Area:
eye development, Notch signaling, ubiquitin pathway, Angelman syndrome
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, Steven A. Vokes is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2012 — 2021 |
Vokes, Steven Alexander |
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. |
Cis-Regulatory Circuitry Underlying Hedgehog Mediated Limb Development @ University of Texas, Austin
DESCRIPTION (provided by applicant): Defects in the Hedgehog (Hh) pathway underlie a vast spectrum of human birth defects, including holoprosencephaly, cleft palate, and polydactyly. Hh signaling controls transcription by regulating the activity of Gli transcription factors. A thorough understanding of how Gli proteins recognize and activate transcriptional targets is therefore necessary to understand the genes and processes that are misregulated in Hh-associated birth defects. However, virtually nothing is known about how Gli proteins recognize target genes and interact with other transcriptional inputs. The aim of this proposal is to define active Gli enhancers and to determine their interactions in a Hh- responsive cis regulatory network that underlies limb development. In the first approach, we will use an innovative approach to identify Hh-responsive, active enhancers different genetic backgrounds. This data will be used to construct a global gene regulatory network, defining an important set of extragenic regions with the collective potential to mediate the transcriptional effects of the Hh pathway. In a second in vivo-centered approach, we will determine the requirement for additional co-activating factors in the transcriptional regulation of Hh target genes. Finally, we will determine if the Hh and BMP pathways co-regulate target genes, focusing on the regulation the developmentally important gene, Gremlin. This study will transform our understanding of limb development by identifying active Gli enhancers and target genes in the limb, defining enhancer domains and determining co-factors. These will provide an invaluable resource for future studies and will provide a solid foundation for a systems-level understanding of limb development. The identification of these enhancers will also provide an important genomic resource for clinical scientists seeking to understand the mechanisms underlying the spectrum of BMP and Hh-associated birth defects and the hundreds of clinically distinct forms of human polydactyly. PUBLIC HEALTH RELEVANCE: The results obtained from these experiments will advance our understanding of how hedgehog signaling leads to a regulated transcriptional response. They will also increase our understanding of transcriptional processes during development. Together, these results will contribute to an understanding of the mechanisms underlying the large number of hedgehog-mediated birth defects.
|
1 |
2017 — 2021 |
Vokes, Steven Alexander Wallingford, John B [⬀] |
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 Genetics of Mammalian Larynx and Vocal Fold Development @ University of Texas, Austin
Abstract: Vocal communication underlies almost every aspect of human social interactions, yet we know almost nothing about the developmental biology of the organs of vocalization, the larynx and vocal folds. This is a significant issue because problems with voice are a common but poorly understood aspect of many human structural birth defects, and the resulting difficulty in communication has a profound effect on patients' quality of life. Here, we propose to develop the mouse as a model for normal and pathological development of the larynx and vocal folds. We will systematically characterize embryonic lineages and gene expression patterns in the diverse tissues of the mouse larynx, and we will characterize pathological laryngeal development in mouse models of human birth defect syndromes. We will also take a systems biology approach to defining gene regulatory circuitry underlying mammalian laryngeal development. By combining genetic fate mapping, molecular genetics, and systems biology, the experiments proposed here will provide a modern foundation from which we can assemble a detailed mechanistic understanding of laryngeal development and gain molecular insights into the etiology of human laryngeal birth defects.
|
1 |