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Validated All-in-One™ qPCR Primer for HRAS(NM_005343.4) Search again
Product ID:
HQP155299
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
C-BAS/HAS, C-H-RAS, C-HA-RAS1, CTLO, H-RASIDX, HAMSV, HRAS1, RASH1, p21ras
Gene Description:
HRas proto-oncogene, GTPase
Target Gene Accession:
NM_005343.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
This gene belongs to the Ras oncogene family, whose members are related to the transforming genes of mammalian sarcoma retroviruses. The products encoded by these genes function in signal transduction pathways. These proteins can bind GTP and GDP, and they have intrinsic GTPase activity. This protein undergoes a continuous cycle of de- and re-palmitoylation, which regulates its rapid exchange between the plasma membrane and the Golgi apparatus.
Gene References into function
- The Tg.AC (v-Ha-ras) transgenic mouse model provides a reporter phenotype of skin papillomas in response to either genotoxic or nongenotoxic carcinogens.
- The Tg.Ac (v-Ha-ras) mouse model was not overly sensitive and possesses utility as an adjunct to the battery of toxicity studies used to establish carcinogenic risk.
- immunohistochemical analysis reveals a protective effect of H-ras expression mediated via apoptosis in node-negative breast cancer patients
- molecular dynamics simulations to show that Ras, a monomeric G protein, can generate mechanical force upon hydrolysis
- Point mutations were identified in DNA from two of the 115 normal individuals. Both mutations resulted in an amino acid substitution at position 12 in H RAS.
- H-Ras/mitogen-activated protein kinase pathway inhibits integrin-mediated adhesion and induces apoptosis in osteoblasts
- H-Ras mutations at the binding site for the GTP nucleotide ring in a human multiple myeloma line leads to transformation and factor-independent cell growth
- HRAS genes are biallelically expressed in multiple fetal and adult tissues both in humans and in mice
- overexpression of PPARalpha or the c-Ha-ras transgene is not associated with the liver tumorigenesis induced by DEHP in rasH2 mice
- steady-state structure of the switch I region of the protein in both the inactive GDP-bound conformation as in the active GTP-bound conformation.
- Ha-ras mutations detected in HPV-induced cervical intraepithelial neoplasia grade II and invasive squamous cell carcinoma
- Results demonstrate the close relationship between Ha-ras expression level and sensitization of 5-flurouracil (5-FU)-treated cells.
- using fragments of the human c-Ha-ras gene containing 8-hydroxyguanine (8-OH-G) in codon 12, evidence for the highly complex biochemical events leading to activation of the oncogene
- the human c-Ha-ras proto-oncogene product does not influence the androgen-dependence of prostate carcinogenesis due to the probasin-mediated SV40 T antigen.
- Ras activates the MAP kinase cascade through simultaneous dual effector interactions: induction of Raf kinase activity and derepression of Raf-MEK complex formation
- When mutated, causes hepatocarcinogenesis in transgenic mice.
- complete loss of p53 is a prerequisite for collaborating with activated Ha-ras to promote bladder tumorigenesis
- H-ras mutations have a role in malignant transformation of aerodigestive spindle cell carcinoma
- a domain of Rap1 acts dominantly on COOH-terminal lipid modification of Ha-Ras, which has been considered to be essential and sufficient for the plasma membrane localization
- Changes in flexibility upon protein-protein complex formation of H-Ras & the Ras-binding domain of C-Raf1 have been investigated using the molecular framework approach FIRST and molecular dynamics simulations of in total approximately 35 ns length.
- ras gene alterations have a specific and early role in the development of follicular type of thyroid tumors in Taiwan.
- Myc rescued cell growth inhibition induced by Ras
- RAS appears to be a pejorative prognostic factor in terms of survival in NSCLC globally, in ADC and when it is studied by PCR.
- No significant correlations were found between mutations in colorect cancer.
- H-Ras-specific activation of Rac-MKK3/6-p38 pathway has a role in invasion and migration of breast epithelial cells
- the mechanism of O2*-mediated Ras guanine nucleotide dissociation is similar to that of NO/O2-mediated Ras guanine nucleotide dissociation
- Ras exists in (at least) two conformational states identifiable by nuclear magnetic resonance spectroscopy: state 2 represents the high-affinity binding state for effectors, while state 1 represents a weak binding state.
