Product nameAnti-Ras antibody [F132-62]
See all Ras primary antibodies
DescriptionMouse monoclonal [F132-62] to Ras
SpecificityReactive with the Ras translational products of the H-, K- and N-ras human, as well as mouse and rat c- and v-ras oncogenes. We have received mixed results for Western Blot.
Tested applicationsSuitable for: ICC/IF, IHC-Fr, IHC-P, IP, ICC, Flow Cytmore details
Species reactivityReacts with: Mouse, Rat, Human
Recombinant full length protein (Human).
- Sw480 or Y1 cells or normal skin tissue.
Storage instructionsStore at +4°C short term (1-2 weeks). Store at +4°C. Avoid freeze / thaw cycle.
Storage bufferPreservative: 0.1% Sodium azide
Constituents: 0.2% Gelatin, 0.82% Sodium phosphate
Concentration information loading...
PurityProtein A purified
Our Abpromise guarantee covers the use of ab16907 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|ICC/IF||Use at an assay dependent concentration.|
|IHC-Fr||Use a concentration of 5 µg/ml.|
|IHC-P||Use a concentration of 5 µg/ml.|
|IP||Use a concentration of 4 µg/ml.|
|ICC||Use a concentration of 2 µg/ml.|
|Flow Cyt||Use 1µg for 106 cells.
ab170192 - Mouse monoclonal IgG2b, is suitable for use as an isotype control with this antibody.
FunctionRas proteins bind GDP/GTP and possess intrinsic GTPase activity.
Involvement in diseaseDefects in HRAS are the cause of faciocutaneoskeletal syndrome (FCSS) [MIM:218040]. A rare condition characterized by prenatally increased growth, postnatal growth deficiency, mental retardation, distinctive facial appearance, cardiovascular abnormalities (typically pulmonic stenosis, hypertrophic cardiomyopathy and/or atrial tachycardia), tumor predisposition, skin and musculoskeletal abnormalities.
Defects in HRAS are the cause of congenital myopathy with excess of muscle spindles (CMEMS) [MIM:218040]. CMEMS is a variant of Costello syndrome.
Defects in HRAS may be a cause of susceptibility to Hurthle cell thyroid carcinoma (HCTC) [MIM:607464]. Hurthle cell thyroid carcinoma accounts for approximately 3% of all thyroid cancers. Although they are classified as variants of follicular neoplasms, they are more often multifocal and somewhat more aggressive and are less likely to take up iodine than are other follicular neoplasms.
Note=Mutations which change positions 12, 13 or 61 activate the potential of HRAS to transform cultured cells and are implicated in a variety of human tumors.
Defects in HRAS are a cause of susceptibility to bladder cancer (BLC) [MIM:109800]. A malignancy originating in tissues of the urinary bladder. It often presents with multiple tumors appearing at different times and at different sites in the bladder. Most bladder cancers are transitional cell carcinomas. They begin in cells that normally make up the inner lining of the bladder. Other types of bladder cancer include squamous cell carcinoma (cancer that begins in thin, flat cells) and adenocarcinoma (cancer that begins in cells that make and release mucus and other fluids). Bladder cancer is a complex disorder with both genetic and environmental influences.
Note=Defects in HRAS are the cause of oral squamous cell carcinoma (OSCC).
Sequence similaritiesBelongs to the small GTPase superfamily. Ras family.
modificationsPalmitoylated by the ZDHHC9-GOLGA7 complex. A continuous cycle of de- and re-palmitoylation regulates rapid exchange between plasma membrane and Golgi.
S-nitrosylated; critical for redox regulation. Important for stimulating guanine nucleotide exchange. No structural perturbation on nitrosylation.
Cellular localizationCell membrane. Golgi apparatus membrane. The active GTP-bound form is localized most strongly to membranes than the inactive GDP-bound form (By similarity). Shuttles between the plasma membrane and the Golgi apparatus.
- Information by UniProt
- C-BAS/HAS antibody
- c-H-ras antibody
- C-HA-RAS1 antibody
Overlay histogram showing HeLa cells stained with ab16907 (red line). The cells were fixed with 4% paraformaldehyde (10 min) and then permeabilized with 0.1% PBS-Tween for 20 min. The cells were then incubated in 1x PBS / 10% normal goat serum / 0.3M glycine to block non-specific protein-protein interactions followed by the antibody (ab16907, 1µg/1x106 cells) for 30 min at 22°C. The secondary antibody used was DyLight® 488 goat anti-mouse IgG (H+L) (ab96879) at 1/500 dilution for 30 min at 22°C. Isotype control antibody (black line) was mouse IgG2b [PLPV219] (ab91366, 2µg/1x106 cells) used under the same conditions. Acquisition of >5,000 events was performed. This antibody gave a positive signal in HeLa cells fixed with 100% methanol (5 min)/permeabilized in 0.1% PBS-Tween used under the same conditions.
This product has been referenced in:
- Choi BH et al. RAS GTPases are modified by SUMOylation. Oncotarget 9:4440-4450 (2018). Read more (PubMed: 29435114) »
- Aguilera O et al. Vitamin C uncouples the Warburg metabolic switch in KRAS mutant colon cancer. Oncotarget 7:47954-47965 (2016). Read more (PubMed: 27323830) »