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Using the system, we detected Circulating tumor cells (CTCs) heterozygosity and heterogeneity in KRAS status among CTCs within a patient and between CTCs and tumor tissues
The G12A mutation reduces intrinsic K-Ras GTP (show AK3 Proteins) hydrolysis by an unexplained mechanism.Study reports crystal structures of G12A K-Ras in complex with GDP, GTP (show AK3 Proteins), GTPgammaS and GppNHp, and of Q61A K-Ras in complex with GDP, G12A K-Ras-GTP (show AK3 Proteins) complex, the switch I region undergoes a significant reorganization such that the Tyr32 side chain points towards the GTP-binding (show RND2 Proteins) pocket and forms a hydrogen bond to the GTP (show AK3 Proteins) gamma-phosphate.
Kras mutation appears to be one of the imperative events in the ovarian mucinous adenoma-borderline tumor-carcinoma sequence, as increased numbers of Kras mutations have been shown to be the strongest predictor of unequivocal malignancy in ovarian mucinous neoplasms.
KRAS Mutation is associated with Recurrence in rectal cancer.
KY1022, a small molecule that destabilizes both beta-catenin (show CTNNB1 Proteins) and Ras by targeting the Wnt (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) pathway, inhibitits cellular events, including epithelial mesenchymal transformation, an initial process of metastasis, and apoptosis in colorectal cancer cells.
The addition of simtuzumab to FOLFIRI did not improve clinical outcomes in patients with metastatic KRAS mutant colorectal carcinoma
The present study demonstrated that pathological stage I adenocarcinoma harboring EGFR and K-ras gene mutations have distinct clinicopathological features. The presence of these mutations alone were not prognostic factors in patients with resected pathological stage I adenocarcinoma.
Results indicate that specific inhibition of PI3K p110alpha (show PIK3CA Proteins) could provide an alternative therapeutic approach for colorectal cancer (CRC (show CALR Proteins)) patients, particularly those harboring KRAS mutations.
Suppression of MEK/ERK pathway in senescent cells provides a new strategy for elimination of Ras-expressing cells.
Reduced insulin receptor substrate-1 (IRS-1 (show IRS1 Proteins)) staining in lung adenocarcinoma tissue microarray displayed a significant survival disadvantage, especially within the Kirsten rat sarcoma viral oncogene (show RAB1A Proteins) homolog (KRAS) mutant subgroup.
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 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.
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 (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
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 Proteins) 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 Proteins)/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 Proteins) 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 Proteins)(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 Proteins) suppress the terminal differentiation and sustain the stem cell-like features in epidermal keratinocytes
This gene, a Kirsten ras oncogene homolog from the mammalian ras gene family, encodes a protein that is a member of the small GTPase superfamily. A single amino acid substitution is responsible for an activating mutation. The transforming protein that results is implicated in various malignancies, including lung adenocarcinoma, mucinous adenoma, ductal carcinoma of the pancreas and colorectal carcinoma. Alternative splicing leads to variants encoding two isoforms that differ in the C-terminal region.
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
, GTPase KRas
, K-Ras 2
, K-ras p21 protein
, PR310 c-K-ras oncogene
, c-Kirsten-ras protein
, cellular c-Ki-ras2 proto-oncogene
, oncogene KRAS2
, v-Ki-ras2 Kirsten rat sarcoma 2 viral oncogene homolog
, v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog
, H-ras 1 protein
, c-Ha-ras p21 protein
, c-Ha-ras transgene
, transforming protein P21
, GTPase NRas
, transforming protein N-Ras