- We found mutations in p53, K-ras, and BRAF genes in 35%, 30%, and 4% of tumors, respectively, and observed a minimal or no co-presence of these gene alterations.
- RAS-MEK-ERK1/2 signaling pathway can sensitize cells to TRAIL-induced apoptosis by up-regulating DR4 and DR5
- Data show that the the RET receptor (RET/PTC), Ras and BRAF function along a linear oncogenic signaling cascade in which RET/PTC induces RAS-dependent BRAF activation and RAS- and BRAF-dependent ERK activation.
- reduced Ras activation in cells harbouring the Hepatitis C virus subgenomic replicon
- K-ras mutations are found in plasma after colorectal tumor resection
- the mechanism for Ras-mediated down-regulation of Par-4 is by promoter methylation
- Ras isoforms have distinct and separate cellular and subcellular distribution that may persist even in the malignantly transformed state in pancreatic disease
- In this study, we probe the cellular and molecular mechanisms of RAS-mediated transformation.
- HRAS oncogene could play an important role in the development of cervical cancer, in addition to the presence of HPV, by reducing the G1 phase and accelerating the G1/S transition of infected cells
- N-Ras(L61) transformed cells lack a G0-G1 arrest upon TGF-beta treatment due to absence of p27.
- Ras activity regulates Fbw7-mediated cyclin E proteolysis; impaired cyclin E proteolysis is a mechanism through which Ras mutations promote tumorigenesis.
- RIG1 exerts inhibitory effect at the level of Ras activation, which is independent of Ras subtype but dependent on membrane localization of RIG1. It may be mediated through downregulation of Ras levels and alteration of Ras subcellular distribution.
- studies provide evidence for the existence of human-specific mechanisms that resist Ras/MEK/ERK-mediated transformation
- in primary fibroblasts stabilization of Ras protein by ROS and ERK1/2 amplifies the response of the cells to growth factors and in systemic sclerosis represents a critical factor in the onset and progression of the disease
- growth factor-induced, Ras-mediated changes of keratinocyte shape may be an important mechanism that determines the speed of wound epitheli
- Germline mutations in HRAS perturb human development and increase susceptibility to tumors.
- Incidence of K-ras mutation and frequencies of COX-2 and gastrin overexpression are high in laterally spreading granular and protruded type colorectal tumors.
- We conclude that in wild-type cells, endogenous Ras does not need to be prenylated to be active.
- IL-24 is a member of IL-10 family of cytokines, and it signals through two hetorodimeric receptors, whose expression is also upregulated by ras oncogenes
- K-ras mutation was found in 29% of sporadic adenocarcinomas respectively and in 0% and 22% of the 9 HNPCC cases.
- Expression of constitutively active Galpha(q)Q209L in cells inhibited Ras activation of the PI3K/Akt pathway but had no effect on Ras/Raf/MEK [MAPK (mitogen-activated protein kinase)/ERK (extracellular-signal-regulated kinase) kinase] signalling
- activation of the PI3K/AKT pathway replaced Ras once tumors formed, although other effectors were still activated independently of Ras, presumably by factors provided upon the establishment of a tumor microenvironment
- APC and K-ras, but not CTNNB1 mutations have roles in regulation of expression of hMLH1 in sporadic colorectal carcinomas
- Oncogenic RAS activity is directly responsible for OPCML promoter hypermethylation & epigenetic gene silencing. Elevation of the RAS signaling pathway may play an important role in epigenetic inactivation of OPCML in human epithelial ovarian cancer.
- Analysus if 2502 patients with acute myeloid leukemia at diagnosis for NRAS mutations around hot spots at codons 12, 13, and 61 and correlation of the the results with cytomorphology, cytogenetics, other molecular markers, and prognosis.
- Ras induces ErbB4 receptor phosphorylation in a non-autocrine manner and this activation depends on multiple Ras effector pathways and on ErbB4 kinase activity.
