Optimized conditions for GTP loading of Ras
Ras and the small GTPase group are essential for myriad cellular processes and cycle between GDP- and GTP-loaded states to allow stringent control of downstream signaling pathways. Biochemical studies of small GTPases can therefore require a specific nucleotide-bound state. Small GTPases possess basal intrinsic activity to process GTP into GDP plus inorganic phosphate; therefore, in vitro exchange of GDP for GTP is necessary for assays on GTP-loaded states. Here, we assess the methodology of in vitro nucleotide exchange for soluble H-Ras. We begin by describing a protocol to quantify the nucleotide-bound content of H-Ras using anion exchange chromatography and use this protocol to investigate optimal strategies for loading Ras with GTP by assessing the effects of time, temperature, H-Ras concentration, magnesium, excess nucleotide, and isoform identity. Together, we achieve a maximum of approximately 80% GTP-loading efficiency. We continue by considering storage of GTP-loaded H-Ras and present optimal conditions to minimize intrinsic GTP hydrolysis. Finally, we conclude by investigating the nucleotide composition of recombinantly expressed H-Ras encompassing cancer mutations at residues Gly12, Gly13, and Gln61 and find each to increase bound GTP compared with wildtype H-Ras. We therefore describe a methodology to quantitatively analyze the nucleotide content of small GTPases and their mutants and demonstrate conditions to achieve efficient GTP loading of Ras.
Authors
- Titus J. Boggon (ORCID: https://orcid.org/0000-0003-2862-1637)
- Kimberly J. Vish (ORCID: https://orcid.org/0000-0002-9394-1218)
- M Paul (ORCID: https://orcid.org/0000-0001-5551-1893)
- Asha P. Rollins (ORCID: https://orcid.org/0009-0004-0907-6295)
Institutions
- Yale Cancer Center (US)
- Yale University (US)
- Quantitative BioSciences (US)
Publication Details
- Journal
- Journal of Biological Chemistry
- Published
- 2025-11-07
- DOI
- https://doi.org/10.1016/j.jbc.2025.110923
- Primary Topic
- Protein Kinase Regulation and GTPase Signaling
- Type
- article
- Field-Weighted Citation Impact
- 0.00