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Ras GTPases

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.

Products
Background
Literature
Gene Data

Inhibitors
Cat No Product Name / Activity
6407 Fendiline Hydrochloride
Inhibits K-Ras localization to the plasma membrane; also L-type calcium channel blocker
5607 GNF 7
Ras signaling inhibitor; inhibits Ack1 and GCK
6429 ML 210
Selectively kills mutant HRAS-expressing cells; glutathione peroxidase inhibitor; induces ferroptosis
5411 RBC8
RalA and RalB inhibitor
4989 Salirasib
Ras inhibitor; also induces autophagy
3101 XRP44X
Ras-Net (Elk-3) pathway inhibitor; also microtubule depolymerization agent and angiogenesis inhibitor
6111 Zoledronic Acid
Ras signaling inhibitor; also potent farnesyl diphosphate (FPP) synthase inhibitor

Other
Cat No Product Name / Activity
5424 Deltarasin
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 Oncoproteins

Therapeutic Vulnerabilities

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.

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RAS Oncoproteins

External sources of pharmacological information for Ras GTPases :

    Literature for Ras GTPases

    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.

    Cancer

    Cancer Research Product Guide

    A collection of over 750 products for cancer research, the guide includes research tools for the study of:

    • Cancer Metabolism
    • Epigenetics in Cancer
    • Receptor Signaling
    • Cell Cycle and DNA Damage Repair
    • Angiogenesis
    • Invasion and Metastasis
    RAS Oncoproteins

    RAS Oncoproteins Scientific Review

    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.

    Cell Cycle & DNA Damage Repair

    Cell Cycle & DNA Damage Repair Poster

    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.

    Epigenetics in Cancer

    Epigenetics in Cancer Poster

    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.

    Ras GTPases Gene Data

    Gene Species Gene Symbol Gene Accession No. Protein Accession No.
    HRas Human HRAS NM_176795 P01112
    Mouse Hras NM_008284 Q61411
    Rat Hras NM_001098241 NP_001091711
    KRas Human KRAS NM_033360 P01116
    Mouse Kras NM_021284 P32883
    Rat Kras NM_031515 NP_113703
    NRas Human NRAS NM_002524 P01111
    Mouse Nras NM_010937 P08556
    Rat Nras NM_080766 NP_542944
    RalA Human RALA NM_005402 P11233
    Mouse Rala NM_019491 P63321
    Rat Rala NM_031093 NP_112355
    RalB Human RALB NM_002881 P11234
    Mouse Ralb NM_022327 Q9JIW9
    Rat Ralb NM_053821 NP_446273