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, Aboozar Monavarfeshani is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2020 — 2021 |
Monavarfeshani, Aboozar |
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. |
Uncovering Novel Targets For Retinal Ganglion Cell Neuroprotection and Axon Regeneration @ Boston Children's Hospital
Project Summary Like other neurons of the central nervous system, retinal ganglion cells (RGCs)?the projection neurons of the retina?fail to regenerate after injury. In glaucoma, a leading cause of blindness, degeneration of RGC axons and their subsequent death are two key pathological events that lead to irreversible loss of vision. However, no effective treatments to prevent RGC vulnerability and loss are available. A critical obstacle toward developing novel therapeutics is our insufficient understanding of mechanisms that regulate RGC survival and axon regeneration. Using mouse optic nerve crush (ONC) model, previously, we discovered that removal of phosphatase and tensin homolog (PTEN) protein significantly promotes axon regeneration. More recently, we leveraged ONC model and undertook a large-scale in vivo CRISPR screen to identify key regulators of such mechanisms. Our screen revealed multiple genes whose removal from retinal cells promoted RGC survival and/or axon regeneration. One of the strongest protective phenotypes belonged to the knockout of the c-Jun N- terminal kinases-Interacting Protein 3 (JIP3). However, knockout of JIP3 not only fails to promote axon regeneration in survived RGCs, it abolishes axon regeneration induced by PTEN deletion. Here, I propose performing transcriptomic analysis of RGCs with or without JIP3 and/or PTEN at different time points after optic nerve injury to further investigate molecular programs underlying JIP3-dependent RGC survival, and PTEN- dependent axon regeneration. Furthermore, I will test the neuroprotective effect of JIP3 in a mouse glaucoma model in which elevation of intraocular pressure causes RGC loss.
|
1 |