Biography:

Professor Ravid has completed his PhD from Tel Avi University in 2001 and postdoctoral studies from University of California, Davis, School of Medicine and fom Yale University, School of Medicine. He is faculty member at the Department of Biological Chemisty, Faculty of Life Sciences, the Hebrew University of Jerusalem, since 2007. His Lab research focuses  on the mechanisms underlying protein quality control and degradation by the ubiquitin-proteasome system, using the budding yeast Saccharomyces cerevisiae as a model organism.

Abstract:

The ubiquitin-proteasome system (UPS) for protein degradation has been under intensive study, and yet, we have only partial understanding of mechanisms by which proteins are selected to be targeted for proteolysis. One of the obstacles in studying these recognition pathways is the limited repertoire of known degradation signals (degrons). To better understand what determines the susceptibility of intracellular proteins to degradation by the UPS, we developed an unbiased method for large-scale identification of eukaryotic degrons. Using a reporter-based high-throughput competition assay, followed by deep sequencing, we measured a degradation potency index for thousands of native polypeptides in a single experiment. We further used this method to identify protein quality control (PQC)-specific and compartment-specific degrons. Our method provides an unprecedented insight into the yeast degrome, and it can readily be modified to study protein degradation signals and pathways in other organisms and in various settings.

Biography:

Bernard Lopez has completed his PhD at the age of 27 years from University of Lyon I and postdoctoral studies from Curie Institute (Paris), followed by a sabbatical from and Brandeis university (Waltham, Ms, USA). He is first class research director at CNRS (French state organisation for basic research). He has published more than 70 papers in reputed journals and has been serving as a scientific advisor of many organizations.

Abstract:

The DNA damage response (DDR) is essential for maintaining genome stability. Here, we discovered that, in a response specific to low-intensity replication stress, primary cells control the production of non-nuclear reactive oxygen species (ROS) by inducing expression of the NADPH oxidases DUOX1 and DUOX2 in an NF-kB-dependent manner. This response does not activate cell cycle arrest but, strikingly, protects against the accumulation of pre-mutagenic DNA lesions such as 8-oxoG. Increasing the replication stress intensity above a threshold triggers the canonical DDR leading to DNA synthesis inhibition and suppression of replication stress-induced ROS (RIR), in a p53/ATM-dependent manner. These data bring to light an actual cell response, specific to low stress intensity that constitutes a “pre-DDR response”. Therefore, cells adapt their response to the severity of stress in the following two distinct phases: a low-intensity stress response, which produces RIR protecting against the accumulation of pre-mutagenic lesions, and, beyond a threshold of stress intensity, a high-intensity stress response that corresponds to the actual canonical DDR and that detoxifies RIR.

Strikingly, RIR are deregulated during the early steps of cancer progression, abolishing the threshold and the distinction between the low and high intensity stress responses. Moreover, nuclear RIR are produced, generating DNA damages. Because ROS generate replication stress, which reciprocally generates ROS, this initiates a vicious circle maintaining and amplifying genetic instability leading to carcinogenesis and fuelling cancer progression.

Biography:

Abstract:

Biography:

Braga E.A. has completed her PhD at the age of 28 at Lomonosov Moscow State University, Bioorganic Chemistry Department. She has taken a part in Russian Human Genome Project and HUGO. She was an Invited Principle Investigator at Karolinska Institute (Stockholm, Sweden, 1999-2000). She completed her full Dr. of Biology Sc. at Engelhardt Institute of Molecular Biology in 2007. She is a head of Laboratory of Pathogenomics and Transcriptomics at Institute of General Pathology and Pathophysiology, Moscow, Russia. She has published more than 70 papers in reputed Journals.

Abstract:

