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, Hongju Wu is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2009 — 2013 |
Wu, Hongju |
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. |
Improving Islet Transplantation Outcome With Akt1 @ Tulane University of Louisiana
DESCRIPTION (provided by applicant): Summary Islet transplantation is becoming a potential cure for type 1 diabetes (T1D). However, the limited supply and significant islet loss in the peritransplant period are cast as the major limitations of this treatment strategy. This project is aimed to improve the therapeutic outcome of islet transplantation by introducing constitutively active Akt1 (CA-Akt1) into the insulin producing 2-cells ex vivo. The serine/threonine protein kinase Akt/PKB is the direct downstream target of PI3 Kinase pathway, and has been found to have dual functions of anti-apoptosis and induction of cell proliferation. Relevance of Akt on 2-cell survival and proliferation has been demonstrated in studies of transgenic and knockout mouse models, as well as using pharmacological methods. Nonetheless, in order to realize the therapeutic potential of CA-Akt1, a safe, efficient and specific vector is needed to deliver Akt1 into islet 2-cells ex vivo. In this regard, adenovirus serotype 5 (Ad5)-based vector is of great interest. Our previous studies have demonstrated the modified Ad5 vector, AdRGDpK7, exhibited significantly higher gene transfer efficiency for the human islet cells. We thus propose to employ Ad5RGDpK7 to deliver Akt1 into islet cells ex vivo. To further diminish the potential adverse effect of CA-Akt1, we will restrict exogenous Akt1 expression in 2-cells by employment of 2-cell specific promoter-rat insulin promoter (RIP) to drive Akt1 expression. In addition, we propose to co-express a dual functional modality, HSV-TK, with CA-Akt1 so that it can be used as both a non-invasive imaging modality to follow the transplanted islets and a suicide gene should malignancy occur. Our specific aims are thus: 1) To develop a 2-cell specific, infectivity-enhanced Ad5 vector that allows efficient and specific CA-Akt1 and HSV-TK gene delivery into 2-cells ex vivo; 2) To examine the capacity of the Ad5 vector developed above to promote islet survival and proliferation while minimizing transformation, thus enhancing the efficacy of islet transplantation; and 3) To evaluate the safety of the Ad5 vector developed above in the context of islet transplantation.
|
1 |
2016 — 2018 |
Wu, Hongju |
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. |
Pax4-Induced Alpha-to-Beta Cell Conversion @ Tulane University of Louisiana
SUMMARY Cell-based therapy is promising strategy for the cure of insulin deficient diabetes. One of such strategies, islet transplantation, has achieved remarkable success over the past decade, but its use is limited due to islet supply and graft survival. Another cell-based strategy is to regenerate the insulin-producing ?-cells from other cell types. In the preliminary studies, we explored a strategy to regenerate ?-cells from the neighboring glucagon-producing ?-cells in pancreatic islets. Specifically, we explored Pax4, a transcription factor critical for the determination of ?- vs ?-cell lineage during development, for this purpose. Our data showed Pax4 gene transfer into ?TC1.9 cells, a clonal ?-cell line, induced them to adopt ?-cell phenotype. We also found Pax4 gene transfer into primary human islets significantly improved ?-cell function, and had circumstantial evidence indicating Pax4 not only promoted ?-cell survival, but also induced ?-to-? cell conversion. Despite the extensive preliminary studies, more investigations are required in order to fully realize the therapeutic potential of Pax4 and to thoroughly understand its actions. We thus propose two specific aims in this project: 1) To investigate whether Pax4 gene transfer into donor human islets improves the therapeutic efficacy of islet transplantation; and 2) To investigate whether Pax4 induces ?-to-? cell conversion in primary islets and in vivo using lineage-tracing technology. Clearly, the project will provide important information regarding the therapeutic actions and potential of Pax4 for diabetes treatment.
|
0.942 |