原癌基因K-ras抗體,Anti-KRAS抗體Background: This gene, a Kirsten ras oncogene homolog from the mammalian ras gene family, encodes a protein that is a member of the small GTPase superfamily. A single amino acid substitution is responsible for an activating mutation. The transforming protein that results is implicated in various malignancies, including lung adenocarcinoma, mucinous adenoma, ductal carcinoma of the pancreas and colorectal carcinoma. Alternative splicing leads to variants encoding two isoforms that differ in the C-terminal region.
Ras, a proto-oncogene, is a small G-protein that has 3 primary isoforms (H-Ras, N-Ras, and K-Ras) that differ in there approximay 20 C-terminal amino acids. H-Ras was first discovered as a transforming product the retrovirus Harvey murine virus and K-Ras of Kirten sarcoma virus. Ras is a heavily studied target of both academic and pharmaceutical research because of its implications in various pathways and diseases as well as being mutated in a large number of human cancers. Ras is most notably the activator of the Erk/MAPK kinase pathway as activator of Raf, as well as an activator of PI3 Kinase (PI3K). In its oncogenic, mutated state, Ras is unable to hydrolyze GTP to GDP, thus staying in an active state and activating numerous pathways including the MAPK pathway through its activation of Raf, but also others as well that include PI3 Kinase and RalGDS. One path that the pharmaceutical industry has taken to control Ras and its activity is by finding what some consider its Achilles’ heel. For its activation, Ras must localize to the plasma membrane, but interestingly, it lacks a transmembrane domain. To achieve this, Ras must first undergo a post-translational modification (PTM) known as prenylation or geranylation at its C-terminal CAAX motif. For this to take place, a controlled three step process must occur. The first step in the process is the prenylation or geranylation of the C in the CAAX motif that is initiated by the covalent attachment of farnesyl groups to the cysteine that is catalyzed by the . After this modification, the and heterodimer enzymes farnesyl transferases –aaX of the motif is proteolytically removed via Rce1 (Ras Converting Enzyme 1), a membrane associated endoprotease, by a mechanism that is still not fully understood. Finally, the C-terminal prenylcysteine is now methlylated by ICMT (Isoprenylcysteine Carboxymethyl Transferase). These drugs have yet to pass clinical trials though and there is doubt that they will ever be successful in treating tumors associated with Ras activation
原癌基因K-ras抗體,Anti-KRAS抗體相關(guān)產(chǎn)品：
Anti-IRAK4(IL-1 Receptor-associated Kinase 4) 白介素-1受體相關(guān)激酶4抗體
Anti-IL-1RA (Interleukin-1 receptor antagonist) 白介素-1受體拮抗劑抗體
Anti-IL-1R1(interleukin-1 receptor type 1 precursor) 白介素1受體1抗體
Anti-IL-1RⅡ(interleukin-1 receptor Ⅱ) 白介素1受體Ⅱ抗體
Anti-IRF-4(Interferon regulatory factor 4) 干擾素調(diào)節(jié)因子4抗體
Anti-ILT2/CD85j(Immunoglobulin-like transcript 2) 細(xì)胞表面免疫球蛋白樣轉(zhuǎn)錄因子2抗體
Anti-IRS P53 (Insulin receptor substrate P53) 胰島素受體底物p53蛋白抗體
Anti-IRS-1 胰島素受體底物-1抗體
Anti-IRS-2 胰島素受體底物-2抗體
Anti-IRS-3 胰島素受體底物-3抗體
Anti-IRS-4 胰島素受體底物-4抗體
Anti-ISR（Insulin Receptor）（hu, cattle, mo, rat, horse, sheep, Rb, dog, chi） 胰島素受體抗體
Anti-ISR-α （Insulin Receptor-α） 胰島素受體-α抗體
Anti-ISR-β （Insulin Receptor-β） 胰島素受體-β抗體
Anti-Integrin α4/CD49d(Integrin alpha 4) 整合素α4抗體
原癌基因K-ras抗體,Anti-KRAS抗體Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
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