- Our data suggest that mutations of PTPN11 as well as RAS play a role in the pathogenesis of not only myeloid hematological malignancies but also a subset of RMS malignancies
- Interplay and transmission of structural information between the switch regions are important factors for Ras function. They propose that initiation of GTP hydrolysis sets off the separation of the Ras/effector complex.
- the H-RAS 81T --> C polymorphism may induce aneuploidy through overexpression of the active p21 isoform of H-RAS
- The IGFBP3, hRas, JunB, Egr-1, Id1 and MIDA1 genes were up-regulated in psoriatic involved skin compared with uninvolved skin.
- intracellular generation of NO* by nNOS leads to S-nitrosylation of H-Ras, which interferes with Raf-1 activation and propagation of signalling through ERK1/2
- In 239 Thai adult AML cases, 35 RAS mutations were found in 32 cases (13%) predominantly classified as M1/M2 (53%) followed by M4/M5 (38%). Ten cases were positive for NRAS codon 12, 11 for NRAS codon 61, 13 for NRAS codon 13, and one for KRAS codon 13.
- Activating RAS mutation is a pivotal molecular lesion that is implicated in the pathogenesis of AML and MDS.
- Ras mutations were significantly more frequent in inv(16) than in t(8;21) subset (36 versus 8%, P=0.001).
- NF1 is a novel regulator of RAS-induced signals in primary vascular smooth muscle cells
- There is a signaling loop between Ras-dependent MAPK cascade activation and p73 function.
- histone deacetylase inhibitor sodium butyrate induces G1/S phase arrest in E1A + Ras-transformed cells through down-regulation of E2F1 activity and stabilization of beta-catenin
- Review. An alternative splice form of c-H-ras, called p19ras, is a positive regulator of p73beta via Mdm2. Implications for this previously unidentified means of regulation are discussed in light of tumor suppression and are extended to p53 and p63.
- K-ras mutations were observed in 68/182 (37.4%) cases of colorectal cancer.
- ras may be involved in early stages of larynx carcinogenesis and may be activated by other mechanisms different from mutations, such as epigenetic events
- Targeted activation of a human oncogenic-ras transgene in rat pancreas can induce carcinomas correspondent to human pancreatic ductal adenocarcinomas.
- These findings indicate that mechanical strain causes ROS-dependent S-glutathiolation of Ras at Cys118, leading to myocyte hypertrophy via activation of the Raf/Mek/Erk pathway.
- The entire Ras/Raf/MEK/ERK pathway is activated by intracellular acidosis, indicating that the initiating acid sensor is found at the level of Ras or above.
- Down-regulation of MIP-1 alpha was not observed following FGFR3 inhibition in MM cells with RAS mutations implicating RAS-MAPK in MIP-1 alpha regulation
- Ras and c-Myc play important roles in the up-regulation of nucleophosmin/B23 during proliferation of cells associated with a high degree of malignancy, thus outlining a signaling cascade involving these factors in the cancer cells.
- Three unrelated Dutch patients with Costello syndrome all have the same mutation, G12S, in HRAS.
- High prevalence of CIMP-high and K-ras mutations in G-LST, especially in the proximal colon, could strongly suggest that G-LST appearance is associated with a unique carcinogenic pathway.
- analysis of H-RAS, K-RAS and N-RAS expression in acute myeloid leukemia
- Ras expression in cervical keratinocyte cell lines containing stably replicating extrachromosomal HPV-16 consistently diminished anchorage-independent growth (AI), reduced E6 and E7 expression, and caused p53 induction in these cells.
- Somatic mosaicism for an HRAS mutation causes Costello syndrome.
- Activation of Ras plays a critical role in modulating the expression of both CXCL10 and CXCR3-B, which may have important consequences in the development of breast tumors through cancer cell proliferation.
- The hydrolysis of guanosine triphosphate (GTP) by p21(ras) (Ras) has been modeled by using ab initio type quantum mechanical-molecular mechanical simulations. The minimum energy reaction path is consistent with a 2-step mechanism of GTP hydrolysis.
- Neurofibromin-deficient mouse embryonic fibroblasts (MEFs) and human NF1 tumor cells were more resistant than neurofibromin-expressing cells to apoptosis mediated by two survival pathways: a Ras-dependent pathway, and a Ras-independent pathway.