Epigenetic mechanisms including DNA methylation and interaction between miRNAs and mRNAs are the most dynamic mechanisms of genes deregulation in cancer. The aim of this study was to identify novel miRNAs, involved in down-regulation of some cancer-associated genes, and could be down-regulated itself by DNA methylation, in breast cancer (BC). We analyzed expression and methylation profiles of 20 tumor-suppressor miRNAs and 15 cancer-associated genes, which interactions were predicted by algorithms of miRWalk 2.0 database. Representative set of 58 paired (tumor/normal) BC samples; methylation-specific PCR, qPCR and the IBM SPSS Statistics Base 20 software package were used. We first observed hypermethylation of MIR-127, -132, -1258, -193a, and hypomethylation of MIR-191. Using qPCR, we established a strong correlation between promoter methylation and expression levels of 12 miRNA genes, confirming the functional importance of altered methylation patterns. The significant negative correlations were revealed between expression level alterations for the following pairs: CCND1 – miR-212-3p, -34a-5p, -34c-3p; BCL2 – miR-24-2-5p, -212-3p, -124-3p; BCL6 – miR-34a-5p, -24-2-5p. The results of transfection of MCF7 cell line with miR-124-3p duplex strengthened hypothesis on direct or indirect interaction of this miRNA with BCL2 mRNA. Thus, systemic role of hypermethylation in deregulation of miRNAs and its targets was shown, and novel potential interactions of 5 miRNAs with CCND1, BCL2, and BCL6, being involved in cell cycle regulation, apoptosis, EMT and metastasis, were suggested, that could be useful as missing chains in signaling pathways and potential targets in complex BC therapy. This work was financially supported by the Russian Science Foundation grant 14-15-00654.

Biography:

Nabieh Ayoub began his scientific career at the Hebrew University (1989-1993) where he received a BSc in Biology. He has done his Master’s degree with distinction in Genetics (1994-1996) studying chromosome X inactivation. Supported by the Levy Eshkool Fellowship from the Israeli Ministry of Science, he pursued his PhD in the study of heterochromatic gene regulation under the supervision of Professor Amikam Cohen at Hadassah Medical School, the Hebrew University (1997-2002). He is an Assistant Professor at the Israel Institute of Technology – Technion. In 2016, he was prompted to the degree of Associate Professor with tenure.

Abstract:

Double-strand breaks (DSBs) trigger rapid and transient transcription pause to prevent collisions between repair and transcription machineries at damage sites. Little is known about the mechanisms that ensure transcription block after DNA damage. Here we reveal a novel role of the negative elongation factor, NELF, in blocking transcription activity nearby DSBs. We show that NELF-E and NELF-A are rapidly recruited to DSB sites. Furthermore, NELF-E recruitment and its repressive activity are both required for switching off transcription at DSBs. Remarkably, using I-Sce-I endonuclease and CRISPR-Cas9 systems, we observed that NELF-E is preferentially recruited, in a PARP1-dependent manner, to DSBs induced upstream transcriptionally active rather than inactive genes. Moreover, the presence of RNA polymerase II is a prerequisite for the preferential recruitment of NELF-E to DNA breakage sites. Additionally, we demonstrate that NELF-E is required for intact repair of DSBs. Altogether, our data identified NELF complex as a new component in the DNA damage response.

Biography:

Peleg Hasson has completed his PhD at the age of 33 years from the Hebrew University, Jerusalem, Israel University and continued his postdoctoral studies at the MRC-National Institute of Medical Research, London. He has started his own lab at the Technion's Rappaport Faculty of Medicine in 2010.

Abstract:

For muscles to function, myofibers have to stretch and anchor at the myotendinous junction (MTJ), a region rich in extracellular matrix (ECM). Integrin signaling is required for MTJ formation, and mutations affecting the cascade lead to muscular dystrophies in mice and humans. Underlying mechanisms for integrin activation at the MTJ and ECM modifications regulating its signaling are unclear. We show that lysyl oxidase-like 3 (LoxL3) is a key regulator of integrin signaling that ensures localized control of the cascade. In LoxL3 mutants, myofibers anchor prematurely or overshoot to adjacent somites, and are loose and lack tension. We find that LoxL3 complexes with and directly oxidizes Fibronectin (FN), an ECM scaffold protein and integrin ligand enriched at the MTJ. We identify a mechanism whereby localized LoxL3 secretion from myofiber termini oxidizes FN, promoting FN polymerization thus priming it for integrin activation at the tips of myofibers and ensuring correct positioning and anchoring of myofibers along the MTJ.

Biography:

Yangyang Yu is professor at center for diabetes, obesity and metabolism in department of physiology, Shenzhen University Health Science Center, Shenzhen, Guangdong province, China.

Abstract:

Toll-like receptors (TLRs) expressed on mast cells are essential for effective host defense against a wide variety of pathogens. Previous studies have demonstrated that TLR2 agonists Pam3CSK4 and PGN both stimulated IL-8 release in human mast cells. To determine the molecular basis for this phenomenon, we utilized a human mast cell line LAD2 cells. We found that only release of IL-8 stimulated by Pam3CSK4 was TLR2-mediated, which was confirmed by specific TLR2 shRNA. Heterotrimeric G proteins have been previously implicated in TLRs signaling in macrophages and monocytes. In the current study, we showed that PamCSK4 induced the activation of MAPKs, NF-κB, PI3K-Akt and Ca2+-calcineurin-NFAT signaling cascades in LAD2 cells. G_o proteins were required for the activation of MAPKs and NF-κB in TLR2 stimulated LAD2 cells. Therefore, genetic depletion of Gα_o proteins also leaded to reduction of IL-8 release in LAD2 cells. Taken together, the data presented here suggest that TLR2 activation in human mast cells promotes the release of inflammatory mediators via distinct signaling pathways that partially depends on G_o protein action.

