Name :
Recombinant Human HRAS Protein (His Tag)
Biological Activity :
Background :
HRas, also known as HRAS, belongs to the small GTPase superfamily, Ras family, and is widely expressed. It functions in signal transduction pathways. HRas can bind GTP and GDP, and they have intrinsic GTPase activity. It undergoes a continuous cycle of de- and re-palmitoylation, which regulates its rapid exchange between the plasma membrane and the Golgi apparatus. Defects in HRAS are the cause of faciocutaneoskeletal syndrome (FCSS). FCSS is a rare condition characterized by prenatally increased growth, postnatal growth deficiency, mental retardation, distinctive facial appearance, cardiovascular abnormalities, tumor predisposition, skin, and musculoskeletal abnormalities. Defects in HRAS also can cause congenital myopathy with excess of muscle spindles. HRAS deficiency may be a cause of susceptibility to Hurthle cell thyroid carcinoma. It has been shown that defects in HRAS can cause susceptibility to bladder cancer which is a malignancy originating in tissues of the urinary bladder. It often presents with multiple tumors appearing at different times and 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. Defects in HRAS are the cause of oral squamous cell carcinoma. Cancer Immunotherapy Immune Checkpoint Immunotherapy Targeted Therapy
Biological Activity :
Testing in progress
Expression Host :
Human
Source :
Baculovirus-Insect Cells
Tag :
Protein Accession No. :
P01112
NCBI Gene ID :
Synonyms :
Synonyms :
Harvey rat sarcoma viral oncogene homolog
Amino Acid Sequence :
Molecular Weight :
The recombinant human HRAS consists of 197 amino acids and predicts a molecular mass of 22.45 kDa. It migrates as an approximately 23 kDa band in SDS-PAGE in SDS-PAGE under reducing conditions.
Purity :
> 94 % as determined by SDS-PAGE
State of Matter :
Product Concentration :
Storage and Stability :
Samples are stable for up to twelve months from date of receipt at -20℃ to -80℃. Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
Endotoxin Level :
< 1.0 EU per μg of the protein as determined by the LAL method
Protein Construction :
A DNA sequence encoding the human HRAS (P01112) (Met 1-Cys 186) was fused with a polyhistidine tag at the C-terminus.
Buffer Solution :
Lyophilized from sterile 50mM Tris, 100mM NaCl, pH 8.0, 10% glyPlease contact us for any concerns or special requirements. Normally 5 % – 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization. Please refer to the specific buffer information in the hardcopy of datasheet.
Shipping :
In general, recombinant proteins are provided as lyophilized powder which are shipped at ambient temperature.Bulk packages of recombinant proteins are provided as frozen liquid. They are shipped out with blue ice unless customers require otherwise.
Redissolution :
A hardcopy of datasheet with reconstitution instructions is sent along with the products. Please refer to it for detailed information.
Synonyms :
C-BAS/HAS Protein, Human; C-H-RAS Protein, Human; C-HA-RAS1 Protein, Human; CTLO Protein, Human; H-RASIDX Protein, Human; HAMSV Protein, Human; HRAS1 Protein, Human; p21ras Protein, Human; RASH1 Protein, Human HRAS 背景信息 HRas, also known as HRAS, belongs to the small GTPase superfamily, Ras family, and is widely expressed. It functions in signal transduction pathways. HRas can bind GTP and GDP, and they have intrinsic GTPase activity. It undergoes a continuous cycle of de- and re-palmitoylation, which regulates its rapid exchange between the plasma membrane and the Golgi apparatus. Defects in HRAS are the cause of faciocutaneoskeletal syndrome (FCSS). FCSS is a rare condition characterized by prenatally increased growth, postnatal growth deficiency, mental retardation, distinctive facial appearance, cardiovascular abnormalities, tumor predisposition, skin, and musculoskeletal abnormalities. Defects in HRAS also can cause congenital myopathy with excess of muscle spindles. HRAS deficiency may be a cause of susceptibility to Hurthle cell thyroid carcinoma. It has been shown that defects in HRAS can cause susceptibility to bladder cancer which is a malignancy originating in tissues of the urinary bladder. It often presents with multiple tumors appearing at different times and 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. Defects in HRAS are the cause of oral squamous cell carcinoma. Cancer Immunotherapy Immune Checkpoint Immunotherapy Targeted Therapy
References & Citations :
Schulten HJ, et al. (2011) Mutational screening of RET, HRAS, KRAS, NRAS, BRAF, AKT1, and CTNNB1 in medullary thyroid carcinoma. Anticancer Res. 31(12):4179-83. Gripp KW, et al. (2011) Molecular confirmation of HRAS p.G12S in siblings with Costello syndrome. Am J Med Genet A. 155A(9):2263-8. Na KY, et al. (2012) Allelic loss of susceptibility loci and the occurrence of BRAF and RAS mutations in patients with familial non-medullary thyroid cancer. J Surg Oncol. 105(1):10-4. Membrino A, et al. (2011) G4-DNA formation in the HRAS promoter and rational design of decoy oligonucleotides for cancer therapy. PLoS One. 6(9):e24421.
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