To determine the molecular mechanisms for mitochondrial autophagy in memory B cells. The functions of novel Nix- and Bnip3-interacting proteins in the regulation of mitochondrial autophagy will be studied. The findings from this study may facilitate the development of better strategies to enhance the efficacy of vaccination against infections by targeting mitochondrial autophagy.
|
0.918 |
2021 |
Wang, Jin |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Targeting the Hiv-1 Reservoir in Myeloid Cells @ Methodist Hospital Research Institute
ABSTRACT HIV is reverse-transcribed and integrated into the DNA of host cells, resulting in persistent infections that are difficult to clear. To date, there is no effective cure to clear the virus from HIV- infected patients. We have shown an approach to eradicate HIV infections by selective elimination of host cells harboring replication-competent HIV (SECH). The SECH treatment can clear HIV-1 in over 50% mice reconstituted with a human immune system, and in blood samples from HIV-1- infected patients. SECH can clear HIV-infection not only in CD4 T cells, but also in macrophages and microglia cells. Experiments are proposed to determine how to improve the efficacy and safety for SECH in clearing HIV-infection in the macrophage lineage: 1) To improve the efficacy and specificity in the killing of HIV-1-infected macrophages. We have found that increased viral reactivation leads to improved viral clearance in humanized mice. We will identify drugs that show greater potentials in virus reactivation that could lead to better HIV clearance. We will examine the inflammatory potentials for IDB and alternative LRAs in macrophages, and determine what inflammatory cytokines may need to be targeted; 2) To determine how to improve the efficacy and safety in the clearance of HIV reservoir in the macrophage lineage in lymphoid organs and in the brain of humanized mice. We will evaluate whether alternative agents can improve the clearance of HIV-1 in humanized mice in vivo. We will also determine whether optimum SECH regimens can induce limited and controllable inflammatory responses. Our proposed work will provide novel insights into how targeting apoptosis and autophagy regulates the clearance of HIV infection in the macrophage lineage. The studies will facilitate the development of SECH clear HIV-1 infection in lymphoid organs and in the brain to achieve complete eradication of HIV-1.
|
0.918 |