HRAS cDNA ORF Clone, Human, His tag

Cat: HG12059-CH

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HRAS cDNA ORF Clone, Human, His tag General Information
NCBI Ref Seq
RefSeq ORF Size
615 bp
Sequence Description
Identical with the Gene Bank Ref. ID sequence.
Full length Clone DNA of Human v-Ha-ras Harvey rat sarcoma viral oncogene homolog with C terminal His tag.
Enhanced CMV promoter
Restriction Sites
KpnI + XbaI(6kb+0.62kb)
Tag Sequence
Sequencing Primers
Quality Control
The plasmid is confirmed by full-length sequencing.
Antibiotic in E.coli
Antibiotic in Mammalian cell
Stable or Transient mammalian expression
Storage & Shipping
Each tube contains lyophilized plasmid.
The lyophilized plasmid can be stored at ambient temperature for three months.
HRAS cDNA ORF Neucleotide Sequence and Amino Acid Sequence Information

**Sino Biological guarantees 100% sequence accuracy of all synthetic DNA constructs we deliver, but we do not guarantee protein expression in your experimental system. Protein expression is influenced by many factors that may vary between experiments or laboratories.**

HRAS cDNA ORF Clone, Human, His tag Validated Images
other Green fluorescent protein / GFP Gene Plasmid Map 5610
HRAS cDNA ORF Clone, Human, His tag Alternative Names
C-BAS/HAS cDNA ORF Clone, Human;C-H-RAS cDNA ORF Clone, Human;C-HA-RAS1 cDNA ORF Clone, Human;CTLO cDNA ORF Clone, Human;H-RASIDX cDNA ORF Clone, Human;HAMSV cDNA ORF Clone, Human;HRAS1 cDNA ORF Clone, Human;p21ras cDNA ORF Clone, Human;RASH1 cDNA ORF Clone, Human
HRAS Background Information

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 arare 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 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. Defects in HRAS are the cause of oral squamous cell carcinoma.

Immune Checkpoint   Immunotherapy   Cancer Immunotherapy   Targeted Therapy

Full Name
Harvey rat sarcoma viral oncogene homolog
  • 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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