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KRAS-Dependent Glycolytic Reprogramming of Endothelial Cells in Sporadic Arteriovenous Malformations

ABSTRACT: Brain arteriovenous malformation (bAVM) is a disease characterized by the formation of tangled blood vessels with direct connections between arteries and veins. There is currently limited understanding of the underlying molecular mechanisms that are responsible for the development of bAVM. Our previous work identified the presence of somatic activating KRAS mutations in endothelial cells (ECs) isolated from clinical bAVM tissue. As such, we performed this proteomics study to profile the molecular impact of mutant KRAS expression on endothelial biology. We engineered a human EC model with doxycycline-inducible expression of mutant KRAS G12V. As mutant KRAS ECs preferentially activated the MAPK/ERK signaling cascade with no change to the activities of PI3K/AKT or MAPK/p38 pathways, we also included a MEK inhibitor (SL327) in this study to delineate MEK-dependent versus MEK-independent proteome changes.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Endothelial Cell

SUBMITTER: Ruilin Wu

LAB HEAD: Jason E.

PROVIDER: PXD062375 | Pride | 2025-12-14

REPOSITORIES: Pride

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			Action	DRS
	38766_HUVEC_KRASTMT16_20220611_NBCC133_88min_F1_20220630003604.raw	Raw
	38767_HUVEC_KRASTMT16_20220611_NBCC133_88min_F2_20220630033041.raw	Raw
	38768_HUVEC_KRASTMT16_20220611_NBCC133_88min_F3_20220630062516.raw	Raw
	38769_HUVEC_KRASTMT16_20220611_NBCC133_88min_F4_20220630091951.raw	Raw
	38770_HUVEC_KRASTMT16_20220611_NBCC133_88min_F5_20220630135400.raw	Raw

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