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Ras GTPases are prototypical members of the RAS superfamily and regulate cytosolic signaling pathways involved in gene expression, as well as regulation of cell proliferation, differentiation and survival. In humans there are 3 Ras genes, which are the most commonly identified oncogenes, found in approximately 20-30% of all cancers.
|Cat No||Product Name / Activity|
|Inhibits K-Ras localization to the plasma membrane; also L-type calcium channel blocker|
|Ras signaling inhibitor; inhibits Ack1 and GCK|
|6429||ML 210 New|
|Selectively kills mutant HRAS-expressing cells; glutathione peroxidase inhibitor; induces ferroptosis|
|RalA and RalB inhibitor|
|Ras inhibitor; also induces autophagy|
|Ras-Net (Elk-3) pathway inhibitor; also microtubule depolymerization agent and angiogenesis inhibitor|
|Ras signaling inhibitor; also potent farnesyl diphosphate (FPP) synthase inhibitor|
|Cat No||Product Name / Activity|
|High affinity PDEδ-KRas interaction inhibitor; binds to PDEδ|
Ras GTPases are prototypical members of the RAS superfamily and regulate signaling pathways involved in gene expression, as well as regulation of cell proliferation, differentiation and survival. They are known to interact with multiple intracellular signaling pathway members, including ERK, MAPK and MEK, as well as the PI3K/AKT/mTOR pathway.
In humans, there are 3 Ras genes; HRas, KRas and NRas, which encode 4 proteins. These genes are the most commonly identified oncogenes in humans and are found in approximately 20-30% of all cancers. Mutations in Ras genes result in the translation of permanently activated proteins, overactivation of pathways controlling cell growth and differentiation, oncogenesis and cancer. As well as the 4 proteins encoded by the Ras genes, the Ras subfamily of GTPases also includes RalA, RalB and Rap GTPases.
RAS proteins function as binary on-off switches that regulate diverse cytoplasmic signaling networks. In cancer and developmental disorders (RASopathies), mutationally activated RAS proteins drive aberrant signal transduction. This webinar discusses the vulnerabilities of RAS that have been exploited for the development of pharmacologic inhibitors of RAS function.Watch Now!
Tocris offers the following scientific literature for Ras GTPases to showcase our products. We invite you to request* or download your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
Written by Kirsten L. Bryant, Adrienne D. Cox and Channing J. Der, this review provides a comprehensive overview of RAS protein function and RAS mutations in cancer. Key signaling pathways are highlighted and therapeutic vulnerabilities are explored. This review also includes a detailed section on RAS drug discovery and targeting synthetic lethal interactors of mutant RAS. Compounds available from Tocris are listed.
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.
Adapted from the 2015 Cancer Product Guide Edition 3, this poster summarizes the main epigenetic targets in cancer. The dysregulation of epigenetic modifications has been shown to result in oncogenesis and cancer progression. Unlike genetic mutations, epigenetic alterations are considered to be reversible and thus make promising therapeutic targets.
|Gene||Species||Gene Symbol||Gene Accession No.||Protein Accession No.|