Product nameAnti-KRAS antibody - C-terminal
See all KRAS primary antibodies
DescriptionRabbit polyclonal to KRAS - C-terminal
SpecificityThe immunogen shares 64.2% sequence homology with RASN_HUMAN(P01111) with stretches of 7 similar amino acids between the two sequences, and 50% sequence homology with RASH_HUMAN(P01112) with stretches of 5 similar amino acids between the two sequences.
Tested applicationsSuitable for: Flow Cyt, WB, ICC/IFmore details
Species reactivityReacts with: Mouse, Human
Predicted to work with: Rat
Synthetic peptide within Human KRAS aa 145-174 (C terminal) conjugated to Keyhole Limpet Haemocyanin (KLH). The exact sequence is proprietary.
Database link: P01116
- Mouse NIH-3T3 cell line lysate, WiDr cells, HeLa cells.
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferPreservative: 0.09% Sodium azide
Constituent: 99.91% PBS
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab172949 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|Flow Cyt||1/10 - 1/50.
ab171870 - Rabbit polyclonal IgG, is suitable for use as an isotype control with this antibody.
|WB||1/100 - 1/500. Predicted molecular weight: 22 kDa.|
|ICC/IF||1/10 - 1/50.|
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
- c Ki ras2 antibody
- c Kirsten ras protein antibody
- c-K-ras antibody
Anti-KRAS antibody - C-terminal (ab172949) at 1/100 dilution + NIH-3T3 cell line lysate at 35 µg
Predicted band size: 22 kDa
Confocal immunofluorescent analysis of WiDr cells labeling KRAS with ab172949 at 1/10 dilution followed by Alexa Fluor 488-conjugated goat anti-rabbit lgG (green). Actin filaments have been labeled with Alexa Fluor 555 phalloidin (red). DAPI was used to stain the cell nuclear (blue).
Flow cytometric analysis of Hela cells (right histogram) compared to a negative control cell (left histogram) labeling KRAS with ab172949 at 1/10 dilution. FITC-conjugated goat-anti-rabbit secondary antibodies were used for the analysis.
This product has been referenced in:
- Zhu Z et al. Knockdown long noncoding RNA nuclear paraspeckle assembly transcript 1 suppresses colorectal cancer through modulating miR-193a-3p/KRAS. Cancer Med 8:261-275 (2019). Read more (PubMed: 30575330) »
- Cimino PJ et al. Plinabulin, an inhibitor of tubulin polymerization, targets KRAS signaling through disruption of endosomal recycling. Biomed Rep 10:218-224 (2019). Read more (PubMed: 30972217) »