HRAS cDNA ORF Clone, Human, N-DDK (Flag®) tag

Cat: HG12059-NF
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HRAS cDNA ORF Clone, Human, N-DDK (Flag®) tag 基本信息
基因
种属
Human
NCBI 参考序列号
参考序列ORF长度
570 bp
序列描述
Identical with the Gene Bank Ref. ID sequence.
描述
Full length Clone DNA of Human v-Ha-ras Harvey rat sarcoma viral oncogene homolog with N terminal Flag tag.
质粒
启动子
Enhanced CMV promoter
载体
pCMV3-N-FLAG
限制性酶切位点
KpnI + XbaI (6kb + 0.62kb)
标签序列
FLAG Tag Sequence: GATTACAAGGATGACGACGATAAG
测序引物
T7( 5' TAATACGACTCACTATAGGG 3' )
BGH( 5' TAGAAGGCACAGTCGAGG 3' )
质控
The plasmid is confirmed by full-length sequencing.
筛选
抗生素(大肠杆菌)
Kanamycin
抗生素(哺乳动物细胞)
Hygromycin
应用
Stable or Transient mammalian expression
储存 & 运输
运输
Each tube contains lyophilized plasmid.
储存
The lyophilized plasmid can be stored at ambient temperature for three months.
HRAS cDNA ORF 核苷酸序列及氨基酸序列信息

**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, N-DDK (Flag®) tag Validated Images
Human aFGF/FGF1 Gene Plasmid Map 5637
Human HRAS Gene Expression validated Image 16172
The plasmid was transfected into 293H adherent cells with Sinofection reagent (Cat# STF02). After 48 h, Immunofluorescence staining of cells. Cells were fixed with 4% PFA, permeabilzed with 0.3% Triton X-100 in PBS, blocked with 10% serum, and incubated with Mouse anti-Flag Tag monoclonal antibody (CST#8146S) at 37℃ 1 hour. Then cells were stained with Goat Anti-mouse IgG secondary antibody. The fluorescent signal is detected by fluorescence microscope. Each expression experiment has negative control.
HRAS cDNA ORF Clone, Human, N-DDK (Flag®) 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
References
  • 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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