This antibody is specific for human K-Ras (K-Ras2, Ki-Ras, c-K-ras, GTPase KRas) protein (accession # NP_004976.2, P01116), which is 100% homologous with mouse, 95% with rat, and 94% with bovine, respectively. Reactivity has been confirmed on western blots with human HeLa and WI-38 cell lysates as well as rat KNRK and mouse NIH 3T3 cell lysates, and identifies the target band at~21 kDa. The reactivity has been also confirmed with rat KNRK cells using immunoprecipitation and with HeLa cells by immunofluorescence. Based on amino acid sequence homology, reactivity with bovine is also expected.
The mammalian Ras oncogene family of retrovirus-associated DNA sequences (ras) originally isolated from Harvey (H-Ras, HaRas, RasH) and Kirsten (K-Ras, Ki-Ras, RasK) murine sarcoma viruses. Ras genes are widely conserved among animal species and sequences corresponding to both H-Ras and K-Ras genes have been detected in human, avian, murine, and non-vertebrate genomes. Multiple transcript variants, which encode different isoforms, have been identified for this gene. The closely related N-Ras gene has been detected in human neuroblastoma and sarcoma cell lines. Among the three Ras proto-oncogenes, K-Ras is the most important in terms of its impact on human cancer. Ras proteins transduce signals from membrane-bound receptors via multiple downstream effector pathways and thereby affect fundamental cellular processes, including proliferation, apoptosis, and differentiation. K-Ras acts as a molecular switch. This protein undergoes a continuous cycle of de- and re-palmitoylation, which regulates its rapid exchange between the plasma membrane and the Golgi apparatus. In its normal form, the protein can be turned on and off to control pathways that regulate cell growth. The mutated form, however, is locked in the ""on"" position, causing cells to grow uncontrollably and, at the same time, turning off apoptosis. The nucleotide GTP (guanidine triphosphate) engages the switch to keep it in the ""on"" state. A portion of the Ras protein has an enzyme activity (a GTPase) which cleaves the GTP. This turns the switch ""off"" after the brief ""on"" period. In reality, the mutations of Ras do indeed inactivate a function, as most mutations are expected to do. The GTPase is inactivated by the mutations. Mutations in this gene cause Costello syndrome, a disease characterized by increased growth at the prenatal stage, growth deficiency at the postnatal stage, predisposition to tumor formation, mental retardation, skin and musculoskeletal abnormalities, distinctive facial appearance, and cardiovascular abnormalities. K-Ras activating mutations play a key role in neoplastic progression and are particularly prevalent in colorectal, pancreatic, and lung cancers. Defects in this gene are also implicated in bladder cancer, follicular thyroid cancer, and oral squamous cell carcinoma. Mutations of the K-Ras gene occur in over 90% of pancreatic carcinomas, making K-Ras proto-oncogene an important candidate for molecular targeted therapy.
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Protein Aliases: C-K-RAS; c-K-ras2 protein; c-Ki-ras; c-Kirsten-ras protein; c-Kirsten-ras proto-oncogene; cellular c-Ki-ras2; cellular c-Ki-ras2 proto-oncogene; GTPase KRas; K-Ras 2; K-ras p21 protein; K-RAS2A; K-RAS2B; K-RAS4A; K-RAS4B; KI-RAS; Kirsten rat sarcoma oncogene 2, expressed; Kirsten rat sarcoma viral oncogene homolog; Kirsten rat sarcoma viral oncogene homologue 2 (active); Kirsten rat sarcoma-2 viral (v-Ki-ras2) oncogene homolog; KRAS1; KRAS2; oncogene KRAS2; p21 protein; PR310 c-K-ras oncogene; RASK; RASK2; transforming protein p21; v-Ki-ras2 Kirsten rat sarcoma 2 viral oncogene homolog; v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog
Gene Aliases: AI929937; C-K-RAS; c-Ki-ras; CFC2; K-ras; K-RAS2A; K-RAS2B; K-RAS4A; K-RAS4B; KI-RAS; KRAS; Kras-2; KRAS1; KRAS2; NS; NS3; p21; p21B; RALD; ras; RASK2