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"Finally, membranes from Rce1-deficient fibroblasts lacked the capacity to proteolytically process farnesylated Ha-Ras, N-Ras, and Ki-Ras or geranylgeranylated Ki-Ras."

"Unraveling the Arl2-mediated release mechanism of farnesylated KRas4B from PDE δ may facilitate therapeutic targeting."

"Furthermore, mutant K-Ras proteins which are farnesylated but which show no, or very weak, membrane association, are active in transformation [111]."

"This value is in similar to the previously published dissociation constant for binding of farnesylated K-Ras to CaM [ xref ]."

"One of the prominent targets of farnesylation in humans is a p21 GTPase, K-Ras4B. Our research demonstrates that K-Ras4B farnesylation increases the binding affinity for CaM."

"However, therapeutic strategies have focused on developing inhibitors that interfere with farnesylation of Kras, which is required for its activation."

"GGTase-I may geranylgeranylate K-Ras4B and other proteins that are typically farnesylated (Fig 3) ."

"Such Ras-binding partners were identified when it was shown that galectin-1 and galectin-3, xref respectively, act as specific binding partners only of farnesylated active H-Ras and K-Ras. xref , xref , xref Hydrophobic binding pockets in these galectins are the putative farnesyl-binding sites. xref , xref Galectin-1 drives the formation and participates as an integral component of H-Ras-GTP nanoclusters, the sites at which Raf is activated. xref Galectin-3 drives K-Ras-GTP nanoclustering, leading to robust Ras signaling. xref Interaction of nucleolin with N-Ras and the epidermal growth factor receptor was recently shown to synergistically support N-Ras transformation in vitro . xref Taken together, and assuming that compounds that block farnesyl-binding sites would act as Ras inhibitors, these findings point to the farnesyl-binding pockets as excellent potential targets for Ras-directed therapy."

"However, it was later found that, while K-Ras and N-Ras are normally farnesylated, they can be alternatively modified by geranylgeranylation [ xref – xref ]."

"FTIs act by inhibiting farnesyl-transferase, which has the downstream effect of impeding KRAS activation, this is because KRAS is farnesylated, which enables it to interact with the membrane and become activated by RAS-guanine nucleotide exchange factors (GEFs)."

"GTP or farnesylated K-Ras."

"GTP, but not non farnesylated K-Ras."

"Given the critical role of prenylation for KRAS membrane association and neoplastic transformation, and farnesylation of KRAS by FTase is the first step in the KRAS post-translational modification, FTase is the ideal target for KRAS-driven cancers."

"Given the critical role of prenylation for KRAS membrane association and neoplastic transformation, and farnesylation of KRAS by FTase is the first step in the KRAS post-translational modification, FTase is the ideal target for KRAS-driven cancers."

"Raltitrexed (Tomudex (R); AstraZeneca Pharmaceuticals, Holland) is a quinazoline folate analogue, which acts as a pure and specific thymidylate synthetase (TS) inhibitor, designed to inhibit K-ras protein farnesylation."

"Targeting Ras membrane association has also received renewed attention, with research focusing on compounds such as deltazinone 1 that compete for the farnesyl-binding pocket on phosphodiesterase-6 de[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

"Raltitrexed (Tomudex (R); AstraZeneca Pharmaceuticals, Holland) is a quinazoline folate analogue, which acts as a pure and specific thymidylate synthetase (TS) inhibitor, designed to inhibit K-ras protein farnesylation."

"Lonafarnib, which inhibits the farnesylation (and thus cell membrane targeting and function) of Kras, as well as the MEK inhibitor PD0325901 inhibited cell proliferation and the phosphorylation of FADD (XREF_FIG)."