Courtney A. Miller

This study identifies ATAT1 as a therapeutic target in glioblastoma by showing its role in promoting tumor invasion, proliferation, and resistance, with potential for combination therapies.

This study shows that Syngap1 haploinsufficiency in mice causes opposing cortical activity patterns, with reduced sensory responses and increased movement/arousal activity, revealing cell-type-dependent effects on network states.

The paper introduces Endo-GeneScreen, a platform that identifies small molecules regulating endogenous protein levels, and demonstrates its application in finding probes for Syngap1-related neurodevelopmental disorder.

This study shows that non-muscle myosin II overactivation occurs in dedifferentiating melanomas adapting to BRAF and MEK inhibitors, and targeting NMII with BMi reduces drug-tolerant persister cell survival.

The paper introduces MesoMap, a mesoscale proximity labeling method to study chromatin occupancy changes, showing how HDAC inhibitors and the drug SR-1815 affect gene expression.

This study shows that Syngap1 in cortical neurons is essential for sensorimotor integration and perception by shaping neural dynamics and connectivity.

This paper develops a selective non-muscle myosin II inhibitor, MT-228, with high brain penetration and efficacy in preclinical models, offering therapeutic potential for diseases like stimulant use disorder.

The paper shows that CRF2 receptor activation in the BLA during learning makes memory vulnerable to NMII inhibition, disrupting METH-associated memory but not COC-associated memory.

This study shows Syngap1 controls membrane excitability in cortical neurons, which is essential for proper circuit assembly during brain development.

The paper shows that specific SynGAP splice variants improve cognitive function and reduce seizures in mice.

This study shows that mice lacking the gastrin-releasing peptide gene exhibit enhanced fear conditioning and impaired extinction, with reduced dopamine-related gene transcription in the basolateral amygdala during stress-enhanced fear learning.

This study shows that SYNGAP1 loss-of-function in human neurons leads to enhanced dendritic morphogenesis, increased excitatory synapses, and altered network activity.

This study shows Syngap1 regulates plasticity of silent neurons in the somatosensory cortex during sensory experience, with implications for neurodevelopmental disorders.

The paper shows that METH learning causes long-lasting NMII-dependent spine motility in BLA neurons, which can be reversed by NMII inhibition.

The paper investigates how the SynGAP-1 PBM regulates NMDA receptor signaling and cognitive function in mice, finding that disrupting the PBM leads to synaptic and cognitive impairments.

The paper identifies mir-135b-5p as a regulator of persistent stress-enhanced memory and a potential therapeutic target and biomarker for PTSD.

This study shows that restoring SynGAP protein in adult Syngap1 heterozygous mice improves memory, seizure susceptibility, and brain activity patterns.

The paper identifies mir-598-3p as a miRNA involved in stress-enhanced fear memory in male mice, but not females, through effects on actin cytoskeleton regulation.

This study identifies long-lasting transcriptional and translational changes in the basolateral amygdala after a single acute stress event using integrative genomic and proteomic approaches.