Frank McCormick, Ph.D., F.R.S., is the David A. Wood Distinguished Professor of Tumor Biology and Cancer Research at the University of California, San Francisco (UCSF) Helen Diller Family Comprehensive Cancer Center, and the leader of the RAS Initiative at the National Cancer Institute. His current research focuses on the understanding of RAS GTPases and how they can be therapeutically targeted in RAS-driven cancers, which are some of the most commonly occurring and most difficult to treat.
SFARI is pleased to announce that it expects to have funded 22 grants in response to the Explorer Awards request for applications (RFA) this year.
New Simons VIP Phase 2 data were recently added to SFARI Base. This data release included data from individuals with 16p11.2 copy number variants, 1q21.1 CNVs and mutations in the following single genes: ADNP, ASXL3, CHAMP1, CHD8, CSNK2A1, DYRK1A, GRIN2B, HIVEP2, HNRNPH2, MED13L, PACS1, PPP2R5D, SCN2A, SETBP1, STXBP1 and SYNGAP1.
Jess Cardin and Michael J. Higley will establish a functional screen (using a CRISPR/Cas9-induced gene disruption system and multiscale in vivo calcium imaging in awake mice) for the assessment of common cellular- and circuit-level cortical dysregulation phenotypes associated with mutations in ASD risk genes.
SFARI is pleased to announce that it intends to fund 36 grants (15 Pilot Awards and 21 Research Awards) in response to the 2018 Pilot and Research Awards request for applications.
The animal models module of SFARI Gene has recently been expanded to include two new species: Drosophila melanogaster and Danio rerio. As of now, the database lists 55 genes for Drosophila models and 24 genes for zebrafish models, in addition to several models induced by biological or chemical agents.
Frank McCormick will address the biochemical mechanism by which mutations in SYNGAP1 drive ASD and intellectual disability. Elucidation of the mechanism of SYNGAP1 negative regulation of RAS and its effector pathways in neurons will further our understanding of the role of this pathway in health and disease, and will shed light on potential ways in which targeted RAS pathway inhibition may be therapeutically relevant.
Sung Eun “Samuel” Kwon plans to use a recently developed optical reporter of ERK activity, combined with a neuronal activity reporter, to monitor the dynamics of ERK signaling and neuronal activity in awake-behaving SynGAP mutant mice.
New Simons VIP Phase 2 data were recently added to SFARI Base. This data release included data from individuals with 16p11.2 copy number variants (CNVs), 1q21.1 CNVs and mutations in the following single genes: ADNP, ASXL3, DYRK1A, FOXP1, GRIN2B, HIVEP2, MED13L, PACS1, PPP2R5D, SCN2A, SETBP1, STXBP1 and SYNGAP1.
Based on the critical role of silent synapses in developmental neurocircuit refinement, Oliver Schlüter aims to assess whether ASD-risk genes encoding proteins associated with glutamate receptor complexes play a common role in silent synapse development. Using three different ASD mouse models (Shank3, Syngap1 and Nlgn3 deficiency), Schlüter will assess whether alterations in silent synapse maturation represent a common mechanistic defect underlying the distinct phenotypic facets of ASDs.
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