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Publisher: Smart Science and Technology LLC   (Total: 21 journals)   [Sort by number of followers]

Showing 1 - 21 of 21 Journals sorted alphabetically
Abdomen     Open Access  
Cancer Cell & Microenvironment     Open Access   (Followers: 9)
Cardiovascular Regenerative Medicine     Open Access  
Evidence-based Medicine & Public Health     Open Access   (Followers: 7)
Immunoendocrinology     Open Access   (Followers: 1)
Inflammation and Cell Signaling     Open Access   (Followers: 3)
Itch & Pain     Open Access   (Followers: 2)
J. of Advanced Nutrition and Human Metabolism     Open Access   (Followers: 14)
Macrophage     Open Access  
Molecular & Cellular Epilepsy     Open Access   (Followers: 2)
Musculoskeletal Regeneration     Open Access   (Followers: 2)
Neurotransmitter     Open Access  
Precision Medicine     Open Access   (Followers: 2)
Receptors & Clinical Investigation     Open Access   (Followers: 1)
RNA & Disease     Open Access   (Followers: 1)
Science Proceedings     Open Access   (Followers: 1)
Stem Cell and Translational Investigation     Open Access   (Followers: 2)
Stem Cell Epigenetics     Open Access   (Followers: 3)
Telomere and Telomerase     Open Access  
Therapeutic Targets for Neurological Diseases     Open Access   (Followers: 1)
Uterus & Ovary     Open Access  
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ISSN (Online) 2375-7795
Published by Smart Science and Technology LLC Homepage  [21 journals]
  • The Subcellular Compartment for Endoplasmic Reticulum-Associated
           Degradation of Exogenous Antigens from dendritic cells

    • Authors: Mayu Otani, Takahiro Sakai, Shinichi Hatta
      Abstract: Dendritic cells (DCs) have the unique ability of processing and presenting exogenous antigens upon major histocompatibility class I (MHC I) molecules. This ability is called antigen cross-presentation (CP) and plays not only in the activation of naïve CD8+ T into anti-infectious and anti-tumoral cytotoxic CD8+ T cells, but also in the inactivation of self-acting naïve T cells by T cell anergy or T cells deletion. Since antigen CP was first described more than four decades ago, so many numbers of studies, by using a variety of sources of antigens and antigen-presenting cells (APCs), had been carried out to solve the cellular process of CP. There are accumulating in vivo and in vitro evidences that endoplasmic reticulum (ER)-associated degradation (ERAD) acts as a key player in CP. But for all these efforts, the precious molecular mechanisms for CP are still remained to be elucidated. It may be partially because there are several pathways for CP running alongside with each other and each cell uses these several pathways redundantly responding against environmental conditions. Here, we review the intracellular transport routes for exogenous antigens and the subcellular compartment in which exogenous antigens undergo ERAD.
      PubDate: 2017-01-17
      DOI: 10.14800/sp.1490
      Issue No: Vol. 4 (2017)
       
  • Rituximab dosing in B cell lymphoma

    • Authors: Mitchell R Smith
      Abstract: Rituximab has been extensively used in the treatment of CD20-expressing B cell neoplasms in the last two decades. Despite that, its dose and scheduling are still being questioned as they are supported my minimal scientific evidence. Our retrospective study of patients with indolent B cell lymphoma showed that older males and patients with higher weight had worse outcomes when treated with first line rituximab-containing chemotherapy, probably due to faster rituximab clearance. This suggests that a subset of patients with indolent B cell lymphoma may be sub-optimally dosed with rituximab as commonly administered. These results are in line with other studies in aggressive lymphoma where rituximab pharmacokinetics were shown to be affected by gender, age and weight and can affect outcomes. Our study also highlights the challenge of presenting the newer anti-CD20 monoclonal antibodies as intrinsically superior to rituximab when they are given at higher dose and more frequent administration.
      PubDate: 2016-12-05
      DOI: 10.14800/sp.1463
      Issue No: Vol. 3 (2016)
       
