Recombinant Human KRAS (mutated Q61H) protein (ab96817)
Key features and details
- Expression system: Escherichia coli
- Purity: > 90% SDS-PAGE
- Tags: His tag N-Terminus
- Suitable for: MS, SDS-PAGE, WB
Description
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Product name
Recombinant Human KRAS (mutated Q61H) protein
See all KRAS proteins and peptides -
Purity
> 90 % SDS-PAGE.
ab96817 is purified using conventional chromatography techniques. -
Expression system
Escherichia coli -
Accession
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Protein length
Full length protein -
Animal free
No -
Nature
Recombinant -
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Species
Human -
Sequence
MGSSHHHHHH SSGLVPRGSH MTEYKLVVVG AGGVGKSALT IQLIQNHFVD EYDPTIEDSY RKQVVIDGET CLLDILDTAG HEEYSAMRDQ YMRTGEGFLC VFAINNTKSF EDIHHYREQI KRVKDSEDVP MVLVGNKCDL PSRTVDTKQA QDLARSYGIP FIETSAKTRQ GVDDAFYTLV REIRKHKEKM SKDGKKKKKK SKTKC -
Predicted molecular weight
23 kDa including tags -
Amino acids
1 to 185 -
Modifications
mutated Q61H -
Tags
His tag N-Terminus -
Additional sequence information
Corresponds to K-Ras4B (Isoform 2B)
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Associated products
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Related Products
Specifications
Our Abpromise guarantee covers the use of ab96817 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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Applications
Mass Spectrometry
SDS-PAGE
Western blot
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Mass spectrometry
MALDI-TOF-TOF -
Form
Liquid -
Additional notes
Isoform 2B
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Concentration information loading...
Preparation and Storage
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Stability and Storage
Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
pH: 8.00
Constituents: 0.0154% DTT, 0.316% Tris HCl, 10% Glycerol, 0.58% Sodium chloride
General Info
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Alternative names
- c Ki ras2
- c Kirsten ras protein
- c-K-ras
see all -
Function
Ras proteins bind GDP/GTP and possess intrinsic GTPase activity. -
Involvement in disease
Defects 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 similarities
Belongs to the small GTPase superfamily. Ras family. -
Cellular localization
Cell membrane. - Information by UniProt
Images
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15% SDS-PAGE showing ab96817 at approximately 23.2 kDa (3 µg).
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MALTI-TOF result: of 23253.422 Da for Human KRAS (mutated Q61H) protein.
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This blot was produced using a 4-12% Bis-tris gel under the MES buffer system. The gel was run at 200V for 35 minutes before being transferred onto a Nitrocellulose membrane at 30V for 70 minutes. The membrane was then blocked for an hour using 5% Bovine Serum Albumin before being incubated with ab84573 overnight at 4°C. Antibody binding was detected using an anti-rabbit antibody conjugated to HRP, and visualised using ECL development solution.
Protocols
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.
Datasheets and documents
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SDS download
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Datasheet download
References (6)
ab96817 has been referenced in 6 publications.
- Sakamoto K et al. Generation of KS-58 as the first K-Ras(G12D)-inhibitory peptide presenting anti-cancer activity in vivo. Sci Rep 10:21671 (2020). PubMed: 33303890
- Sutton MN et al. DIRAS3 (ARHI) Blocks RAS/MAPK Signaling by Binding Directly to RAS and Disrupting RAS Clusters. Cell Rep 29:3448-3459.e6 (2019). PubMed: 31825828
- Xie C et al. Identification of a New Potent Inhibitor Targeting KRAS in Non-small Cell Lung Cancer Cells. Front Pharmacol 8:823 (2017). PubMed: 29184501
- Carné Trécesson S et al. BCL-XLdirectly modulates RAS signalling to favour cancer cell stemness. Nat Commun 8:1123 (2017). PubMed: 29066722
- Siprashvili Z et al. The noncoding RNAs SNORD50A and SNORD50B bind K-Ras and are recurrently deleted in human cancer. Nat Genet 48:53-8 (2016). PubMed: 26595770
- Lesur A et al. Screening protein isoforms predictive for cancer using immunoaffinity capture and fast LC-MS in PRM mode. Proteomics Clin Appl 9:695-705 (2015). PubMed: 25656350