Murat Günel

This study shows human claustrum neurons encode uncertainty and prediction errors during aversive learning, with distinct temporal profiles compared to anterior cingulate cortex.

This study identifies multicellular spatial molecular programs in meningiomas using multi-omic data and develops a model to infer these programs from histopathology.

The paper shows mitochondrial state in zebrafish tip cells encodes brain collateral network topology, with microRNA-125a regulating mitochondrial function to influence vascular resilience.

The paper identifies phenotype-specific signaling networks in glioblastoma cells, showing that invasive spread is linked to DNA damage response and AKT-mTOR activation, with 14-3-3 proteins mediating phosphorylation and predictive phospho-site signatures for patient survival.

This study uses endoluminal biopsy and single-cell proteomics to analyze immune profiles in intracranial aneurysms, identifying immune signatures linked to aneurysm stability and rupture.

This study investigates the role of cytokine and FGF2 signaling in inducing entosis and vasculogenic mimicry in glioblastoma, linking macrophage activity to alternative vascularization mechanisms.

This study shows PTEN mutations cause ventriculomegaly and cortical network dysfunction through neural precursor and interneuron dysregulation, with mTORC1 inhibition offering therapeutic potential.

The paper identifies genetic variants in RASA1 and EPHB4 associated with vein of Galen malformations through exome analysis and single-cell transcriptomics.

The paper introduces spARC, a method to recover spatial signaling networks in gliomas, revealing an Osteopontin-CD44 interaction enriched in grade IV astrocytomas.

The paper identifies a recurrent start codon mutation in UGP2 causing a severe epileptic encephalopathy, showing that isoform-specific expression loss of an essential gene can lead to disease.

This study uses an AAV-mediated CRISPR screen in mice to identify functional suppressors of glioblastoma, revealing novel and canonical tumor suppressors and their interactions.