  • Effects of Acrolein on Adrenal Glands

    • Authors: Kai-Lee Wang
      Abstract: Aldosterone and cortisol, two major hormones secreted from adrenal glands, are vital to life by maintaining electrolyte, body fluid and energy homeostasis in human. Both of hormones are regulated precisely. Acrolein, the well-known cytotoxic agent released during the incomplete combustion. It abounds in the smoke of cigarette and in enclosed fires. Previous studies have demonstrated that smoking has the adverse effects on cardiovascular, nerve and other system. In particular, the pathogenic functions of tobacco inhalation in cardiovascular disorders as well as alters plasma electrolyte levels have been well documented. It is thus important to evaluate cellular/molecular mechanisms of smoking that change these responses. In a recent paper published in Steroids, we demonstrated that the major chemical in cigarette, acrolein, has the abilities to enhance aldosterone secretion and decrease corticosterone secretion. These effects may associate with the progression of cardiovascular and other diseases.
      PubDate: 2016-09-26
      DOI: 10.14800/sp.1428
      Issue No: Vol. 3 (2016)
       
  • Dual-targeting of MEK and CDK4/6 in KRAS-mutated Non-Small Cell Lung
           Cancer

    • Authors: Justin M Le Blanc, Nicholas G Zaorsky, Bo Lu
      Abstract: Discovering new ways to modulate the responsiveness of non-small cell lung cancer (NSCLC) to treatment represents one of the forefronts of cancer research. KRAS mutations, present in roughly 30% of NSCLCs, lead to increased levels of cellular proliferation and decreased responsiveness to treatment modalities. The present study examined the RB/p16/CDK4 pathway as a way to modulate the responsiveness of these cell lines. The diverse downstream effects of these pathways suggest that molecular profiling of NSCLCs may assist clinicians and researchers to predict the effectiveness in the application of particular therapeutics.
      PubDate: 2016-07-05
      DOI: 10.14800/sp.1363
      Issue No: Vol. 3 (2016)
       
  • Novel role of Parkinson’s protein DJ-1/Park7 in the development of
           Foxp3+ regulatory T cells

    • Authors: Yogesh Singh, Madhuri S Salker, Florian Lang
      Abstract: Parkinson’s protein DJ-1/Park7, is a key regulator of redox signalling in neurons and muscles by regulating reactive oxygen species (ROS) production. Defects in DJ-1 are suggested to cause autosomal recessive early-onset Parkinson's disease. Further, deregulated DJ-1 signalling has been ascribed to other pathologies including diabetes (type II) and in obesity. How DJ-1/Park7 is involved in the maintenance of immune T cells especially suppressor regulatory T cells (Tregs) is not well defined. We explored this important question by using DJ-1 knock-out mice at cellular and molecular level. We found that DJ-1 is involved, both in vivo and in vitro, in the development of natural and induced Tregs. Differentiation of induced Tregs is regulated by mammalian target of rapamycin (mTOR)/Serum and glucocorticoid kinase 1 (Sgk1) and ROS/NFƙB pathway. Thus, our data highlights the importance of DJ-1 in the development of Tregs.
      PubDate: 2016-05-09
      DOI: 10.14800/sp.1285
      Issue No: Vol. 3 (2016)
       
  • Conceptual design for critically-high power generation efficiency by using
           multi-stage solid oxide fuel cells (SOFCs) or proton-conducting ceramic
           fuel cells (PCFCs)

