Oncogenic K-Ras proteins, such as K-RasG12D, accumulate in the active, guanosine
triphosphate (GTP)–bound conformation and stimulate signaling through effector kinases …

When overexpressed in primary erythroid progenitors, oncogenic Ras leads to the
constitutive activation of its downstream signaling pathways, severe block of terminal …

How do Ras isoforms attain oncogenic specificity at the membrane? Oncogenic KRas,
HRas, and NRas (K-Ras, H-Ras, and N-Ras) differentially populate distinct cancers. How …

Defining how cancer-associated mutations perturb signaling networks in stem/progenitor
populations that are integral to tumor formation and maintenance is a fundamental problem …

Depending on the cellular context, Ras can activate characteristic effectors by mechanisms
still poorly understood. Promotion by galectin-1 of Ras activation of Raf-1 but not of …

About 18% of all human cancers carry a mutation in the KRAS gene making it among the
most sought-after anti-cancer targets. However, mutant KRas protein has proved remarkably …

Reversing the aberrant biochemical output of oncogenic Ras proteins is one of the great
challenges in cancer therapeutics; however, it is uncertain which Ras effectors are required …

Somatic KRAS mutations are highly prevalent in many cancers. In addition, a distinct
spectrum of germline KRAS mutations causes developmental disorders called RASopathies …

Activating mutations in the K-Ras small GTPase are extensively found in human tumors.
Although these mutations induce the generation of a constitutively GTP-loaded, active form …

Fine tuning of Ras activity is widely known as a mechanism to induce different cellular
responses. Recently, we have shown that calmodulin (CaM) binds to K-Ras and that K-Ras …