Overview
| 别名 | GTPase KRas; K-Ras 2; Ki-Ras; c-K-ras; c-Ki-ras) [Cleaved into: GTPase KRas; N-terminally processed] |
| 基因名 | KRAS |
| UniProt ID | P01116 |
| 反应种属 | Human |
| 应用 | IHC-P |
| 宿主 | Mouse |
| 偶联物 | Unconjugated |
| 修饰 | Unmodified |
| 亚型 | IgG2a |
| 克隆号 | 5D3-F6-M4 |
| 克隆性 | Monoclonal Antibody |
| 分子量 | Calculated MW: 21 kDa |
| 纯化方式 | Affinity Purified |
| 产品形式 | Liquid |
| 推荐稀释比 | IHC-1:250-1:500 |
| 存储缓冲液 | Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.09% sodium azide |
| 保存温度 | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| 背景信息 | KRAS proto-oncogene, GTPase (KRAS) is a small membrane-bound protein that functions as a molecular switch in signal transduction pathways regulating cell proliferation, differentiation, and survival. It cycles between an active GTP-bound state and an inactive GDP-bound state, a process tightly regulated by guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs). Once activated, KRAS triggers key downstream effector cascades, including the MAPK and PI3K/AKT pathways. The protein is anchored to the plasma membrane via a farnesylated C-terminal hypervariable region. KRAS is one of the most frequently mutated oncogenes in human cancer; specific hotspot mutations at residues G12, G13, and Q61 lock the protein in a constitutive GTP-bound state. These mutations are well-established drivers of tumorigenesis and therapy resistance, particularly in pancreatic, colorectal, and non-small cell lung cancers, where they correlate with aggressive disease and poor clinical outcomes. |
检测原理