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We show that whereas Ras drives a global increase in protein translation, it suppresses TXNIP protein synthesis by reducing the rate at which ribosomes transit the coding region of TXNIP mRNA. The N terminus of the growing TXNIP polypeptide is the target for Ras-dependent translational repression.
Simultaneous phosphorylation of synGAP by Plk2 and CDK5 at distinct sites produces an additive increase in GAP activity toward HRas ( approximately 230%) and a smaller, non-additive increase in activity toward Rap1 ( approximately 15%).
Study identifies WD40-repeat protein 76 (WDR76) as one of the HRAS binding proteins using proteomic analyses of hepatocellular carcinomas tissue form human patients and mouse diethylnitrosamine-induced liver carcinogenesis model and demonstrates that WDR76 functions as a tumor suppressor via RAS degradation.
results demonstrate that adenomyoepitheliomas are genetically heterogeneous, and qualify mutations in HRAS, a gene whose mutations are vanishingly rare in common-type breast cancers, as likely drivers of ER-negative adenomyoepitheliomas
Plasma membrane polyphosphoinositides depletion caused rapid translocation of K-Ras4B but not H-Ras from the plasma membrane to the Golgi.
Data show that an indispensable beta-subunit of the voltage-gated Ca(2+) channel Cav1.2 interaction with H-Ras is independently of Ca(2+) flux, suggesting the regulatory role of beta2 in transcriptional activation via the ERK/CREB pathway.
This study demonstrated that Oligodendrocyte RasG12V expressed in its endogenous locus disrupts myelin structure through increased MAPK, nitric oxide, and notch signaling.
Data indicate dynamic of H-Ras functional cycle as controlled by son of sevenless homolog 1 (Sos).
Our data support the idea that a variable range of dysregulated HRAS-dependent signalling dynamics, rather than static activation of HRAS-dependent signal flow, may underlie the phenotypic variability in CS.
AF6 employs a non-canonical, evolutionarily conserved alpha-helix to bind RAS, unique to AF6 and the classical RASSF effectors.
Case Report: somatic HRAS mutation in pigmented trichoblastoma developed in a sebaceous nevus.
our identification of the novel interaction between Aurora A and H-Ras as a mechanism by which Aurora A can activate Ras-MAPK signaling opens the way for studies into perturbation of the Aurora A/H-Ras interaction and the effect on Ras-MAPK signaling.
Peroxiredoxin I (Prx I) increased in tumors of hepatocellular carcinoma (HCC) patients that aligned with overexpression of oncogenic H-ras.
Familial alcohol dependence was associated with hypomethylation of CpG sites in the HRAS promoter region.
Suppression of MEK/ERK pathway in senescent cells provides a new strategy for elimination of Ras-expressing cells.
ESR1 inhibits senescence-like phenotype and facilitates transformation induced by oncogenic ras in human mammary epithelial cells
Data show that STK38 supports Ras-driven transformation through promoting detachment-induced autophagy.
Data indicate acquired KRAS, NRAS or HRAS mutations in more than one third of patients after cetuximab exposure.
HRAS mutations were more common in epithelial-myoepithelial carcinomas (EMCAs) with intact PLAG1 and HMGA2. Most EMCAs arose ex pleomorphic adenoma (PA)and the genetic profile of EMCA varies with the absence or presence of preexisting PA and its cytogenetic signature. Progression to higher grade EMCA with intact PLAG1 and HMGA2 correlates with the presence of TP53, FBXW7 mutations, or SMARCB1 deletion.
Analysis of HRAS mutations and their respiratory phenotype revealed that the common p.Gly12Ser mutation is more often associated with transient respiratory distress and other respiratory diagnoses.
Kita driven expression of oncogenic HRAS leads to early onset and highly penetrant melanoma in zebrafish
Data demonstrate that H-Ras activation is important in the activation of the specific signaling events leading to the accelerated retinal capillary cell apoptosis in hyperglycemic conditions.
Activation of H-Ras and its downstream signaling pathway in the retina and its vasculature could be under the control of superoxide, and H-Ras activation in diabetes can be prevented by inhibiting superoxide accumulation.
Thrombospondin 1, fibronectin, and vitronectin are differentially dependent upon RAS, ERK1/2, and p38 for induction of vascular smooth muscle cell chemotaxis.
gene expression profiles of each of the Ras isoforms in a panel of mouse tissues derived from a full developmental time course, are reported.
This study demonstrates that H- ras deletion protects against AngII-induced cardiac remodeling, possibly via a mechanism in which PKG-Ibeta overexpression could play a partial role, and points to H-Ras and/or downstream proteins as potential therapeutic targets in cardiovascular disease.
