James M. Tepper
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View article: Temporal control of sgRNA library activation unlocks large-scale <i>in vivo</i> CRISPR screens
Temporal control of sgRNA library activation unlocks large-scale <i>in vivo</i> CRISPR screens Open
Functional genomics screens have illuminated genetic dependencies in cancer, but conventional in vitro approaches fail to capture vulnerabilities shaped by the tumor microenvironment. Here, we implement CRISPR-StAR (Stochastic Activation b…
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplementary Figure 4: Overexpression of RAC1 P29S increases cell viability of A375 to RAF and MEK inhibitor treatment.
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplementary Table 4. STR profiles for cell lines used in this study.
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplementary Table 3. IC50s (nM) and fold changes (FC) comparing IC50s of RAC1 wild-type and P29S mutant to GFP are shown for indicated drug, cell lines and expression plasmid.
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplementary Figure 5: Overexpression of RAC1 P29S increases cell viability of MALME-3M to RAF inhibitor treatment.
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplemental Figure Legends
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplementary Figure 4: Overexpression of RAC1 P29S increases cell viability of A375 to RAF and MEK inhibitor treatment.
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplementary Figure 6: RAC1 P29S knockdown increases sensitivity of IGR1 melanoma cell lines to MAPK inhibition.
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplementary Table 2. % viability at 1uM drug treatment compared to DMSO control for the NRAS Q61K mutant cell lines, CP66, HMVII, and WM3060 (expresses RAC1 P29S) are shown.
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplementary Figure 7. RAC1 P29S decreases effect of RAF inhibitor treatment on tumor growth in vivo.
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplementary Figure 1: Identification of RAC1 P29S mutant melanoma cell lines.
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplementary Figure 7. RAC1 P29S decreases effect of RAF inhibitor treatment on tumor growth in vivo.
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplementary Figure 5: Overexpression of RAC1 P29S increases cell viability of MALME-3M to RAF inhibitor treatment.
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplementary Table 4. STR profiles for cell lines used in this study.
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplementary Table 1. (Top) IC50 (nM), fold changes (FC) and (Bottom) % viability at 10uM drug treatment compared to DMSO control for BRAF mutant cell lines, A375, MALME-3M, 451Lu and IGR1 (expresses RAC1 P29S) are shown.
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplementary Table 3. IC50s (nM) and fold changes (FC) comparing IC50s of RAC1 wild-type and P29S mutant to GFP are shown for indicated drug, cell lines and expression plasmid.
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplementary Figure 6: RAC1 P29S knockdown increases sensitivity of IGR1 melanoma cell lines to MAPK inhibition.
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplementary Figure 3: Overexpression of RAC1 P29S increases cell viability of 451Lu cells to RAF and MEK inhibitor treatment.
View article: Data from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Following mutations in BRAF and NRAS, the RAC1 c.85C>T single-nucleotide variant (SNV) encoding P29S amino acid change represents the next most frequently observed protein-coding hotspot mutation in melanoma. However, the biologic and clin…
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplementary Figure 2: RAC1 P29S mutant melanoma cell lines have higher levels of activated RAC1.
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplementary Figure 1: Identification of RAC1 P29S mutant melanoma cell lines.
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplementary Table 1. (Top) IC50 (nM), fold changes (FC) and (Bottom) % viability at 10uM drug treatment compared to DMSO control for BRAF mutant cell lines, A375, MALME-3M, 451Lu and IGR1 (expresses RAC1 P29S) are shown.
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplementary Figure 3: Overexpression of RAC1 P29S increases cell viability of 451Lu cells to RAF and MEK inhibitor treatment.
View article: Data from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Following mutations in BRAF and NRAS, the RAC1 c.85C>T single-nucleotide variant (SNV) encoding P29S amino acid change represents the next most frequently observed protein-coding hotspot mutation in melanoma. However, the biologic and clin…
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplementary Figure 2: RAC1 P29S mutant melanoma cell lines have higher levels of activated RAC1.
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplemental Figure Legends
View article: Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF
Data Supplement from The RAC1 P29S Hotspot Mutation in Melanoma Confers Resistance to Pharmacological Inhibition of RAF Open
Supplementary Table 2. % viability at 1uM drug treatment compared to DMSO control for the NRAS Q61K mutant cell lines, CP66, HMVII, and WM3060 (expresses RAC1 P29S) are shown.
View article: Cholinergic control of striatal GABAergic microcircuits
Cholinergic control of striatal GABAergic microcircuits Open
Cholinergic interneurons (CINs) are essential elements of striatal circuits and functions. Although acetylcholine signaling via muscarinic receptors (mAChRs) has been well studied, more recent data indicate that postsynaptic nicotinic rece…
View article: Neuropilin 2/Plexin-A3 Receptors Regulate the Functional Connectivity and the Excitability in the Layers 4 and 5 of the Cerebral Cortex
Neuropilin 2/Plexin-A3 Receptors Regulate the Functional Connectivity and the Excitability in the Layers 4 and 5 of the Cerebral Cortex Open
The functions of cortical networks are progressively established during development by series of events shaping the neuronal connectivity. Synaptic elimination, which consists of removing the supernumerary connections generated during the …
View article: Cholinergic control of striatal GABAergic microcircuits
Cholinergic control of striatal GABAergic microcircuits Open
A bstract Cholinergic interneurons (CINs) are essential elements of striatal circuits and behaviors. While acetylcholine signaling via muscarinic receptors (mAChRs) have been well studied, more recent data indicate that postsynaptic nicoti…