    • Authors: Yoshio Matsuzaki, Yuya Tachikawa, Takaaki Somekawa, Koki Sato, Hiroshige Matsumoto, Shunsuke Taniguchi, Kazunari Sasaki
      Abstract: Recently we have developed the conceptual design for realizing a critically-high electrical efficiency with solid oxide fuel cells (SOFCs). SOFCs are promising electrochemical devices that enable the highest fuel-to-electricity conversion efficiencies under high operating temperatures. The concept of multi-stage electrochemical oxidation using SOFCs has been proposed and studied over the past several decades for further improving the electrical efficiency. However, the improvement is limited by fuel dilution downstream of the fuel flow. Recently we developed and reported a conceptual design that has a potential to realize a critically-high fuel-to-electricity conversion efficiency of up to as high as 85% (LHV, gross DC), in which a high-temperature multi-stage solid oxide fuel cells (SOFCs) is combined with a proton-conducting solid oxide electrolyte. Switching a solid electrolyte material from a conventional oxide-ion conducting material to a proton-conducting material under the high-temperature multi-stage electrochemical oxidation mechanism has proven to be highly advantageous for the electrical efficiency. The DC efficiency of 85% (LHV) corresponds to a net AC efficiency of approximately 77% (LHV), where the net AC efficiency refers to the transmission-end AC efficiency. This evolved concept will yield a considerably higher efficiency with a much smaller generation capacity than the state-of-the-art several tens-of-MW-class most advanced combined cycle (MACC). In the conceptual design the proton-conducting electrolyte was assumed to have a protonic transport number of 1. However, the protonic transport number of the proton-conducting solid oxide electrolyte depends on the material and operating conditions such as temperature, oxygen partial pressure, kinds of fuel and so on, and would affect the electrical efficiency. Therefore, to realize the critically-high electrical efficiency by using the multi-stage electrochemical oxidation, proton-conducting solid oxide having a high ionic transport number should be developed.
      PubDate: 2016-05-02
      DOI: 10.14800/sp.1272
      Issue No: Vol. 3 (2016)
       
  • Nicotine and the taste allure for salty food

    • Authors: Albertino Bigiani
      Abstract: Smoking has been recognized as one agent that may decrease the effectiveness of the gustatory system to detect salt (Na+) in foodstuffs. As a consequence, smokers tend to ingest saltier foods than nonsmokers. An increase in sodium intake has been associated with hypertension: thus, smoking may concur to the development of  hypertension by impairing salt perception. Understanding the mechanisms underlying the action of smoking on salty taste represents the premise to design proper intervention aiming at restoring normal sensitivity to sodium in smokers. I addressed this issue by studying the effect of nicotine, one of the main components of tobacco smoke, on the sodium detection mechanism in rat taste cells. Electrophysiological analysis of these cells revealed that long-term exposure to nicotine reduced the ion current mediated by the Epithelial Sodium Channel (ENaC), one of the sodium receptors occurring in taste cells. As to the molecular mechanism responsible for such a current decrease, data were consistent with a reduction in the number of functional ENaCs in the membrane of taste cells. Therefore, nicotine reduces the capability of taste cells to respond to sodium ions. This might explain, at least in part, why smokers tend to use salt more abundantly when flavoring their food: they are just boosting the sensory information to be relayed to the brain.
      PubDate: 2016-01-04
      DOI: 10.14800/sp.1133
      Issue No: Vol. 3 (2016)
       
  • Osteogenic Differentiation of Adipose-Derived Stromal Cells: Advancements
           and Future Directions for Bone Tissue Engineering

    • Authors: Graham G Walmsley, Alexander T Cheung, Michael S Hu, H. Peter Lorenz, Michael T Longaker
      Abstract: Adipose-derived stromal cells (ASCs) present a promising cell source for tissue engineering applications. ASCs are attractive due to their abundance and ease of procurement through subcutaneous liposuction and subsequent isolation from lipoaspirates. ASCs are also preferable to more controversial stem cell sources due to ethical considerations and potential for teratoma formation. Recent approaches to promote osteogenesis have incorporated potent agents such as exogenous osteogenic growth factors, substrate-induced differentiation using mechanical properties of scaffolds, and genetic modification using viral vectors, RNAi, and nanotechnology. In this manuscript we review current literature on methods for the differentiation of ASCs for the purpose of improving bone tissue engineering.
      PubDate: 2016-01-04
      DOI: 10.14800/sp.1085
      Issue No: Vol. 3 (2016)
       