HRas (G12V/G12V) mice showed robust upregulation of ERK signaling, neuronal hypertrophy, increased brain volume, spatial learning deficits, and impaired mGluR-dependent long-term depression (LTD).
the oncogenic Hras mutation modulates energy homeostasis in vivo.
Loss of wild-type Hras promotes the earliest stages of pancreatic tumorigenesis, and moreover results in more rapid progression of the disease. As such, mechanisms leading to activation of wild-type Ras proteins, including but not limited to redox-dependent reactions, may influence the development of pancreatic cancer.
High HRAS expression is associated with hepatocarcinogenesis.
p21-associated inhibition of early-stage malignant progression and the intense expression in papilloma outgrowths, identifies a novel, significant antagonism between p21 and ras(Ha)/ROCK2/NF-kappaB signalling in skin carcinogenesis.these data show that ROCK2 activation induces malignancy in ras(Ha)-initiated/promoted papillomas in the context of p53 loss and novel NF-kappaB expression
this study shows that retinoic acid stabilizes HRas protein during neurogenesis.
we provide genetic evidence that the wild-type H-Ras and K-Ras proteins are bioequivalent in spite of their different structural and biological properties
loss of one allele of Hras increased the sensitivity of mice to this carcinogen, and this effect was further exacerbated by the loss of the second Hras allele. However, loss of one or both alleles of Nras failed to alter tumor burden, either in the absence or presence of Hras, after exposure to urethane.
H-ras isoform mediates protection against pressure overload-induced cardiac dysfunction in part through activation of AKT/PI3K signaling pathway.
The long intergenic non-coding RNA CCR492 functions as a let-7 competitive endogenous RNA to de-repress c-Myc expression and to promote cell transformation assisted by the constitutively active H-Ras.
these contrasting signatures precisely match those proposed to confer bias toward Hras(CAA61CTA) versus Braf(GTG636GAG) mutations in the original tumor sets. Our findings highlight a novel mechanism whereby exposure history acts through strand-biased mutagenesis to specify activation of preferred oncogenes
The abnormal expression of epidermal cytokeratins suggests that Ha-Ras and Bcl-2 suppress the terminal differentiation and sustain the stem cell-like features in epidermal keratinocytes
Ras (G12V)-induced cyclin D1 protein synthesis was markedly suppressed by the knockdown of IL-33.
We find that the tumor suppressive effects of Hras are nullified in a homozygous mutant p53 background. As such, loss of wild-type Hras fosters the earliest stages of pancreatic cancer in a p53-dependent manner.
This study establishes a role for the loss of microRNA-203 in promoting selection and expansion of Hras mutated cells and identifies a mechanism through which microRNA-203 antagonizes Hras-mediated tumorigenesis.
The data suggest a role for redox-dependent activation of wild-type KRAS through cysteine 118 in oncogenic HRAS-driven tumorigenesis.
Phenotypic Screening Identifies Protein Synthesis Inhibitors as H-Ras-Nanocluster-Increasing Tumor Growth Inducers.
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. Mutations in this gene cause Costello syndrome, a disease characterized by increased growth at the prenatal stage, growth deficiency at the postnatal stage, predisposition to tumor formation, mental retardation, skin and musculoskeletal abnormalities, distinctive facial appearance and cardiovascular abnormalities. Defects in this gene are implicated in a variety of cancers, including bladder cancer, follicular thyroid cancer, and oral squamous cell carcinoma. Multiple transcript variants, which encode different isoforms, have been identified for this gene.
GTP- and GDP-binding peptide B
, GTPase HRas
, Ha-Ras1 proto-oncoprotein
, Ras family small GTP binding protein H-Ras
, c-has/bas p21 protein
, c-ras-Ki-2 activated oncogene
, p19 H-RasIDX protein
, transformation gene: oncogene HAMSV
, transforming protein p21
, v-Ha-ras Harvey rat sarcoma viral oncogene homolog
, Transforming protein p21
, neuroblastoma ras oncogene
, v-Ha-ras Harvey rat sarcoma viral oncogene-like protein
, Harvey ras1 protein
, Harvey rat sarcoma viral (v-Ha-ras) oncogene homolog
, ras p21
, small G-protein H-Ras
, GTPase HRas (Transforming protein p21) (H-Ras-1) (c-H-ras)
, Harvey ras 1
, H-ras 1 protein
, c-Ha-ras p21 protein
, c-Ha-ras transgene
, transforming protein P21