Granton A. Jindal
Princeton University
15 Papers
20 Citations
Granton A. Jindal is an academic researcher from Princeton University. The author has contributed to research in topics: Enhancer & Biology. The author has an hindex of 9, co-authored 11 publications. Previous affiliations of Granton A. Jindal include California Institute of Technology & University of California, San Diego.
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Papers
Enhancer grammar in development, evolution, and disease: dependencies and interplay.
Granton A. Jindal,Emma K. Farley +1 more
TL;DR: In this paper, the authors introduce dependency grammar, a model where enhancers encode information based on dependencies between enhancer features shaped by mechanistic, evolutionary, and biological constraints, and classify enhancers based on the types of dependencies.
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RASopathies: unraveling mechanisms with animal models
Granton A. Jindal,Yogesh Goyal,Rebecca D. Burdine,Katherine A. Rauen,Stanislav Y. Shvartsman +4 more
TL;DR: An up-to-date review of animal models of RASopathies at the molecular and functional level, and how increasingly sophisticated techniques of genetic engineering can be used to rigorously connect changes in specific components of the Ras-MAPK pathway with observed functional and morphological phenotypes is discussed.
Gdf3 is required for robust Nodal signaling during germ layer formation and left-right patterning
TL;DR: The data indicate that gdf3 is critical for robust Nodal signaling at multiple stages in zebrafish embryonic development, including proper development of regional cell morphology in Kupffer’s vesicle and the establishment of southpaw expression in the lateral plate mesoderm.
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Divergent effects of intrinsically active MEK variants on developmental Ras signaling
Yogesh Goyal,Granton A. Jindal,Jose L Pelliccia,Kei Yamaya,Eyan Yeung,Alan S. Futran,Rebecca D. Burdine,Trudi Schüpbach,Stanislav Y. Shvartsman +8 more
TL;DR: Surprisingly, it is discovered that intrinsically active MEK variants can both increase and reduce the levels of pathway activation in vivo, implying that some of the emerging phenotypes in RASopathies may be caused by increased, as well as attenuated, levels of Ras signaling.
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In vivo severity ranking of Ras pathway mutations associated with developmental disorders.
Granton A. Jindal,Yogesh Goyal,Kei Yamaya,Alan S. Futran,Iason Kountouridis,Courtney A Balgobin,Trudi Schüpbach,Rebecca D. Burdine,Stanislav Y. Shvartsman +8 more
TL;DR: A quantitative, inexpensive, and rapid framework that relies on the early zebrafish embryo to assess mutational effects on a common scale is developed, providing the first step in the development of rational guidelines for patient-specific diagnostics and treatment of RASopathies.
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