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High-probability grants
According to our matching algorithm, Barrington G. Burnett is the likely recipient of the following grants.
| Years |
Recipients |
Code |
Title / Keywords |
Matching
score |
| 2016 — 2020 |
Burnett, Barrington G |
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 Ubiquitin Proteasome System to Treat Spinal Muscular Atrophy @ Henry M. Jackson Fdn For the Adv Mil/Med
? DESCRIPTION (provided by applicant): Spinal muscular atrophy (SMA) is the most common inherited cause of death in infants and young children. SMA is caused by the deletion or mutation in the survival of motor neuron 1 (SMN1) gene, leading to a deficiency of the ubiquitously expressed SMN protein. Currently, there is no effective treatment option available for SMA. Evidence from studies in humans and rodents suggests that increasing SMN protein levels in the central nervous system is sufficient to ameliorate the disease phenotype and prolong survival. To identify protective modifiers of SMN protein levels we performed a genome-wide RNAi screen. Genes we identified in this screen will allow us to investigate genetic modifiers and molecular pathways that regulate SMN protein levels. These targets and pathways should provide novel avenues for therapeutic development for the treatment of SMA.
|
0.913 |
| 2021 |
Burnett, Barrington G
Flagg, Thomas |
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. |
Calcium Dysregulation and Cell Function in Spinal Muscular Atrophy @ Henry M. Jackson Fdn For the Adv Mil/Med
PROJECT SUMMARY/ABSTRACT Spinal muscular atrophy (SMA) is one of the most common inherited cause of death in infants and young children. SMA is caused by the deletion or mutation in the survival of motor neuron 1 (SMN1) gene, leading to a deficiency of the ubiquitously expressed SMN protein. Recent approved therapies increase SMN protein and partially correct the motor neuron loss and muscle degeneration that are hallmarks of the disease. However, SMA patients require critical care as a result of cardiopulmonary impairment and opportunistic infections. This observation, together with extensive new preliminary data, leads us to hypothesize that SMN-deficiency impairs cardiomyocyte function, representing a previously unrecognized contribution of the cardiovascular system on SMA disease pathology. To test this hypothesis, we will use primary cardiomyocytes from a mouse model of the disease and human cardiomyocytes derived from SMA patient induced pluripotent stem cells (iPSC) to determine the consequences of SMN deficiency on contractile function (Aim 1), the molecular mechanisms leading to impaired contraction (Aim 2), and characterize cardiovascular deficiencies following SMN restoration in SMA mice (Aim 3). The preliminary results using our unique approach are already providing novel mechanistic insight into a poorly understood aspect of the SMA disease process which could be critically important when designing strategies to manage the disease clinically.
|
0.913 |