9 research outputs found

    53rd National Meeting of the Italian Society of Biochemistryand Molecular Biology (SIB)andNational Meeting of Chemistry of Biological Systems – Italian Chemical Society (SCI - Section CSB)

    Get PDF
    The 53rd National Congress of the Italian Society of Biochemistry and Molecular Biology (SIB), which will be held in Riccione from 23 to 26 September, is characterised by the elevated scientific level and interdisciplinary interest of the numerous sessions in which it is organised. The Scientific Programme comprises three joint Symposia of the SIB and the Chemistry of Biological Systems section of the Italian Chemistry Society (SCI) on Molecular Systems Biology, Chemistry of Nucleic Acids, Protein and Drug Structure, and Environmental Biotechnology. These Symposia address groundbreaking arguments, making the joint interest of the two societies particularly fascinating; the joint organisation of these events in fact signals the shared intention to proceed along the path of scientific exchange. The topics of the other sessions have been chosen by the Scientific Committee on the basis of their scientific relevance and topicality, with particular attention paid to the selection of the speakers. The SIB sessions will range from Signal Transduction and Biomolecular Targets, Protein Misfolding and its Relationship with Disease, Emerging Techniques in Biochemistry, Gene Silencing, Redox Signalling and Oxidative Stress, Lipids in Cell Communication and Signal Transduction, Mitochondrial Function and Dysfunction

    53rd National Meeting of the Italian Society of Biochemistry and Molecular Biology (SIB) and National Meeting of Chemistry of Biological Systems – Italian Chemical Society (SCI - Section CSB)

    Get PDF
    Il 53° Congresso Nazionale della Società Italiana di Biochimica e Biologia Molecolare che si tiene a Riccione dal 23 al 26 Settembre si distingue per l'alto livello scientifico e l'interesse interdisciplinare delle numerose sessioni nelle quali è strutturato. Il Programma scientifico vede tre Simposi congiunti della SIB con la Sezione della Chimica dei Sistemi Biologici della Società Italiana di Chimica (SCI) su Molecular Systems Biology, Chemistry of Nucleic Acids, Protein and Drug Structure, Environmental Biotechnology. Questi Simposi, riguardano argomenti di avanguardia per i quali fa piacere l'interesse condiviso delle due Società, che per la prima volta organizzano dei Simposi congiunti a significare l'intento di procedere insieme negli scambi scientifici. Gli argomenti delle altre sessioni sono stati scelti dal comitato scientifico in base alla loro rilevanza e attualità scientifica, con particolare cura nella individuazione dei relatori. Le sessioni SIB spazieranno da Signal Transduction and Biomolecular Targets, Protein Misfolding and its Relationship with Diseases, Emerging Techniques in Biochemistry, Gene Silencing, Redox Signalling and Oxidative Stress, Lipids in Cell Communication and Signal Transduction, Mitochondrial Function and Dysfunction

    Pancreatic Cancer

    Get PDF
    This book provides the reader with an overall understanding of the biology of pancreatic cancer, hereditary, complex signaling pathways and alternative therapies. The book explains nutrigenomics and epigenetics mechanisms such as DNA methylation, which may explain the etiology or progression of pancreatic cancer. Book also summarizes the molecular control of oncogenic pathways such as K-Ras and KLF4. Since pancreatic cancer metastasizes to vital organs resulting in poor prognosis, special emphasis is given to the mechanism of tumor cell invasion and metastasis. Role of nitric oxide and Syk kinase in tumor metastasis is discussed in detail. Prevention strategies for pancreatic cancer are also described. The molecular mechanisms of the anti-cancer effects of curcumin, benzyl isothiocyante and vitamin D are discussed in detail. Furthermore, this book covers the basic mechanisms of resistance of pancreatic cancer to chemotherapy drugs such as gemcitabine and 5-flourouracil

    Dichotomic role of NAADP/two-pore channel 2/Ca2+ signaling in regulating neural differentiation of mouse embryonic stem cells

