Recombinant Human H-Ras (G12V) protein (Tagged) (ab90627)
Key features and details
- Expression system: Escherichia coli
- Purity: > 95% SDS-PAGE
- Tags: GST tag N-Terminus
- Suitable for: SDS-PAGE, Functional Studies
Description
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Product name
Recombinant Human H-Ras (G12V) protein (Tagged)
See all H-Ras (G12V) proteins and peptides -
Purity
> 95 % SDS-PAGE. -
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
MTEYKLVVVG AGGVGKSALT IQLIQNHFVD EYDPTIEDSY RKQVVIDGET CLLDILDTAG QEEYSAMRDQ YMRTGEGFLC VFAINNTKSF EDIHQYREQI KRVKDSDDVP MVLVGNKCDL AARTVESRQA QDLARSYGIP YIETSAKTRQ GVEDAFYTLV REIRQHKLRK LNPPDESGPG CMSCKCVLS -
Predicted molecular weight
21 kDa -
Amino acids
1 to 189 -
Modifications
mutated G12V -
Tags
GST tag N-Terminus -
Additional sequence information
(NP_005334)
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Associated products
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Related Products
Specifications
Our Abpromise guarantee covers the use of ab90627 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
SDS-PAGE
Functional Studies
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Form
Liquid -
Additional notes
The mutation G12V leads to elimination of the intrinsic GTPase activity.
ab90627 is effective in activation of PI3K and PKB.
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Concentration information loading...
Preparation and Storage
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Stability and Storage
Shipped on dry ice. Upon delivery aliquot and store at -80ºC. Avoid freeze / thaw cycles.
pH: 7.50
Constituents: 0.87% Sodium chloride, 0.395% Tris HCl, 0.039% Beta mercaptoethanol, 0.0475% Magnesium chloride
General Info
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Alternative names
- c-H-ras
- CBAS/HAS
- CHARAS1
see all -
Function
Ras proteins bind GDP/GTP and possess intrinsic GTPase activity. -
Tissue specificity
Widely expressed. -
Involvement in disease
Defects 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 similarities
Belongs to the small GTPase superfamily. Ras family. -
Post-translational
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.
The covalent modification of cysteine by 15-deoxy-Delta12,14-prostaglandin-J2 is autocatalytic and reversible. It may occur as an alternative to other cysteine modifications, such as S-nitrosylation and S-palmitoylation. -
Cellular localization
Cell membrane. Cell membrane. Golgi apparatus. 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 and Nucleus. Cytoplasm. Cytoplasm > perinuclear region. Colocalizes with GNB2L1 to the perinuclear region. - Information by UniProt
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 (1)
ab90627 has been referenced in 1 publication.
- Kovalski JR et al. The Functional Proximal Proteome of Oncogenic Ras Includes mTORC2. Mol Cell 73:830-844.e12 (2019). PubMed: 30639242