Lane 1: MCF-7 cell lysate
Lane 2: 293T cell lysate
Lane 3: mouse brain tissue lysate
Recombinant Rabbit monoclonal primary
Recombinant Ras Monoclonal Antibody (ET1601-16)
Synthetic peptide within human ras aa 20-50.
MCF-7 cell lysate, 293T cell lysate, mouse brain tissue lysate, Hela.
Store at +4C after thawing. Aliquot store at -20C or -80C. Avoid repeated freeze / thaw cycles.
1*TBS (pH7.4), 0.05% BSA, 40% Glycerol. Preservative: 0.05% Sodium Azide.
Protein A affinity purified.
C-BAS/HAS antibody; c-H-ras antibody; C-HA-RAS1 antibody; CTLO antibody; GTPase HRas antibody; GTPase KRas antibody; GTPase NRas antibody; H-Ras-1 antibody; H-RASIDX antibody; Ha-Ras antibody; HAMSV antibody; HRAS antibody; HRAS1 antibody; K RAS2A antibody; K RAS2B antibody; K RAS4A antibody; K RAS4B antibody; K-RAS antibody; KRAS antibody; KRAS1 antibody; KRAS2 antibody; N-RAS antibody; N-terminally processed antibody; NRAS antibody; NRAS1 antibody; p21ras antibody; RASH_HUMAN antibody; RASH1 antibody; RASK2 antibody; Transforming protein p21 antibody; v Ha ras Harvey rat sarcoma viral oncogene homolog antibody; v Ki ras2 Kirsten rat sarcoma viral oncogene homolog antibody; v ras neuroblastoma RAS viral oncogene homolog antibody
Belongs to the small GTPase superfamily. Ras family.
Palmitoylated by the ZDHHC9-GOLGA7 complex. Depalmitoylated by ABHD17A, ABHD17B and ABHD17C. A continuous cycle of de- and re-palmitoylation regulates rapid exchange between plasma membrane and Golgi.; Acetylation at Lys-104 prevents interaction with guanine nucleotide exchange factors (GEFs).; Ubiquitinated by the BCR(LZTR1) E3 ubiquitin ligase complex at Lys-170 in a non-degradative manner, leading to inhibit Ras signaling by decreasing Ras association with membranes.; Phosphorylation at Ser-89 by STK19 enhances NRAS-association with its downstream effectors.
Cytoplasm, Cell membrane, Golgi apparatus.
Ras superfamily is a protein superfamily of small GTPases, which are all related, to a degree, to the Ras protein subfamily (the key human members of which are KRAS, NRAS, and HRAS). Receptor tyrosine kinases and G protein-coupled receptors activate Ras, which then stimulates the Raf-MEK-MAPK pathway. GTPase-activating proteins (GAP) normally facilitate the inactivation of Ras. However, research studies have shown that in 30% of human tumors, point mutations in Ras prevent the GAP-mediated inhibition of this pathway. The most common oncogenic Ras mutation found in tumors is Gly12 to Asp12 (G12D), which prevents Ras inactivation, possibly by increasing the overall rigidity of the protein. This antibody is predicted to react with H-Ras, N-Ras and K-Ras.