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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.
we found that H-Ras proteins and particularly the G12V and G13D variants are significantly more flexible than their K-Ras counterparts.while most of the simulated proteins sampled the effector-interacting state 2 conformational state, G12V and G13D H-Ras adopted an open switch state 1 conformation that is defective in effector interaction
The HRAS mutation p.T58I could manifest with severe early-onset but stabilizing cardiomyopathy. The dysmorphic features are mild compared with the features of Costello syndrome. The phenotypic variability makes the diagnosis challenging, suggesting that this variant of Costello syndrome might go undiagnosed.
Age at diagnosis of follicular thyroid cancer (FTC (show FUT2 ELISA Kits)) and frequency of extrathyroidal extension have changed over four decades; prevalence of RAS mutations has decreased; HRAS/NRAS (codon 61) and TERT (show TERT ELISA Kits) (promoter) mutations may be associated with poor clinical outcomes in FTC (show FUT2 ELISA Kits), especially when two mutations coexist; this retrospective study was conducted in Seoul.
Knockdown of forkhead Box M1 (FoxM1 (show FOXM1 ELISA Kits)) reduced Prx (show PRDX6 ELISA Kits) II levels in H-ras(G12V)-hepatocellular carcinoma (HCC (show FAM126A ELISA Kits)) cells, indicating FoxM1 (show FOXM1 ELISA Kits) as a direct transcription factor of Prx (show PRDX6 ELISA Kits) II in HCC (show FAM126A ELISA Kits).
we found that ectopic expression of oncogenic KRas and HRas in cells resulted in elevated CIB1 (show CIB1 ELISA Kits) expression. We previously described the Ca(2 (show CA2 ELISA Kits)+)-myristoyl switch function of CIB1 (show CIB1 ELISA Kits), and its ability to facilitate agonist-induced plasma membrane localisation of sphingosine kinase 1 (SK1 (show SPHK1 ELISA Kits)), a location where SK1 (show KCNN1 ELISA Kits) is known to elicit oncogenic signalling.
Data suggest that isoform-specific sequences in the allosteric lobes of HRAS, KRAS, and NRAS (show NRAS ELISA Kits) have an impact on biocatalysis (kinetics of GTP (show AK3 ELISA Kits) hydrolysis) and interaction with c-Raf (show RAF1 ELISA Kits) kinase, which must be due to allosteric effects on dynamics and conformational states, given the identical active sites of these isoenzymes.
Data suggest HRas activates both p110alpha and p110delta isoforms; membrane-resident HRas, not soluble HRas, increases membrane recruitment of both p110alpha and p110delta. (HRas = v-Ha-ras Harvey rat sarcoma viral oncogene homolog; p110alpha = class IA phosphoinositide 3-kinases, subunit p110alpha; p110delta = class IA phosphoinositide 3-kinases, subunit p110delta)
Our data suggest that testing for any RAS mutation is unlikely to change the clinical management of thyroid nodules that have indeterminate cytology
Equilibrium dissociation constants were determined for the binding of HRAS, KRAS, NRAS and RRAS2 to the RAS binding (RB) domain of binding proteins.
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 (show THBS1 ELISA Kits), fibronectin (show FN1 ELISA Kits), and vitronectin (show VTN ELISA Kits) are differentially dependent upon RAS, ERK1/2 (show MAPK1/3 ELISA Kits), and p38 (show MAPK14 ELISA Kits) for induction of vascular smooth muscle cell chemotaxis.
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 (show ROCK2 ELISA Kits)/NF-kappaB (show NFKB1 ELISA Kits) signalling in skin carcinogenesis.these data show that ROCK2 (show ROCK2 ELISA Kits) activation induces malignancy in ras(Ha)-initiated/promoted papillomas in the context of p53 (show TP53 ELISA Kits) loss and novel NF-kappaB (show NFKB1 ELISA Kits) 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 (show NRAS ELISA Kits) 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 (show AKT1 ELISA Kits)/PI3K signaling pathway.
The long intergenic non-coding RNA CCR492 functions as a let-7 competitive endogenous RNA to de-repress c-Myc (show MYC ELISA Kits) 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 (show BRAF ELISA Kits)(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 (show BCL2 ELISA Kits) suppress the terminal differentiation and sustain the stem cell-like features in epidermal keratinocytes
Ras (G12V)-induced cyclin D1 (show CCND1 ELISA Kits) protein synthesis was markedly suppressed by the knockdown of IL-33 (show IL33 ELISA Kits).
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