- HRAS mutations represent independent but cooperating events to uniparental disomy during embryonic rhabdomyosarcoma development.
- The activation of HRAS was inhibited by 25.1% or 81.4% in cells cotransfected with wild-type or Golgi-targeted RIG1, respectively.
- Taken together, the observations indicate that both H-Ras(G12V) and K-Ras4B(G12V) activates non-conventional and perhaps unique effector pathways to induce cytoplasmic vacuolation in glioblastoma cells.
- Ras and Ral mediate BCR-controlled activation of JUN/ATF2 and NFAT transcription factors
- Ras is able to promote monocyte lineage selection via PKC and PDK1.
- Transfection of U266 cells with constitutively activated H-Ras (Q61L) attenuated ERK1/2 inactivation and dramatically diminished the lethality of statins + UCN-01 regimen.
- One female patient exhibiting the distal phalangeal creases had a mutation in the HRAS gene.
- K-ras mutations may play a less important role in the tumorigenesis of ovarian serous tumor of the Chinese patients.
- The subcellular distribution of K-Ras is driven by electrostatic interaction of the polybasic region of the protein with negatively charged membranes.
- We identified two known activating and two novel germline HRAS mutations in four patients with an unusual form of congenital myopathy histologically charactered by an excess of muscle spindles.
- Study identified Crk adapter proteins, Rac1 and H-Ras, but not RhoA or Cdc42 as crucial components of the Helicobacter pylori CagA protein-induced phenotype.
- The evaluation of a large number of actinic keratoses specimens have found a low gene mutation rate in low-graded AK lesions. p53 mutations rather than p16(INK4a) and/or Ha-ras mutations may be an early event in the development of AK to cutaneous SCC.
- low rate of RAS-RAF mutations (2/22, 9.1%) observed in Spitz melanocytic nevi suggests that these lesions harbor as yet undetected activating mutations in other components of the RAS-RAF-MEK-ERK-MAPK pathway
- De novo germline HRAS (G12A) and KRAS (F156L) mutations in two siblings with short stature and neuro-cardio-facio-cutaneous features.
- In contrast to C-RAF that requires farnesylated H-Ras, cytosolic B-RAF associates effectively and with significantly higher affinity with both farnesylated and nonfarnesylated H-Ras.
- BCR/ABL-Y177 plays an essential role in Ras and Akt activation and in human hematopoietic progenitor transformation in chronic myelogenous leukemia
- Erf provides a direct link between the RAS/ERK signaling and the transcriptional regulation of c-Myc and suggests that RAS/ERK attenuation actively regulates cell fate
- No mutations in HRAS was found in pilocytic astrocytomas.
- H-Ras mutation defines a molecular subtype of oral carcinoma with favourable outcome and unique biology
- a potential key role for activated members of ras family genes in terms of their contribution to the development of nasal polyposis as well as to the hypertrophy of adjacent turbinates.
- Examination of various growth-regulatory pathways suggested that Bmi-1 overexpression together with H-Ras promotes human mammary epithelial cell transformation and breast oncogenesis by deregulation of multiple growth-regulatory pathways.
- These data show that a RAS mutation that only perturbs guanine nucleotide binding has similar functional consequences as mutations that impair GTP hydrolysis and causes human disease.
- These findings suggest that the activation of Ras signaling pathways promotes the generation of brain cancer stem-like cells from p53-deficient mouse astrocytes by changing cell fate and transforming cell properties.
- Four cases of Costello syndrome had an unusually severe phenotype, associated in three cases with two unusual mutations, c.35G>A, p.G12D in two cases and c.34G>T, p.G12C in the other.
- the results of HRAS, BRAF and MAP2K1/2 mutation screening in a large cohort of patients with CS and CFC
- H-Ras interacts with Spry2-binding partners, c-Cbl and CIN85, in a Spry2-dependent manner.
- V12 H-Ras oncogenic signaling may contribute to anchorage-independent growth and tumorigenesis by promoting the final cleavage furrow ingression during cytokinesis.
