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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 Proteins), fibronectin (show FN1 Proteins), and vitronectin (show VTN Proteins) are differentially dependent upon RAS, ERK1/2, and p38 (show MAPK14 Proteins) for induction of vascular smooth muscle cell chemotaxis.
Kita driven expression of oncogenic HRAS leads to early onset and highly penetrant melanoma in zebrafish
Age at diagnosis of follicular thyroid cancer (FTC (show FUT2 Proteins)) and frequency of extrathyroidal extension have changed over four decades; prevalence of RAS mutations has decreased; HRAS/NRAS (codon 61) and TERT (show TERT Proteins) (promoter) mutations may be associated with poor clinical outcomes in FTC (show FUT2 Proteins), especially when two mutations coexist; this retrospective study was conducted in Seoul.
Knockdown of forkhead Box M1 (FoxM1 (show FOXM1 Proteins)) reduced Prx (show PRDX6 Proteins) II levels in H-ras(G12V)-hepatocellular carcinoma (HCC (show FAM126A Proteins)) cells, indicating FoxM1 (show FOXM1 Proteins) as a direct transcription factor of Prx (show PRDX6 Proteins) II in HCC (show FAM126A Proteins).
we found that ectopic expression of oncogenic KRas and HRas in cells resulted in elevated CIB1 (show CIB1 Proteins) expression. We previously described the Ca(2 (show CA2 Proteins)+)-myristoyl switch function of CIB1 (show CIB1 Proteins), and its ability to facilitate agonist-induced plasma membrane localisation of sphingosine kinase 1 (SK1 (show SPHK1 Proteins)), a location where SK1 is known to elicit oncogenic signalling.
Data suggest that isoform-specific sequences in the allosteric lobes of HRAS, KRAS, and NRAS (show NRAS Proteins) have an impact on biocatalysis (kinetics of GTP (show AK3 Proteins) hydrolysis) and interaction with c-Raf (show RAF1 Proteins) 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.
Studies indicate that RAS proteins were among the first oncogenes identified and are mutationally activated in 30% of all cancer types.
6 of 7 (86%) malignant ectomesenchymomas had HRAS mutations
RAS-positive thyroid cancer most often demonstrates indolent sonographic features and more commonly associates with lower risk, "indeterminate" cytology.
Study underscores genomic alterations that represent early events in the development of Kras mutant LUAD following Gprc5a (show GPRC5A Proteins) loss and tobacco carcinogen exposure.
High HRAS expression is associated with hepatocarcinogenesis.
In the absence of TP53, chronic imflammaiton leads to the development of several rare K-ras-independent forms of PC, with infrequent PDAC.
KrasG12D-driven proliferation of pancreatic ductal epithelial cells (PDECs) depends on an EGFR (show EGFR Proteins) signaling loop engaging the oncogenic transcription factor c-MYC (show MYC Proteins).
median survival of KPIC mice was longer than that of LSL-KrasG12D; Ink4flox/flox; Ptf1/p48 (show PTF1A Proteins)-Cre mice (KIC) (89 vs 62 days) and shorter than that of KRAS (KrasG12D), TP53 (show TP53 Proteins) (Trp53R172H/+) and Ptf1/p48 (show PTF1A Proteins)-Cre (KPC) mice
Loss of N-cadherin in the context of oncogenic K-ras leads to increased pancreatic intraepithelial neoplasia (PanIN) incidence and progression.
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 Proteins)/NF-kappaB (show NFKB1 Proteins) signalling in skin carcinogenesis.these data show that ROCK2 (show ROCK2 Proteins) activation induces malignancy in ras(Ha)-initiated/promoted papillomas in the context of p53 (show TP53 Proteins) loss and novel NF-kappaB (show NFKB1 Proteins) expression
activating mutations in GNAS and Kras cooperatively promote murine pancreatic tumorigenesis
the Kras(mut (show MUT Proteins)) allele was heterogenous in primary tumors yet homogenous in metastases, a pattern consistent with activated Kras(mut (show MUT Proteins)) signaling being a driver of progression to metastasis.
Using an extensive collection of novel murine cell lines we have identified distinct roles for Kras and Pten on MUC1 (show MUC1 Proteins) and EMT (show ITK Proteins) in vivo and in vitro. The data has implications for future design of combination therapies targeting Kras mutations, Pten deletions and MUC1 (show MUC1 Proteins) vaccines.
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.
v-Ha-ras Harvey rat sarcoma viral oncogene homolog
, small G-protein H-Ras
, Harvey ras 1
, p19 H-RasIDX protein
, GTPase HRas (Transforming protein p21) (H-Ras-1) (c-H-ras)
, GTPase HRas
, Transforming protein p21
, neuroblastoma ras oncogene
, GTP- and GDP-binding peptide B
, Ha-Ras1 proto-oncoprotein
, Ras family small GTP binding protein H-Ras
, c-has/bas p21 protein
, c-ras-Ki-2 activated oncogene
, transformation gene: oncogene HAMSV
, transforming protein p21
, Harvey ras1 protein
, Harvey rat sarcoma viral (v-Ha-ras) oncogene homolog
, H-ras 1 protein
, c-Ha-ras p21 protein
, c-Ha-ras transgene
, transforming protein P21
, GTPase NRas
, transforming protein N-Ras
, v-Ha-ras Harvey rat sarcoma viral oncogene-like protein
, ras p21
, GTPase KRas
, K-Ras 2
, Kirsten rat sarcoma oncogene 2, expressed
, p21 protein