Key features and details
- Expression system: Baculovirus infected Sf9 cells
- Purity: >= 90% SDS-PAGE
- Active: Yes
- Tags: His tag N-Terminus
- Suitable for: SDS-PAGE, Functional Studies
Product nameRecombinant human KRAS (mutated G13D) protein (Active)
See all KRAS proteins and peptides
Intrinsic GTPase reaction of KRAS (G13D) was conducted at room temperature for 60 min using 1 µM GTP.
Purity>= 90 % SDS-PAGE.
Expression systemBaculovirus infected Sf9 cells
Protein lengthProtein fragment
Predicted molecular weight22 kDa including tags
Amino acids2 to 185
TagsHis tag N-Terminus
Additional sequence informationGenbank: NM_033360
Our Abpromise guarantee covers the use of ab271580 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
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Preparation and Storage
Stability and Storage
Shipped on Dry Ice. Store at -80°C. Avoid freeze / thaw cycle.
Preservative: 1.22% Imidazole
Constituents: 0.63% Tris HCl, 0.64% Sodium chloride, 0.02% Potassium chloride, 0.04% Tween, 20% Glycerol, 0.05% DTT
This product is an active protein and may elicit a biological response in vivo, handle with caution.
- c Ki ras2
- c Kirsten ras protein
FunctionRas proteins bind GDP/GTP and possess intrinsic GTPase activity.
Involvement in diseaseDefects in KRAS are a cause of acute myelogenous leukemia (AML) [MIM:601626]. AML is a malignant disease in which hematopoietic precursors are arrested in an early stage of development.
Defects in KRAS are a cause of juvenile myelomonocytic leukemia (JMML) [MIM:607785]. JMML is a pediatric myelodysplastic syndrome that constitutes approximately 30% of childhood cases of myelodysplastic syndrome (MDS) and 2% of leukemia. It is characterized by leukocytosis with tissue infiltration and in vitro hypersensitivity of myeloid progenitors to granulocyte-macrophage colony stimulating factor.
Defects in KRAS are the cause of Noonan syndrome type 3 (NS3) [MIM:609942]. Noonan syndrome (NS) [MIM:163950] is a disorder characterized by dysmorphic facial features, short stature, hypertelorism, cardiac anomalies, deafness, motor delay, and a bleeding diathesis. It is a genetically heterogeneous and relatively common syndrome, with an estimated incidence of 1 in 1000-2500 live births. Rarely, NS is associated with juvenile myelomonocytic leukemia (JMML). NS3 inheritance is autosomal dominant.
Defects in KRAS are a cause of gastric cancer (GASC) [MIM:613659]; also called gastric cancer intestinal or stomach cancer. Gastric cancer is a malignant disease which starts in the stomach, can spread to the esophagus or the small intestine, and can extend through the stomach wall to nearby lymph nodes and organs. It also can metastasize to other parts of the body. The term gastric cancer or gastric carcinoma refers to adenocarcinoma of the stomach that accounts for most of all gastric malignant tumors. Two main histologic types are recognized, diffuse type and intestinal type carcinomas. Diffuse tumors are poorly differentiated infiltrating lesions, resulting in thickening of the stomach. In contrast, intestinal tumors are usually exophytic, often ulcerating, and associated with intestinal metaplasia of the stomach, most often observed in sporadic disease.
Note=Defects in KRAS are a cause of pylocytic astrocytoma (PA). Pylocytic astrocytomas are neoplasms of the brain and spinal cord derived from glial cells which vary from histologically benign forms to highly anaplastic and malignant tumors.
Defects in KRAS are a cause of cardiofaciocutaneous syndrome (CFC syndrome) [MIM:115150]; also known as cardio-facio-cutaneous syndrome. CFC syndrome is characterized by a distinctive facial appearance, heart defects and mental retardation. Heart defects include pulmonic stenosis, atrial septal defects and hypertrophic cardiomyopathy. Some affected individuals present with ectodermal abnormalities such as sparse, friable hair, hyperkeratotic skin lesions and a generalized ichthyosis-like condition. Typical facial features are similar to Noonan syndrome. They include high forehead with bitemporal constriction, hypoplastic supraorbital ridges, downslanting palpebral fissures, a depressed nasal bridge, and posteriorly angulated ears with prominent helices. The inheritance of CFC syndrome is autosomal dominant.
Note=KRAS mutations are involved in cancer development.
Sequence similaritiesBelongs to the small GTPase superfamily. Ras family.
Cellular localizationCell membrane.
- Information by UniProt
To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.
ab271580 has not yet been referenced specifically in any publications.