• Animal cells and systems
• /
• v.13 no.4
• /
• pp.399-403
• /
• 2009

$p19^{ras}$ is an alternative splicing variant of the proto-oncogene c-H-ras pre-mRNA of $p21^{ras}$. In contrast to $p21^{ras}$, $p19^{ras}$ does not have a C-terminal CAAX motif that targets the plasma membrane and is localized to both the cytoplasm and nucleus. We found that $p19^{ras}$ activated the transcriptional activity of $p73{\beta}$ through protein-protein interactions in the nucleus. p73 is known to play an important role in cellular damage responses such as apoptosis. Although p73 is a structural and functional homologue of p53, p73-mediated apoptosis has not yet been clearly elucidated. In this study, we demonstrate that the interaction between $p19^{ras}$ and $p73{\beta}$ accelerated $p73{\beta}$-induced apoptosis through a caspase-3 dependent pathway. Treatment with DEVD-CHO, a caspase inhibitor, also strengthened $p73{\beta}$-mediated apoptosis through a caspase-3 dependent pathway. Furthermore, the enhanced transcriptional activity of endogenous $p73{\beta}$ by treatment with Taxol was amplified by $p19^{ras}$ overexpression, which markedly increased caspase-3 dependent apoptosis in the p53-null SAOS2 cancer cell line. Our findings indicate a functional linkage between $p19^{ras}$ and p73 in caspase-3 mediated apoptosis of cancer cells.

• Asian Pacific Journal of Cancer Prevention
• /
• v.13 no.11
• /
• pp.5535-5538
• /
• 2012

Background: There have been case reports of oral squamous cell carcinoma arising from gingival overgrowth induced by phenytoin - an antiepileptic drug. However, a detailed analysis for the presence of mutations in p53 and ras genes, which are the two most frequently mutated genes in cancers, in phenytoin induced gingival overgrowth tissues has hitherto not been performed. Methods: Cellular DNA isolated from twenty gingival overgrowth tissues collected from patients undergoing phenytoin therapy were amplified using primers for p53 (exons 5-8) and H-ras (exons 1-2) genes. The PCR amplicons were then gel purified and subjected to direct sequencing analysis to screen for mutations. Results: Direct sequencing of twenty samples of phenytoin induced gingival growth did not identify mutations in any of the exons of p53 and H-ras genes that were analyzed. Conclusion: Our result indicates that mutational alteration of p53 and H-ras genes is infrequent in phenytoin induced gingival growth, which thus suggests a non malignant nature of this pathology. The findings in the present study are clinically significant as a large number of epileptic patients are treated with phenytoin.

• Proceedings of the PSK Conference
• /
• 2003.10b
• /
• pp.168.3-169
• /
• 2003

The matrix metalloproteases (MMPs) play important roles in invasion, metastasis and angiogenesis in various cell types. Tissue inhibitor of metalloprotease (TIMP)-2, an endogenopus inhibitor of MMP-2, has been shown to inhibit invasion and metastasis. We have previously shown that MMP-2 is responsible for the H-ras-induced invasive and migrative phenotypes in MCF10A human breast epithelial cells. Here, we investigated the effect of TlMP-2 overexpression on invasion and migration in H-ras MCF10A cells. (omitted)

• Proceedings of the Korean Society of Toxicology Conference
• /
• 2002.05a
• /
• pp.76-77
• /
• 2002

Ras expression has been suggested as a marker for tumor aggressiveness of breast cancer including the degrees of invasion and tumor recurrence. Expression of H-, K-, and N-ras is regulated in a tissue-specific manner and during development, indicating that ras proteins may have different cellular functions.(omitted)

• BMB Reports
• /
• v.36 no.4
• /
• pp.399-402
• /
• 2003

Early detection of bladder cancer is particularly important since it dramatically affects the survival rates. However, neither urinary cytology nor tumor markers that are currently used are sensitive enough for the early detection of bladder cancer or recurrent disease. The ras genes are frequently mutated in cancer. In this study, we investigated the diagnostic potential of ras mutation analysis in urinary sediments of patients with bladder cancer using a single-strand conformation polymorphism analysis and polymerase chain reaction. Mutation in codon 12 of the H-ras gene was observed in 39% of the patients. Our results indicate that this approach may significantly improve diagnostic sensitivity in detecting bladder tumors.

