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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 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.
Kita driven expression of oncogenic HRAS leads to early onset and highly penetrant melanoma in zebrafish
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.
It has been concluded that VMP1-mediated autophagy cooperated with Kras to promote pancreatic ductal adenocarcinoma initiation.
High KRAS expression is associated with Gastric Tumorigenesis.
Study underscores genomic alterations that represent early events in the development of Kras mutant LUAD following Gprc5a (show GPRC5A ELISA Kits) 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 ELISA Kits) signaling loop engaging the oncogenic transcription factor c-MYC (show MYC ELISA Kits).
median survival of KPIC mice was longer than that of LSL-KrasG12D; Ink4flox/flox; Ptf1/p48 (show PTF1A ELISA Kits)-Cre mice (KIC) (89 vs 62 days) and shorter than that of KRAS (KrasG12D), TP53 (show TP53 ELISA Kits) (Trp53R172H/+) and Ptf1/p48 (show PTF1A ELISA Kits)-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 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
activating mutations in GNAS and Kras cooperatively promote murine pancreatic tumorigenesis
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