Key features and details
- Produced recombinantly (animal-free) for high batch-to-batch consistency and long term security of supply
- Rabbit monoclonal [EPR20141-212] to GTPase HRAS
- Suitable for: Sandwich ELISA
- Reacts with: Human
Product nameAnti-GTPase HRAS antibody [EPR20141-212]
See all GTPase HRAS primary antibodies
DescriptionRabbit monoclonal [EPR20141-212] to GTPase HRAS
Tested applicationsSuitable for: Sandwich ELISAmore details
Species reactivityReacts with: Human
The details of the immunogen for this antibody are not available.
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 bufferpH: 7.2
Preservative: 0.02% Sodium azide
Concentration information loading...
PurityProtein A purified
Our Abpromise guarantee covers the use of ab222550 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|Sandwich ELISA||Use at an assay dependent concentration.|
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
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.
ab222550 has not yet been referenced specifically in any publications.