Biography:

Rinat Arbel-Goren completed her PhD in 2002 in Life Sciences at the Department of Molecular Biology of the Cell, Weizmann Institute of Science Rehovot, Israel, under Prof. Y. Zick. From 2002-2005, she carried out a Postdoc in the Department of Immunology, under Prof Y. Reisner. Since 2006 she is a Staff Scientist in the Department of Physics of Complex Systems, Weizmann Institute of Science, in the lab of Prof. J. Stavans. In addition to the above, her current research topics include:Effects of post-transcriptional regulation by small-RNAs on phenotypic variability; Effects of phenotypic variability during development in cyanobacteria.

Abstract:

During horizontal gene transfer processes, imported exogenous DNA sequences integrate at unique sites in the host bacterial genome, driving genetic diversity. One example is viral infection, which is known to allow the acquisition of pathogenic traits.After entering an Escherichia coli cell, the ∼5x10⁴-long bacteriophage λ DNA must locate a unique site among ∼5x10⁶ possible sites on the bacterial genome, with high efficiency and within physiological times, to integrate and establish lysogeny. What are the mechanisms that allow it to do it?We followed the targeting process in individual live E. coli cells in real-time, by marking fluorescently both the phage DNA after entry into the host, and a chromosomal sequence near the integration site. Surprisingly, we found that λ DNA does not carry out an active search. Instead, it remains confined near its entry point into the cell following infection, preferentially at the poles, where it undergoes limited diffusion. The encounter between the 15 bp-long target sequence on the chromosome and the recombination site on the viral genome is facilitated by thedirected motion of bacterial DNA generated during chromosome replication and segregation.A different mechanism of target location is observed during conjugation betweenB. subtilis cells:  integrating conjugating elements imported from donor cells carry out anomalous diffusion within host cellsin their search for their target insertion sites, which move concomitantly, driven by replication of the host genome. These finding demonstrate that there are different solutions to the target location problemduring horizontal gene transfer processes.

Biography:

Peng-Sheng Wei completed his PhD in Mechanical Engineering department at University of California, Davis, in 1984. He has been a Professor in Department of Mechanical and Electro-Mechanical Engineering of National Sun Yat-Sen University, Kaohsiung, Taiwan, since 1989. He has contributed to advancing the understanding of and to the applications of electron and laser beam, plasma, and resistance welding through theoretical analyses coupled with verification experiments. He has published more than 80 journal papers and given keynote or invited speeches in international conferences more than 70 times. He was a Fellow of American Welding Society (AWS) in 2007 and a Fellow of American Society of Mechanical Engineers (ASME) in 2000. He has been the Xi-Wan Chair Professor at National Sun Yat-sen University (NSYSU) since 2009.

Abstract:

Pore formation and its shape in solid influence not only microstructure of materials, but also contemporary issues of various biology and medical sciences, etc. How to produce lotus-type porous material chosen as a scaffold is a challenging topic in tissue engineering. A pore in solid is usually resulting from entrapment of a nucleated bubble due to super-saturation by a solidification front. This work account for mass and momentum transport across a coupled shape of the bubble cap in physico-chemical interfacial equilibrium beyond the solidification front. Accurate determination of contact angle from a realistic shape of the cap is essentially required to predict the relevant shape of the pore in solid. It is systematically found that there are two different solute transport models subject to thin and thick thicknesses of concentration boundary layers on the solidification front. Case 1 accounts for species transport from the pore across an emerged cap through a thin concentration boundary layer on the solidification front into surrounding liquid in the early stage, whereas, case 2 is subject to species transport from the surrounding liquid across a submerged cap within a thick concentration boundary layer into the pore. The analytical results show the effects of initial conditions such as bond number and initial solute concentration in the liquid on development of the pore shape in solid. The predicted pore shape agrees with experimental data. How to select initial conditions to control porosity in solid has therefore been revealed.

