LEADER 01100cam0-22003371i-450- 001 990004087810403321 005 20050614164807.0 035 $a000408781 035 $aFED01000408781 035 $a(Aleph)000408781FED01 035 $a000408781 100 $a19990604d1978----km-y0itay50------ba 101 0 $aeng 102 $aUS 105 $ay-------001yy 200 1 $aEpistemology and the history of mankind in Lucretius "De rerum natura" 5 and 6$fArnold Sidney Cohen 210 $aAnn Arbor(Michigan)$cUniversity Microfilms international$d©1978 215 $a84 p.$d20 cm 300 $aThe Ohio State University, Ph. D., 1978 325 $aIl v. è una ripr. facs. 610 0 $aLucrezio$aEpicureismo$aFilosofia antica 676 $a871.01 676 $a187 700 1$aCohen,$bArnold Sidney$0385403 801 0$aIT$bUNINA$gRICA$2UNIMARC 901 $aBK 912 $a990004087810403321 952 $aP2B-650-LUCR.-8C.A.S.-1978$bIFC.10048$fFLFBC 959 $aFLFBC 996 $aEpistemology and the history of mankind in Lucretius "De rerum natura" 5 and 6$9479528 997 $aUNINA LEADER 00897nam0-22003011i-450- 001 990006802890403321 005 20001010 035 $a000680289 035 $aFED01000680289 035 $a(Aleph)000680289FED01 035 $a000680289 100 $a20001010d--------km-y0itay50------ba 101 0 $aita 105 $ay-------001yy 200 1 $a<>PRINCIPI dell'Ottantanove$fJ. Imbert ... (e altri)$ga cura e con saggio introduttivo di Paolo Bagnoli$gprefazionedi Ettore A. Albertoni e Henri Morel. 210 $aMilano$cA. Lombardi$d1990. 215 $a288 p.$d22 cm 225 1 $aSaggi$v2 702 1$aBagnoli,$bPaolo$f<1947- > 702 1$aImbert,$bJean 801 0$aIT$bUNINA$gRICA$2UNIMARC 901 $aBK 912 $a990006802890403321 952 $aXII A 1214$b23768$fFSPBC 959 $aFSPBC 996 $aPRINCIPI dell'Ottantanove$9633733 997 $aUNINA DB $aGEN01 LEADER 03999nam 2200445z- 450 001 9910261134603321 005 20210211 035 $a(CKB)4100000002484746 035 $a(oapen)https://directory.doabooks.org/handle/20.500.12854/44997 035 $a(oapen)doab44997 035 $a(EXLCZ)994100000002484746 100 $a20202102d2017 |y 0 101 0 $aeng 135 $aurmn|---annan 181 $ctxt$2rdacontent 182 $cc$2rdamedia 183 $acr$2rdacarrier 200 00$aDiacylglycerol Kinase Signalling 210 $cFrontiers Media SA$d2017 215 $a1 online resource (96 p.) 225 1 $aFrontiers Research Topics 311 08$a2-88945-335-9 330 $aDiacylglycerol kinases (DGKs) phosphorylate diacylglycerol (DG), catalyzing its conversion into phosphatidic acid (PA). This reaction attenuates membrane DG levels, limiting the localization/activation of signaling proteins that bind this lipid. Initially recognized as modulators of classical and novel PKC family members, the function of the DGK has further expanded with the identification of novel DG effectors including Ras Guanyl nucleotide-releasing proteins (RasGRP) and chimaerin Rac GTPases. The product of the DGK reaction, PA, is also a signaling lipid that mediates activation of multiple proteins including the mammalian target of rapamycin (mTOR). The DGK pathway thus modulates two lipids with important signaling properties that are also key intermediates in lipid metabolism and membrane trafficking. The DGK family in eukaryotes comprises 10 different members grouped into five different subfamilies characterized by the presence of particular regulatory motifs. These regions allow the different DGK isoforms to establish specific complexes and/or to be recruited to specific subcellular compartments. The subtle regulation of DG and PA catalyzed byspecific DGKs is sensed by a restricted set of molecules, providing the means for spatio-temporal regulation of signals in highly specialized cell systems. In the recent years, multiple studies have unveiled the functions of specific isoforms, their mechanisms of regulation and their participation in different pathways leading to and from DG and PA. Animal models have greatly helped to understand the specialized contribution of DGK mediated signals, particularly in the immune and central nervous systems. Mice deficient for individual DGK isoforms show defects in T and B cell functions, dendritic spine maintenance, osteoclast and mechanical-induced skeletal muscle formation. Studies in flies and worms link DGK mediated DAG metabolism with mTOR- mediated regulation of lifespan and stress responses. In plants DGK mediated PA formation contributes to plant responses to environmental signals. Aberrant DGK function has been recently associated with pathological states, an expected consequence of the essential role of these enzymes in the regulation of multiple tissue and systemic functions. DGK mutations/deletions have been related to human diseases including diabetes, atypical hemolytic-uremic syndrome, Parkinson disease and bipolar disorders. On the contrary DGK upregulation emerges as a non-oncogenic addition of certain tumors and represents one of the main mechanism by which cancer evades the immune attack. As a result, the DGK field emerges an exciting new area of research with important therapeutic potential. 606 $aBiology, life sciences$2bicssc 610 $acytotoxic T cells 610 $aimmune system 610 $aimmunotherapy of cancer 610 $alipid signaling 610 $asynaptic plasticity (LTP/LTD) 610 $asynaptic transmission 610 $aT cell receptor 610 $atolerance 615 7$aBiology, life sciences 700 $aAndrea Graziani$4auth$01320420 702 $aFumio Sakane$4auth 702 $aIsabel Merida$4auth 906 $aBOOK 912 $a9910261134603321 996 $aDiacylglycerol Kinase Signalling$93034285 997 $aUNINA