  • The role of the tumor suppressor PTEN in Chronic Myeloid Leukemia
           pathogenesis

    • Authors: ALESSANDRO MOROTTI
      Abstract: The tumor suppressive properties of Phosphatase and Tensin homolog PTEN are exerted within two different cellular compartments. In the cytoplasm/membrane, it regulates cellular proliferation, survival and metabolisms, through the de-phosphorylation of the phosphatidylinositol (3,4,5) triphosphate (PIP3), therefore counteracting the PI3K-AKT pathway. In the nucleus, it regulates proliferation and genomic stability through phosphatase independent mechanisms. Chronic Myeloid Leukemia is a myeloproliferative disorder characterized by the translocation t(9;22) coding for the chimeric protein BCR-ABL. PTEN was shown to play an essential role in the CML pathogenesis in a murine model. We and others have demonstrated that PTEN is affected in human CML though non genomic loss of function mechanisms. Furthermore, we proposed strategies to reactivate PTEN in CML cells, with relevant therapeutic implications. 
      PubDate: 2015-02-15
      DOI: 10.14800/sp.638
      Issue No: Vol. 3 (2015)
       
  • Manipulating Host Signaling for Pathogenic Purposes: Hijacking of the
           Transcriptional Activity of the Host Protein Nrf2 by Kaposi’s
           Sarcoma-Associated Herpesvirus

    • Authors: Olsi Gjyshi, Bala Chandran
      Abstract: Kaposi’s sarcoma-associated herpesvirus (KSHV) is the etiological agent of two highly aggressive AIDS-related malignancies, endothelial Kaposi’s sarcoma (KS) and B cell primary effusion lymphoma (PEL). Although current antiretroviral therapy (ART) methods have decreased the overall morbidity and mortality in immunocompromised and AIDS patients, KS and PEL remain difficult to treat. Thus, novel therapeutic methods are essential to significantly improve the life expectancy and quality of life of PEL and KS patients, respectively. One of the signaling pathways that is highly modulated during KSHV infection is oxidative stress, which is a well-known inducer of the transcription factor Nrf2. Because Nrf2 plays an important role in the biology of several viral infections, and is an important agent in cancer progression and chemotherapeutic resistance, we recently undertook a study to investigate its role in KSHV infection of endothelial cells. Here, we provide important highlights of our recent findings, including the importance of oxidative stress and PKCζ in Nrf2 activation, a newly discovered feed-forward loop between Nrf2 and COX-2, and the impact of Nrf2 activation on host and KSHV gene expression and pathogenesis. Lastly, we provide insights on the potential therapeutic implications of Nrf2 modulation in KSHV and other virus-associated pathologies. 
      PubDate: 2015-02-15
      DOI: 10.14800/sp.599
      Issue No: Vol. 3 (2015)
       
  • MSC Functional Phenotype: Assay, Age and Source Dependence

    • Authors: Yuko Ujiie, Kazuhiro Gomi, John Edward Davies
      First page: 10
      Abstract: We recently reported the use of human umbilical cord perivascular cells (HUCPVCs), delivered in a collagen sponge, in the healing of calvarial osteotomies in immune-suppressed rats, following their osteogenic differentiation in vitro. We compared these cells with a human bone marrow (BM) immortalized cell line, and also used conditioned medium from the latter to stimulate the osteogenic differentiation of the HUCPVCs. Our results showed that HUCPVCs provided statistically significant bony repair compared to controls, but failed to show osteogenic differentiation in vitro. On the contrary, BM cells exhibited high levels of alkaline phosphatase expression in vitro, in osteogenic assays, but when loaded onto collagen scaffolds and implanted did not produce a statistically different amount of bone from either sham or collagen-only controls. Our results demonstrated that the in vitro assays employed did not predict in vivo outcomes, and that the BM-MSC cell line employed, or CM from such cells, provided no osteogenic advantage over the use of HUCPVCs alone in vivo. Here, we discuss these findings in light of the contradictory findings of the functional phenotype of MSC within the context of the assay employed, the age of the donor, and the tissue source of the cells. From a therapeutic perspective, it is clear that only in vivo assays should be employed as predictors of clinical performance and that cells sourced from tissue originating from younger donors may be functionally more potent than adult tissue derived MSC sources. 
      PubDate: 2015-08-13
      DOI: 10.14800/sp.934
      Issue No: Vol. 2, No. 2 (2015)
       
  • Multiparameter monitoring for optimal T-cell adoptive therapy.