• The Korean Journal of Physiology and Pharmacology
• /
• v.1 no.2
• /
• pp.151-159
• /
• 1997

In an attempt to investigate whether hemorrhage affects the gene expression of the renin-angioteusin system (RAS) components in the brain and peripheral angiotensin-generating tissues, changes in mRNA levels of the RAS components in response to hemorrhage were measured in conscious unrestrained rats. Wistar rats were bled at a rate of 3 ml/kg/min for 5 min, and then decapitated 7 h after hemorrhage. Levels of mRNA for renin, angiotensinogen and angiotensin $II-AT_1$ receptor subtypes ($AT_{1A}$ and $AT_{1B}$) were determined with the methods of northern blot and reverse transcriptase-polymerase chain reaction (RT-PCR). Hemorrhage produced a profound hypotension with tachycardia, but blood pressure and heart rate recovered close to the basal level at 7 h. Plasma and renal renin levels were significantly increased at 7 h. Hemorrhage induced rapid upregulation of gene expression of both $AT_{1A}$ and $AT_{1B}$ receptor subtypes in the brainstem and hypothalamus, downregulation of them in the adrenal gland and liver. However, renin mRNA level increased in the brainstem, decreased in the liver, but was not changed in the hypothalamus, kidney and adrenals after hemorrhage. Angiotensinogen mRNA level was not significantly changed in any of the tissue except a slight increase in the liver. The kidney and liver did not show any significant change in gene expression of the RAS components. These results suggest that gene expression of the RAS in central and peripheral tissues are, at least in part, under independent control and the local RAS in each organ plays specific physiologic role.

• International Journal of Naval Architecture and Ocean Engineering
• /
• v.12 no.1
• /
• pp.881-891
• /
• 2020

In recent years robotics has become an important resource in engineering. Adoption of Robotics and Autonomous Systems (RAS) in activities related to ship inspections has obvious potential advantages, but also arises particular challenges, both from technical and legal viewpoints. The ROBINS project (ROBotics technology for INspection of Ships) is a collaborative project co-funded within the H2020 EU Research and Innovation programme call, aimed at filling the gap between current ship inspections approach and available robotic technology, both from technological and regulatory point of view. Main goal of the present work is to highlight how ship inspections are currently carried out by humans, how they could be improved using RAS, even if not completely autonomous for the time being, at least in selected operational scenarios and how the performances of RAS platforms can be tested to assess their effectiveness in carrying out surveys onboard. In such a framework, a testing facility aimed at assessing RAS' capabilities as well as providing suitable environment for their development has been built and it is still under development along with dedicated testing protocols, able to assess the equivalence between human and RAS inspection of ship and marine structures. The features of a testing facility where RAS can be tested and the testing protocols are presented, showing how technological and regulatory gaps are filled.

• Proceedings of the Korea Environmental Mutagen Society Conference
• /
• 2003.05a
• /
• pp.100-101
• /
• 2003

• Proceedings of the Korean Society of Toxicology Conference
• /
• 2003.10b
• /
• pp.144-144
• /
• 2003

Phosphatidylinositol 3-kinase (PI3K) and Rac play important roles that regulate cellular functions including cell survival and .migration. In the present study, we investigated the functional roles of PI3K and Rac1 pathways in H-ras-induced invasive phenotype and motility of MCF10A cells.(omitted)

• Journal of Life Science
• /
• v.18 no.4
• /
• pp.461-466
• /
• 2008

Transforming growth $factor-{\beta}$ ($TGF-{\beta}$)-dependent apoptosis is important in the elimination of damaged or abnormal cells from normal tissues in vivo. Gadd45b has been known to participate in $TGF-{\beta}-induced$ apoptosis by the activation of p38 kinase. In this report, we show that Gadd45b is an immediate-early response gene for $TGF-{\beta}$ during apoptosis in EpH4 cells. To elucidate the molecular mechanism of $TGF-{\beta}-induced$ Gadd45b gene expression, we cloned the 5'-flanking region of the mouse Gadd45b gene. When transfected into EpH4 cells, this 5'-flanking region conferred promoter activity and inducibility by $TGF-{\beta}$. Deletion analyses demonstrated that the minimal promoter activity was detected in the proximal region 220 bp upstream of the transcription initiation site. We also found that the proximal Gadd45b promoter is activated by $TGF-{\beta}$ through the action of Smad2, Smad3, and Smad4. Finally, we show that the expression of Gadd45b gene by $TGF-{\beta}$ is suppressed in EpRas cells in which $TGF-{\beta}$ could not induce apoptosis, suggesting that Gadd45b may be a crucial target for $TGF-{\beta}-induced$ apoptosis in EpH4 cells.