HRAS Research Reagents

GTPase HRas also known as transforming protein p21 is an enzyme that in humans is encoded by the HRAS gene. The HRAS gene is located on the short (p) arm of chromosome 11 at position 15.5, from base pair 522,241 to base pair 525,549. HRas is a small G protein in the Ras subfamily of the Ras superfamily of small GTPases. Once bound to Guanosine triphosphate, H-Ras will activate a Raf kinase like c-Raf, the next step in the MAPK/ERK pathway.

The following HRAS reagents supplied by CUSABIO are manufactured under a strict quality control system. Multiple applications have been validated and solid technical support is offered.

HRAS Antibodies

HRAS Antibodies for Homo sapiens (Human)

HRAS Antibodies for Rattus norvegicus (Rat)

HRAS Proteins

HRAS Proteins for Homo sapiens (Human)

HRAS Proteins for Rattus norvegicus (Rat)

HRAS Proteins for Gallus gallus (Chicken)

HRAS Proteins for Mesocricetus auratus (Golden hamster)

HRAS Proteins for Mus musculus (Mouse)

HRAS Background

The Harvey rat sarcoma viral proto-oncogene homolog (HRAS), the first identified human proto-oncogene [1], is one of the RAS oncogene family related to the transforming genes of mammalian sarcoma retroviruses [2][3]. The product of this gene HRAS protein mediates many intracellular signaling pathways involved in controlling cell growth, differentiation, and apoptosis. HRAS undergoes a continuous cycle of de- and re-palmitoylation, which regulates its rapid exchange between the plasma membrane and the Golgi apparatus. As a GTPase, HRAS is active in the GTP bound state and inactive in the GDP bound state, just like a switch [4]. The switching between the two is regulated by guanine nucleotide exchange factors (GEF) [5]. HRAS is activated through the epidermal growth factor (EGF) receptor tyrosine kinase (RTK). The RTK recruits a GEF protein known as Son-of-sevenless (SOS) that promotes the GTP-bound state allowing activation of Ras via RTK. The activation of HRAS leads to further downstream direct activation of Raf serine/threonine kinase (activated via phosphorylation) [6]. Activated Raf subsequently turns on MEK1/2 protein kinase and then results in activation of ERK1/2 that leads to intranuclear activation of transcription factors. This process is the Ras/Raf/MEK/ERK cascade pathway, which plays a variety of roles in cell cycle regulation, apoptosis, and cell differentiation [7]. Somatic mutations in HRAS are present in many cancers, and the vast majority of mutations affect codons 12 and 13, leading to a constitutively active protein. Germline mutations in HRAS cause Costello syndrome (CS), which is a congenital disease characterized by postnatal growth retardation, short stature, tumor predisposition, developmental delay, and abnormalities of the heart (cardiomyopathy), skin and skeletal muscles [8]. Besides, the expression of activated H-Ras was shown to be sufficient to promote cardiomyocyte hypertrophy [9-11]. Sheng H et al. delineated an important role for PI3K/Akt in HRas-mediated transformation of intestinal epithelial cells [12].

[1] Parada LF, Tabin CJ, et al. Human EJ bladder carcinoma oncogene is homologue of Harvey sarcoma virus ras gene [J]. Nature 1982, 297: 474–478.
[2] Wong-Staal F, Dalla-Favera R, et al. Three distinct genes in human DNA related to the transforming genes of mammalian sarcoma retroviruses [J]. Science. 1981, 213 (4504): 226–8.
[3] Russell MW, Munroe DJ, et al. A 500-kb physical map and contig from the Harvey ras-1 gene to the 11p telomere (PDF) [J]. Genomics. 1986, 35 (2): 353–60.
[4] Vetter, I.R., and Wittinghofer, A. The guanine nucleotide-binding switch in three dimensions. Science 294, 2001, 1299–1304.
[5] D. Esser, B. Bauer, et al. Structure determination of the ras-binding domain of the Ral-specific guanine nucleotide exchange factor Rlf [J]. Biochemistry, 1998, vol. 37, no. 39, pp. 13453–13462.
[6] Drosten, M., Dhawahir, A., et al. Genetic analysis of Ras signalling pathways in cell proliferation, migration and survival. EMBO J. 2010, 29, 1091–1104.
[7] Steelman LS, Pohnert SC, et al. JAK/STAT, Raf/MEK/ERK, PI3K/Akt and BCR-ABL in cell cycle progression and leukemogenesis [J]. Leukemia. 2004 Feb; 18(2):189-218.
[8] Gripp KW, Lin AE, et al. HRAS mutation analysis in Costello syndrome: genotype and phenotype correlation [J]. Am J Med Genet 2006, 140A: 1–7.
[9] Thorburn A, Thorburn J, et al. HRas-dependent pathways can activate morphological and genetic markers of cardiac muscle cell hypertrophy [J]. J Biol Chem. 1993; 268:2244–2249.
[10] Ramirez MT, Sah VP, et al. The MEKK-JNK pathway is stimulated by alpha1-adrenergic receptor and ras activation and is associated with in vitro and in vivo cardiac hypertrophy [J]. J Biol Chem. 1997; 272:14057–14061.
[11] LaMorte VJ, Thorburn J, et al. Gq- and ras-dependent pathways mediate hypertrophy of neonatal rat ventricular myocytes following alpha 1-adrenergic stimulation [J]. J Biol Chem. 1994; 269:13490–13496.
[12] Sheng H, Shao J, et al. Akt/PKB activity is required for Ha-Ras-mediated transformation of intestinal epithelial cells [J]. J Biol Chem. 2001 Apr 27;276(17):14498-504.

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