    • Authors: Valérie Janelle, Cédric Carli, Jean-Sébastien Delisle
      First page: 10
      Abstract: Adoptive transfer of ex vivo-expanded antigen-specific T cells is a promising therapeutic approach for the treatment of cancer and infectious diseases. Clinical studies have proven the feasibility and potency of this procedure but several limitations need to be overcome before this form of immunotherapy reach its full potential. For instance, the efficacy of the transferred cells is often impeded by terminal effector differentiation and exhaustion acquired during in vitro expansion. This would notably explain the lack of further in vivo proliferation and persistence in many trials. However, the factors that induce T-cell differentiation and functional impairment in culture remain poorly defined. Using the model antigen HA-1, we determined that phenotypic and functional features indicating T-cell exhaustion/dysfunction may not be detected simultaneously and depend on the method of expansion as well as the antigenic repertoire stimulated. Thus, our study has defined critical parameters to monitor in order to optimally differentiate and expand antigen-specific T cells in culture prior to adoptive transfer.
      PubDate: 2015-08-06
      DOI: 10.14800/sp.913
      Issue No: Vol. 2, No. 2 (2015)
       
  • The effects of simulated microgravity on the human nervous system: the
           proposal of a three-dimensional glia–neuron co-culture cell model

    • Authors: Maria A Mariggiò, Giorgio Fanò Illic
      Pages: 10 - 14800/sp.8
      Abstract: Over the last few decades, the increasing number of spaceflights and the permanence of astronauts in orbit to maintain satellites and space stations have focused attention on the effects induced by altered gravitation on the human body, and in particular on bone, skeletal muscle,and brain function. The study of the mechanisms that underlie the effects induced by microgravity and the search for protection strategies are made difficult by limitations due to logistic difficulties (such as the operators and/or automatic processes of measurement during flights) and limitations in the gathering of enough material from astronauts. This has prompted the need to develop and improve alternative models of a simulated weightless environment that can be used to overcome these critical phases. In addition, the use of in-vitro cell models can allow in-depth studies of cellular targets of the extracellular mechanical forces that are modified by variations in gravity. This overview highlights some aspects of the research in this field that are focused on the effects of microgravity on nerve cells,whereby their modified functions might be related to sensory/motor impairment as well as to the disorders of mood, behavior and cognition experienced after spaceflights.
      PubDate: 2015-07-13
      DOI: 10.14800/sp.892
      Issue No: Vol. 2, No. 2 (2015)
       
  • Altered Calcium and Red-ox homeostasis underline defective haematopoiesis
           in Fanconi Anemia.

    • Authors: Paolo Degan, cesare usai, silvia ravera, paola cuccarolo, isabella panfoli, carlo dufour, enrico cappelli
      First page: 10
      Abstract: A defective hematopoiesis underlies the severe pathophysiological conditions of Fanconi anemia (FA) patients. A fine tuning of the bone marrow (BM) niche micro environment appear crucial in myeloproliferation and hematopoiesis where molecular events associated with calcium and red-ox gradients dictates the process. Calcium and red-ox signaling are complex regulatory networks which might play both agonistic as well as antagonistic roles. Both modulates structural and functional elements of the process. In FA the peculiar association between a low [Ca2+]i and an high pro-oxidative metabolism may distinguish its pathological drifting and cancer-proneness. Notably these conditions are associated with specific leukemic contexts typical in FA. Whether the dysregulated calcium metabolism observed in FA be a useful diagnostic tool and/or a predictivity marker of FA associated outcome appear however unlikely given the difficulty to manipulate it.
      PubDate: 2015-07-06
      DOI: 10.14800/sp.880
      Issue No: Vol. 2, No. 2 (2015)
       