Biography:

Peter Waziri completed his MSc at University of Nottingham in 2013. He is currently a PhD student in Medicinal Chemistry at University of Putra, Malaysia. In the last two years, he majored on “The isolation of bioactive components in plants for use in cancer therapy”.

Abstract:

Liver cancer is a leading cause of death in the world with an increasing burden in Asia and sub-Saharan Africa. The therapeutic options for liver cancers are inadequate and survival after diagnosis is very low. This situation actually creates the need for studies on natural products that can complement and provide suitable alternatives to the current therapeutic measures. In the current study, we used clausenidin isolated from Clausena excavata Burm. f. to treat liver cancer (hepG2) cells. The plant is a shrub used in Asian folk medicine to treat cancer patients locally but there is little or no scientific evidence supporting its therapeutic use. We evaluated the cytotoxicity of clausenidin as well as its effect on reactive oxygen species production in hepG2 cells. In addition, we carried out an ultra-structural investigation of the clausenidin-treated cells to identify potential mechanisms through which clausenidin induce cell death in hepG2 cells. Our results reveal that clausenidin induces cytotoxic effects in hepG2 cells in a dose dependent manner with significant increase in the production of reactive oxygen species. Cell death was found to have occurred via apoptotic and non-apoptotic routes as revealed by the results of DNA fragmentation analysis and transmission electron microscopy respectively. The present study lends credence to the use of Clausena excavata to treat cancer patients in Asia and demonstrates the potential of clausenidin in the biotherapy of liver cancer.

Biography:

Jun Yao completed his PhD at Pennsylvania State University, Department of Biology, USA in 2007. He is a Principal Investigator of School of Life Sciences at Tsinghua University, China. In recent years, he has published more than 10 papers in reputed journals.

Abstract:

Bipolar disorder (BD) is a complex neuropsychiatric disorder that is characterized by intermittent episodes of mania and depression; without treatment, 15% of patients commit suicide. Hence, BD has been ranked by the WHO as a top disorder of morbidity and lost productivity. Previous neuropathological studies have revealed a series of alterations in the brains of BD patients or animal models, such as reduced glial cell number in the patient prefrontal cortex, up-regulated activities of the PKA/PKC pathways, and changes in neurotransmission. However, the roles and causation of these changes in BD have been too complex to exactly determine the pathology of the disease. Furthermore, while some patients show remarkable improvement with lithium treatment, for yet unknown reasons, other patients are refractory to lithium treatment. Therefore, developing an accurate and powerful biological model for BD has been a challenge. The introduction of induced pluripotent stem cell (iPSC) technology has provided a new approach. Here, we developed a human BD iPSC model and investigated the cellular phenotypes of hippocampal dentate gyrus-like neurons derived from patient iPSCs. Guided by RNA-seq expression profiling, we detected mitochondrial abnormalities in young BD neurons using mitochondrial assays and, using both patch clamp recording and somatic Ca²⁺ imaging, we observed hyperactive action potential (AP) firing. This hyperexcitability phenotype of young BD neurons was selectively reversed by lithium treatment only in neurons derived from the patients who also responded to lithium treatment. Therefore, hyperexcitability is one early endophenotype of BD, and our BD iPSC model may be useful for the development of new therapies and drugs aimed at clinical treatment of this disease.

Biography:

Dennis M Lox is a world renowned Sports and Regenerative Medicine Expert. He has lectured internationally with some of the most acclaimed Regenerative Medicine and Stem Cell researchers in the world. He has a special interest in Regenerative and Stem Cell Medicine as it relates to athletes, the aging population, osteoarthritis, and Avascular Necrosis (AVN). He has edited two medical textbooks, eight medical textbook chapters, authored numerous scientific articles and abstracts. He continues to maintain an active sport and regenerative medicine practice in Beverly Hills, California and Tampa Bay, Florida region. He has treated patients from around the globe. These diverse patients include professional athletes to patients in their nineties. Utilizing this experience, he incorporates an individualized approach to each patient.

Abstract:

The use of various scaffolds, matrix materials, and stem cells in regenerative medicine and tissue engineering has proliferated in the last decade. The inter-lapping nature of regenerative medicine and tissue engineering, has explored the fundamentals of bioscience, cellular signaling, and aging. The various engineered scaffolds have included synthetic, allogenic, autologous, xenographic, natural matrix substrates and 3-D bio-printing. Cellular medicine has also explored various types of cells including autologous, allogenic, and perinatal. The animal model has yielded promising results, yet a fundamental difference in human diverse behavior and inter-patient variability, may ultimately prove impossible to extrapolate from more simplistic animal model studies. The inherent nature of degenerative osteoarthritis of the knee is a progressive phenomenon. The role of cellular medicine and bio-scaffolds may alter the nature of osteoarthritis over time, thus impacting functional level and quality of life (QoL). The future of improving quality of life (QoL) may find a common thread in preventative and regeneration medicine.