    Get PDF
    Poster Presentation - Stem Cells and Pluripotency: abstract no. 1866The mobilization of intracellular Ca2+stores is involved in diverse cellular functions, including cell proliferation and differentiation. At least three endogenous Ca2+mobilizing messengers have been identified, including inositol trisphosphate (IP3), cyclic adenosine diphosphoribose (cADPR), and nicotinic adenine acid dinucleotide phosphate (NAADP). Similar to IP3, NAADP can mobilize calcium release in a wide variety of cell types and species, from plants to animals. Moreover, it has been previously shown that NAADP but not IP3-mediated Ca2+increases can potently induce neuronal differentiation in PC12 cells. Recently, two pore channels (TPCs) have been identified as a novel family of NAADP-gated calcium release channels in endolysosome. Therefore, it is of great interest to examine the role of TPC2 in the neural differentiation of mouse ES cells. We found that the expression of TPC2 is markedly decreased during the initial ES cell entry into neural progenitors, and the levels of TPC2 gradually rebound during the late stages of neurogenesis. Correspondingly, perturbing the NAADP signaling by TPC2 knockdown accelerates mouse ES cell differentiation into neural progenitors but inhibits these neural progenitors from committing to the final neural lineage. Interestingly, TPC2 knockdown has no effect on the differentiation of astrocytes and oligodendrocytes of mouse ES cells. Overexpression of TPC2, on the other hand, inhibits mouse ES cell from entering the neural lineage. Taken together, our data indicate that the NAADP/TPC2-mediated Ca2+signaling pathway plays a temporal and dichotomic role in modulating the neural lineage entry of ES cells; in that NAADP signaling antagonizes ES cell entry to early neural progenitors, but promotes late neural differentiation.postprin

    Annual Report

    Get PDF

    Genes: Multigene Families, Control of Gene Expression, Genetic contributions to Human Diseases, including Chromosomal Fragile Sites and ‘Dynamic’ and ‘Non-self’ Mutations

    Get PDF
    The early work in this thesis utilizes the general approach of comparative analysis. In order to find out the relationship between entities (either functional or genetic) my colleagues and I have attempted to identify the important elements by detecting similarity between those entities that act in a similar manner. The philosophy behind this approach is simply that when two distinct objects perform a similar process then the requirements essential for that process will be revealed as similarities between those objects above a noise of difference between them. The use of comparative analysis in biological systems is an attempt to identify natural order from apparent chaos. This work includes but is not limited to :- 1. discovery of the family of kallikrein genes and exploration of their roles in biology, 2. identification of the DNA sequence elements required for hormonal and heavy metal control of metallothionein gene expression 3. discovery of at least some of the necessary and sufficient conditions for the appearance of fragile sites on chromosomes, and their consequent contributions to disease, 4. the molecular properties of repeat DNA sequence expansion that lead to dynamic mutation and consequent fragile site expression and / or disease pathogenesis. In a sense the use of genetic animal models in order to study gene function and pathogenesis follows similar logic of comparative analysis – the mutation of a single endogenous gene or the expression of a single introduced mutated gene in a (presumed) constant genetic background to enable the biological consequences of the genetic mutation or aberrant gene expression by comparing animals from the ‘wild-type’ or parent line with those that now carry the mutation or altered gene. This approach has been utilized in the most recent work contained herein as a means to determine gene function and / or to model human genetic disease pathogenesis, specifically pathogenic mechanisms of the protein WWOX in cancer and expanded repeat RNAs in neurodegenerative diseases. The culmination of this recent work is the development of an hypothesis – 4. that expanded repeat double-stranded RNA leads to neurodegeneration through its recognition by the RNA-binding pattern recognition receptors as a ‘non-self’ or foreign nucleic acid due to a paucity of RNA modification. The resultant pathogenic mechanism is therefore autoinflammatory disease. Given the wide range and variety of evidence of inflammatory activation in neurodegenerative diseases in general, this mechanism is therefore hypothesized to be the general causal mechanism for most (or all) of these diseases. A specific Introduction - highlighting the nature and significance of the work, and a Conclusion – of how this work has contributed to knowledge, are given at the start of each chapter, while the impact of the various components of this work is indicated by the number of citations for each of the included publications. Authorship contributions to each of the included publications in this work are also indicated with each specific reference.Thesis (DSc) -- University of Adelaide, School of Biological Sciences, 202
    corecore