  • Extracellular signal-Regulated Kinases 1/2 and their role in cardiac
           diseases

    • Authors: Maria Chatzifrangkeskou, Antoine Muchir
      Abstract: Mitogen-activated protein (MAP) kinases comprise a well-studied family of serine/threonine protein kinases involved in signal transduction pathways that control multiple cellular processes. The extracellular signal-regulated kinase (ERK1/2) cascade is a central MAP kinase pathway that transmits signals from the cell surface to substrates either in the nucleus or in the cytoplasm. The transmission of the signal through the ERK1/2 cascade is mediated by phosphorylation and activation of protein kinases. Abnormal regulation of the ERK1/2 signals has been linked to diseases and recent work clearly implicated ERK1/2 signaling in the development of cardiac pathologies. Understanding the underlying mechanism and the consequences of the aberrant modulation of ERK1/2 cascade will lead to the development of pharmacologic inhibitors for the treatment of these cardiac disorders. 
      PubDate: 2014-12-19
      DOI: 10.14800/sp.457
      Issue No: Vol. 3 (2014)
       
  • Chloroquine as a promising adjuvant chemotherapy together with sunitinib

    • Authors: Amal Kamal Abdel-Aziz, Samia Shouman, Ebtehal El-Demerdash, Mohamed Elgendy, Ashraf B. Abdel-Naim
      Abstract: Chloroquine - a clinically available and cheap antimalarial drug - might have potential usefulness as adjuvant chemotherapy when combined with sunitinib, reports a preclinical study recently published online in Chemico-biological Interactions.  Just few years after its FDA approval to be used in renal cell carcinoma, imatinib resistant gastrointestinal tumor and pancreatic neuroendocrine tumor, increasing studies shed light on the limited clinical efficacy of sunitinib as well as rapid development of resistant cells when used as monotherapy presumably through lysosomal sequestration. Abdel-Aziz and her colleagues now showed that chloroquine augments sunitinib anticancer activity in vitro human cancer cell lines of breast, colorectal, cervical, laryngeal, liver and prostate origin and in vivo in murine Ehrlich ascites carcinoma tumor model. Furthermore, Abdel-Aziz and her colleagues showed that chloroquine interrupts autophagic flux which was induced by sunitinib. They noted that chloroquine when combined with sunitinib showed further activation of apoptosis in cancer cells. The observed synergy was associated with increased nitric oxide level and reduced reactive oxygen species levels. The present findings warrant further studies to explore the safety profile of the combination regimen and its clinical usefulness in vivo and then controlled clinical trials.
      PubDate: 2014-10-26
      DOI: 10.14800/sp.384
      Issue No: Vol. 3 (2014)
       
  • THE ROLE OF JAK2 INHIBITORS IN THE MANAGEMENT OF CML: CAN WE REST THE
           CASE'

    • Authors: Paolo Gallipoli
      Abstract: Chronic myeloid leukaemia (CML) is a clonal myeloproliferative disorder arising as a result of the reciprocal translocation between the long arms of chromosomes 9 and 22 (t9;22), leading to the formation of the fusion oncogene BCR-ABL. BCR-ABL has constitutive tyrosine kinase (TK) activity which is necessary for the transformed phenotype. The introduction at the end of the last century of BCR-ABL TK inhibitors (TKI) has dramatically changed the management of CML however despite their great efficacy, TKI are not curative. Disease persistence in CML patients treated with TKI lies in the insensitivity of the most primitive CML leukaemia stem cell (LSC). CML LSCs are not addicted to BCR-ABL kinase activity but rather rely on other stem cell intrinsic pathways for their survival. The main focus in the CML field is therefore to identify these pathways while also trying to exploit them therapeutically to achieve CML LSC eradication and as a result disease cure. Here we briefly review recent research on the role of the intracellular janus kinase (JAK) 2 in CML LSC survival and proliferation and discuss its putative role as a therapeutic target in CML. We discuss evidence supporting or dismissing a role for JAK2 in CML LSC survival and provide a possible explanation to reconcile the contrasting data published.  We finally outline the future challenges which lie ahead of the CML community in trying to elucidate further the mechanisms of action of JAK2 and to translate into clinical practice the use of JAK2 inhibitors in CML.
      PubDate: 2014-10-26
      DOI: 10.14800/sp.383
      Issue No: Vol. 3 (2014)
       
