Figure 2.

KRAS signaling in non-small-cell lung cancer (NSCLC). Schematic presentation of signaling pathways initiated by oncogenic KRAS aberrations is illustrated in a simplified fashion. RAF: rat fibrosarcoma; MEK: mitogen-activated protein kinase kinase; ERK: extracellular regulated kinase; PI3K: phosphoinositide 3-kinase; AKT: protein kinase B; mTOR: mechanistic target of rapamycin kinase; RALGDS: Ral guanine nucleotide dissociation stimulator; KRAS: Kirsten rat sarcoma viral oncogene homolog; CDK4/6: cyclin-dependent kinase 4/6; RHOA: Ras homolog family member; FAK: focal adhesion kinase; IKK: IkappaB kinase; IκB: nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor; NF-κB: nuclear factor ‘kappa-light-chain-enhancer’ of activated B-cells; Bad: BCL2-associated agonist of cell death; BCL-XL: B-cell lymphoma-extra large; RAL: Ras-like protein; PLD1: phospholipase D1; TBK1: TANK binding kinase 1; TIAM1: T lymphoma invasion and metastasis-inducing protein 1; RAC: Ras-related C3 botulinum toxin substrate 1; JNK: c-Jun N-terminal kinase.