Anti-HRAS Magnetic Beads-IP Kit Product Components
| Components | Storage |
| Anti-HRAS Magnetic Beads1,3 | 2-8℃ for 12 months |
| NP40 Cell Lysis Buffer2 | -20℃ for 12 months |
| 5×TBST（pH7.4） | |
| 1×TBST（pH7.4） | |
| ddH2O | |
| CD166 Positive Cell Lysate | -20℃ for 12 months |
| Alkaline Elution Buffer | 2-8℃ for 12 months |
| Acidity Elution Buffer | 2-8℃ for 12 months |
| Neutralization Buffer | 2-8℃ for 12 months |
[1] The IP KIT contains anti-HRAS magnetic Beads (2 mg/mL) in phosphate buffered saline (PBS, pH 7.4) with sodium azide (0.1%).
[2] Using NP-40 cell lysate buffer in the kit is required,otherwise,the magnetic beads may be precipitated.
[3] Shipping: Magnetic Beads kits are shipped at ambient temperature in which magnetic beads are provided in liquid buffer.
Anti-HRAS Magnetic Beads-IP Kit Product Description
The Anti-HRAS magnetic Beads, conjugated with Anti-HRAS antibody, are used for immuneprecipitation (IP) of HRAS proteins which expressed in vitro expression systems. For IP, the beads are added to a sample containing HRAS proteins to form a bead-protein complex. The complex is removed from the solution manually using a magnetic separator. The bound HRAS proteins are dissociated from the magnetic beads using an elution buffer. Anti-HRAS Magnetic Beads-IP Kit Antibody Information
Immunogen
Recombinant Human HRAS protein (Catalog#12059-H08B)
Species Reactivity
Human HRAS
Source
Polyclonal Human Rabbit IgG
Preparation
Produced in rabbits immunized with purified, recombinant Human HRAS (rh HRAS; Catalog#12059-H08B; P01112; Met1-Cys186). HRAS specific IgG was purified by Human HRAS affinity chromatography.
Applications
Immunoprecipitation (IP), Minimum Protein Purification
Anti-HRAS Magnetic Beads Immunoprecipitation (IP) Kit Alternative Names
Anti-C-BAS/HASALCAM Magnetic Beads-Immunoprecipitatiopn (IP) Kit;Anti-C-H-RASALCAM Magnetic Beads-Immunoprecipitatiopn (IP) Kit;Anti-C-HA-RAS1ALCAM Magnetic Beads-Immunoprecipitatiopn (IP) Kit;Anti-CTLOALCAM Magnetic Beads-Immunoprecipitatiopn (IP) Kit;Anti-H-RASIDXALCAM Magnetic Beads-Immunoprecipitatiopn (IP) Kit;Anti-HAMSVALCAM Magnetic Beads-Immunoprecipitatiopn (IP) Kit;Anti-HRAS1ALCAM Magnetic Beads-Immunoprecipitatiopn (IP) Kit;Anti-p21rasALCAM Magnetic Beads-Immunoprecipitatiopn (IP) Kit;Anti-RASH1ALCAM Magnetic Beads-Immunoprecipitatiopn (IP) Kit
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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