  • Allele imbalance in the transcriptome of human hepatocellular carcinoma:
           stress-induced gene plays a role.

    • Authors: Ming Liu, Xin-Yuan Guan
      Abstract: The two alleles of a gene are usually expressed equally in a normal cell, however, high incidence of allele-specific imbalance is frequently observed in cancer cells. Chromosomal regions with recurrent allele-specific imbalance usually harbor risk alleles and critical genes associated with cancer susceptibility and progression. With the development of large scale transcriptome sequencing technology, systematic analysis of the allele imbalance in the cancer transcriptome could be achieved at the single nucleotide resolution. In the April 2014 issue of Gastroenterology, we reported that the allele-specific imbalance of Oxidative Stress Induced Growth Inhibitor 1 (OSGIN1) can significantly contribute to the progression of HCC. OSGIN1 is a stress-induced pro-apoptotic protein. By validating the sequencing results in a cohort of HCC patients, we found the variant 438H form of OSGIN1 was specifically overrepresented in the tumor tissues. Functional studies indicated that OSGIN1 has strong tumor suppressive function in HCC both in vitro and in vivo. The pro-apoptotic function of the variant form of OSGIN1 was found to be less potent than the wild-type form, and the functional defects might be due to its poor efficiency to localize to the mitochondria. Clinical pathological analysis further revealed that the expression and genotype of OSGIN1 are closely associated with the prognosis of HCC patients. Taken together, our study linked the stress-induced genes with allele imbalance in HCC transcriptome, and proposed OSGIN1 to be an important tumor suppressor gene in the progression of HCC. Further characterization of OSGIN1 might help predict the prognosis of HCC patients and their responses to chemotherapeutic drugs.
      PubDate: 2014-10-26
      DOI: 10.14800/sp.382
      Issue No: Vol. 3 (2014)
       
  • EIF5A2 promotes tumor metastasis and angiogenesis

    • Authors: Yan Li, Xin-Yuan Guan
      Abstract: N/A
      PubDate: 2014-10-26
      DOI: 10.14800/sp.381
      Issue No: Vol. 3 (2014)
       
  • Posttranscriptional Regulation of Glycolytic Enzyme Phosphoglycerate
           Mutase

    • Authors: Takumi Mikawa, Koji Okamoto, Matilde E LLeonart, Yoshinori Yoshida, Akifumi Takaori-Kondo, Masayuki Yokode, Nobuya Inagaki, Hiroshi Kondoh
      Abstract: While glycolysis is vitally essential metabolism for energy production in cells, its enhancement is frequently observed in cancers, known as the Warburg effect. Although the clinical significance of the Warburg effect is well established, it is still not clear how the Warburg effect is coupled to the other cancerous hallmark, e.g. immortalization. Glycolysis would be dysregulated in cancers, which is supported by recent findings on their transcriptional regulation. But among others, phosphoglycerate mutase, PGAM, is an outlier, as the heavy posttranscriptional regulation is operating for it. Here we review about the posttranscriptional regulation of PGAM, especially its ubiquitination by Mdm2 as we reported recently.
      PubDate: 2014-10-26
      DOI: 10.14800/sp.380
      Issue No: Vol. 3 (2014)
       
 
 
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