Biography:

Shorayeva Kamshat Abitkhanovna is a Researcher of Molecular Biology and Genetic Engineering at Research Institute for Biological Safety Problems. She is a Specialist in the field of Molecular Biology, Biochemistry, Biotechnology and Diagnostics of Viral Infections. She is involved in performing international and national research projects and has more than 30 publications in scientific journals.

Abstract:

Diversity of avian viral diseases impedes their diagnosis by traditional research methods. To solve the problem, we developed a new oligonucleotide microchip for rapid simultaneous diagnosis of viral diseases in birds such as avian influenza (AI), Newcastle disease (ND), infectious bronchitis (IB) and infectious bursal disease (IBD). The designed oligonucleotide microchip consists of 16 identical subarrays for simultaneous rapid detection of avian viruses: AIV, NDV, IBV and IBDV in single- and mixed-virus infections. Probes for the proposed microarray are designed on the basis of conserved regions from gene fragments encoding the major viral proteins: NP and M (AIV), NP (VBI), VP2 (VIBB) and S1 (VIB), provided in GenBank database. Versatility of test makes it suitable for a wide use in veterinary laboratories for rapid detection of avian infections. So, the developed microarray for rapid diagnosis of avian viral diseases can be used in mass analysis in the system of routine epidemiological surveillance owing to its ability to test one sample for simultaneous detection of AIV, NDV, IBV and IBDV in cases of single and mixed viral infections. At the same time, duration of the analysis decreases dozen times versus classical methods and the proposed scheme of specimen preparation allows conducting assays immediately in small veterinary laboratories thus avoiding transportation of thermolabile RNA.

Biography:

Hyeon-Ju Lee has done her graduation from Dankook University. She is currently a PhD candidate in the Department of Molecular Medicine, Ewha Womans University Medical School. She has published six papers in reputed international journals.

Abstract:

Zearalenone (ZEN), a non-steroidal estrogenic mycotoxin produced from Fusarium species, is reported to induce damage of a variety of cells such as primary Leydig cells, human bronchial epithelial cells, and human HepG2 hepatocytes. However, to date such study has never been conducted in endothelial cells (EC). In this study, using bovine aortic EC (BAEC), we examined whether and how ZEN affects nitric oxide (NO) production in EC, which is commonly used as an index of EC function. ZEN significantly decreased NO production which was accompanied by a dose- and time-dependent decreases in endothelial NO synthase (eNOS) protein expression. It also decreased eNOS mRNA expression in a dose- and time-dependent manner. Treatment with ICI 182,780, a specific estrogen receptor (ER) antagonist, did not reverse ZEN-induced decrease in eNOS protein and mRNA expression, suggesting no evidence of involvement of ER. Treatment with MG132, a specific proteasome inhibitor, and mithramycin A, a specific Sp1 inhibitor, however, clearly reversed the observed inhibitory effects of ZEN on eNOS protein and mRNA expression. However, the eNOS gene promoter activity analysis revealed that MG132 did not reverse the decreased eNOS gene promoter activity by ZEN, suggesting a possible role for mRNA stability. Altogether, ZEN decreases NO production at least by decreasing eNOS expression at multiple levels including eNOS mRNA transcription/stability and protein degradation, indicating that this mycotoxin may profoundly alter vessel function.

Biography:

J Espina is pursuing his PhD from University of Oviedo, Spain.

Abstract:

Nanoparticles (particles ranging from 1 to 100 nm) are widely used in many fields such as biomedicine, optics, electronics, chemistry, etc. It is in the biomedical field where nanoparticles show impressive potential applications. Fluorescent semiconductor metal nanocrystals (quantum-dots) are commonly used as fluorescent probes because of its high photoluminescence quantum yield and tunability. Nevertheless, the toxicity of quantum dots limits its application, so it is common to coat them with inert materials such as silica in order to lower the toxicity. Likewise, depending on the aim of the quantum dot, other co-functionalizations might be necessary, but it is difficult to combine both needs. Carbon dots are a good choice to solve this problem as they have similar fluorescent properties to quantum dots, but are easier to modify chemically. Carbon dots are carbon-based non-toxic, water-soluble nanoparticles which show good cell membrane permeability, high photostability and a very versatile surface chemistry. Thus, carbon dots are a good alternative to the use of quantum dots as fluorescent imaging probes. In this work, we describe the synthesis of highly luminescent carbon dots from citric acid by a hydrothermal carbonization method. After that we functionalized the surface with α-cyclodextrin, β-cyclodextrin and glucose. This functionalization increases its ability to go through the cell membrane and the space inside the cyclodextrin glucose ring might allow incorporating doxorubicin (chemotherapy medication) and transporting them inside the cell. Carbon dots showed high fluorescence emission at 433 nm (347 nm excitation). U2OS and 293T line cells as well as confocal microscopy were used to check the ability of carbon dots to enter inside the cell using a 405 nm laser. All these characteristics make carbon dots good candidates as cancer treatment agent in the future.

Biography:

Tania Fontanil López is a PhD student from University of Oviedo.

Abstract:

The extracellular matrix (ECM) of the central nervous system (CNS) has several aspects that make it unique and different from the ECM of other tissues. This includes the presence of proteoglycans such as versican, brevican and neurocan. Some of these chondroitin-bearing ECM components have been found to be substrates for several members of the ADAMTSs (a disintegrin and metalloproteinase with thrombospondin motifs) family of secreted metallo-proteases. Moreover, different studies have highlighted the ADAMTSs contribution to repair processes in central nervous system. In this regard, participation of ADAMTSs has been described in the recovery following degradation of glial scar and in stimulating axonal growth, thus enhancing neuronal synaptic plasticity induced after brain injury. However, the role of ADAMTSs in chronic diseases of the central nervous system is complex and not fully understood. A current challenge will consists in unveiling the precise role of ADAMTSs in both normal and pathological processes in the central nervous system. One of the members of this family, ADAMTS-12, has been recently genetically linked to some neuropathologies such as schizophrenia. ADAMTS-12 is known to be implicated in the degradation of some components of the ECM like COMP and aggrecan and thus related with musculoskeletal degenerative diseases. In our search for new substrates for this metallo-protease, we have found neurocan as a novel substrate which, in addition is also linked to neuropathies. Taking into account that previous studies have separately described the involvement of ADAMTS-12 and neurocan in schizophrenia, it could be speculated that the relationship between ADAMTS-12 and neurocan may have an important impact in this neurological disorder. Our ongoing studies are aimed to elucidate the relevance of the degradation of neurocan by ADAMTS-12 in neuropathies through the use of cell-based models and the phenotypic characterization of the ADAMTS-12 deficient mouse.

Biography:

Mária Golda earned her Master’s degree in Molecular Biology from the Faculty of Medicine, University of Debrecen. She has done her PhD under the supervision of Dr. József TÅ‘zsér in Retroviral Biochemistry Laboratory (LRB), in the Department of Biochemistry and Molecular Biology (University of Debrecen).

Abstract:

The Paternally Expressed Gene10 (PEG10) is a retrotransposon-derived imprinted gene in the human genome. Mutation in the coding sequence of the gene is lethal in embryological age due to defects of placental development. PEG10 has been implicated in the development of pancreatic cancer, embryonic kidney Wilms tumor, hepatocellular carcinoma and lymphocytic leukemia, suppressing apoptosis. PEG10 mRNA encodes for two protein isoforms, the reading frame 1 (PEG10- RF1) Gag-like protein and reading frames 1 and 2 (PEG10- RF1/2) Gag-Pol-like polyprotein, which is translated by a typical retroviral frameshift mechanism. The RF2 protein contains an -Asp-Ser-Gly- sequence which corresponds to the consensus active-site motif of retroviral aspartic proteases. We hypothesized that activity of this protease might be required for the strongly observed oncogenic effect of PEG10, in inducing cellular proliferation and suppressing apoptosis. Therefore, PEG10 protease (PR) may be regarded as a chemotherapeutic target. In order to investigate PEG10 PR, the amplified wild-type RF1/2 sequence was cloned into a pQE-TriSystem expression vector. We have also created an inactive PR mutant RF1/2 (D370A) to analyze the activity of the PR. To study the implication of PEG10 PR in cellular proliferation and viability, RF1/2 plasmids containing either a wild-type PEG10 PR or a D370A mutant were transfected into HEK mammalian cells. Our results indicate that overexpression of PEG10 PR may indeed result in the induction of cellular proliferation. Interestingly, when cell viability was assessed, transfection with wild-type PEG10 had a detrimental effect on cell viability.