- Trafficking of H-Ras was examined to determine whether it can enter cells through clathrin-independent endocytosis (CIE).
- K-ras mutations were detected in only one of the Hungarian cases; Eight of 19 (42.1%) Japanese cases were MSI-high (presence of novel peaks in more than one of the five loci analyzed), whereas only 1 of 15 (6.7%) Hungarian cases was MSI-high (P = 0.047
- study reports on two patients with novel HRAS mutations affecting amino acids 58 (T58I) and 146 (A146V), respectively; both patients show many of the physical and developmental problems characteristic for Costello syndrome
- Taken together, these results reveal a novel role for fad24 in the repression of NF-kappaB activity and H-ras-mediated transformation.
- Some smoking characteristics, i.e. being an ex-smoker, frequency and inhalation, may be associated with risk for colorectal cancer characterized by the wild-type KRAS gene, especially in men.
- Hras mutation is associated with familial non-medullary thyroid carcinoma
- The redox sensitive p21Ras-ERK pathway plays a critical role in sensing and delivering the pro-apoptotic signaling mediated by S-nitrosoglutathione.
- Results correlate P53 status and mutation site/type with nuclear protein accumulation, clinicopathologic variables and data on K-ras mutations and high-level microsatellite instability.
- high frequency of mutations in the PIK3CA, HRAS and KRAS genes leads us to believe that dysregulation of the phosphatidylinositol 3-kinase or Ras pathway is significant for the development and progression of penile carcinoma.
- K-RAS and BRAF mutations are a frequent genetic event in our samples of sporadic papillary and medullary thyroid carcinoma.
- K-ras and p53 genes are altered in Tamoxifen-associated endometrial carcinoma
- Study shows that SOS responds to the membrane density of Ras molecules, to their GTP loading and to the concentration of phosphatidylinositol-4,5-bisphosphate, and that the integration of these signals potentiates the release of autoinhibition.
- Report extremely weak tumor-promoting effect of troglitazone on splenic hemangiosarcomas in rasH2 mice induced by urethane.
- RAS signalling may play an important role in neuronal susceptibility to Sindbis virus infection
- p19(ras) interaction with p73beta amplifies p73beta-induced apoptotic signaling responses including Bax mitochondrial translocation, cytochrome c release, increased production of reactive oxygen species and loss of mitochondrial transmembrane potential.
- p21 Ras/Imp regulate cytokine production and migration in CD4 T cells
- Presence of K-ras mutations might be associated with lack of response to panitumumab alone and inferior survival in patients with metastatic colorectal cancer.
- Scribble is an important mediator of MAPK signalling and cooperates with H-ras to promote cell invasion.
- k-ras may have a role in progression of rectal cancer after resection
- K-Ras mutations have a role in treatment outcome in colorectal cancer patients receiving exclusive fluoropyrimidine therapy
- Low-penetrant RB allele in small-cell cancer shows geldanamycin instability and discordant expression with mutant ras.
- This review will summarize the chemical biology of Ras and discuss in more detail the biophysical and structural features of the membrane bound C-terminus of the protein.
- the H-RAS T81C polymorphism might be a low penetrance gene predisposition factor for gastric cancer in the Chinese population
- Ca(2+) may activate Ras signaling pathway by interaction with Ras, providing clues to understand the role of calcium in regulating Ras function in physiological environments.
- This study revealed S100A8/A9 genes as candidate markers for metastatic potential of breast epithelial cells.
- The secondary structure of membrane-bound, lipidated Ras is similar to that determined for the nonlipidated truncated Ras protein for the highly conserved G-domain.
- Hdm2 is expressed in pancreatic cancer cells as a result of activated Ras signaling, and regulates cellular proliferation and the expression of target genes by p53-independent mechanisms.
- The Snail-p53 binding as the new therapeutic target for K-Ras-mutated cancers including pancreatic, lung, and colon cancers.
- Women with the NAT2 fast acetylator genotype may exhibit a higher risk of CRC with increased occurrence of K-RAS mutation.
- K-RAS point mutations, and anomalies of p16-RB1-cyclin D pathway could occur before LOH on 10q23 (PTEN) and microsatellite instability during tumor progression.