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Peer Reviewed Papers, Books, Chapters

Year Title Citation Authors Review type Summary Keywords File filename File mime type
1. 2010 Akt / protein kinase B in skeletal muscle physiology and pathology. J Cell Physiol. 2010 Jul 29
2. 2010 Key role of phosphoinositide 3-kinase class IB in pancreatic cancer. Clin Cancer Res. 2010 Oct 15;16(20):4928-37.
3. 2010 e putative cannabinoid receptor GPR55 defines a novel autocrine loop in cancer cell proliferation Oncogene. 2010 Sep 13
4. 2010 Phosphoinositide 3-kinase/Akt signalling pathway-specific inhibitors: A novel strategy to sensitize cancer cells to anticancer drugs Curr Pharm Des 2010, 16(12):1410-6.
5. 2010 A novel inhibitor of the PI3K/Akt pathway based on the structure of inositol 1,3,4,5,6-pentakisphosphate. Br J Cancer. 2010, 102:104-114
6. 2009 Anticancer activity of the bioactive compound inositol pentakisphosphate Phytochem Rev 2009 8:369-374.
7. 2009 Rethinking phosphatidylinositol 3-monophosphate BBA - Molecular Cell Research 2009 1793: 1795-1803.
8. 2009 A Phosphoinositide 3-Kinase/Phospholipase Cgamma1 Pathway Regulates Fibroblast Growth Factor-Induced Capillary Tube Formation. PLoS One 2009, 4(12):e8285
9. 2008 Insulin resistance and the sugar-lipid connection Cell Science 2008 4:36-43
10. 2008 Phospholipase C gamma1 is required for metastasis development and progression Cancer Research 2008 68:10187-10196.
11. 2007 Phosphoinositide 3-kinase-dependent regulation of phospholipase Cgamma. Biochem Soc Trans. 35:229-230, 2007
12. 2007 Role of class II phosphoinositide 3-kinase in cell signalling Biochem Soc Trans. 35:211-214, 2007
13. 2007 Role of phosphoinositide 3-kinase C2alpha in insulin signaling. J Biol Chem. 2007 282:28226-28236.
14. 2006 Emerging roles of phosphatidylinositol 3-monophosphate as a dynamic lipid second messenger Arch Physiol Biochem. 112:274-284, 2006
15. 2005 Class II phosphoinositide 3-kinase defines a novel signalling pathway in cell migratio The Journal of Cell Biology 169, 789-799, 2005.
16. 2005 Inhibition of the PI3-K/Akt pathway by inositol pentakisphosphate results in anti-angiogenic and anti-tumour effect. Cancer Research 65:8339-8349, 2005.
17. 2004 Inositol Pentakisphosphate promotes apoptosis through the PI 3-K/Akt pathway Oncogene, 23, 1754-1765, 2004
18. 2003 Insulin induces phosphatidylinositol 3-phosphate formation through TC10 activation. EMBO J., 22, 4178-4189, 2003.
19. 2003 Quon and M. Falasca. Role of Pleckstrin Homology domain in regulating membrane targeting and metabolic function of insulin receptor substrate-3. Mol. End., 17, 1568-1579, 2003.
20. 2003 Pyk2 regulates multiple signaling events crucial for macrophage morphology and migration Proc. Natl. Acad. Sci. USA. 100, 10740-10745, 2003
21. 2002 The mechanism involved in the regulation of PLC1 activity in cell migration. Oncogene 21, 6520-6529, 2002.
22. 2001 Modulation of Oncogenic DBL activity by phosphatidylinositol phosphate binding to PH domain J. Biol.Chem. 276, 19524-19531, 2001
23. 2001 Specificity in pleckstrin homology (PH) domain membrane targeting: a role for a phosphoinositide-protein co-operative mechanism FEBS Letters 506, 173-179, 2001.
24. 2000 Different subcellular localisation and phosphoinositides binding of insulin receptor substrate proteins pleckstrin homology domains. Mol. End. 14, 823-836, 2000
25. 2000 Novel functional PI 3-kinase antagonists inhibit cell growth and tumorigenicity in human cancer cell lines FASEB J. 14, 1179-1187, 2000
26. 2000 A novel positive feedback loop mediated by the docking protein Gab1 and PI-3 kinase in EGF receptor signalling Mol.Cell.Biol., 20, 1448-1459, 2000
27. 2000 Pattern within protein/polyphosphoinositide interactions provide specific targets for therapeutic intervention FASEB J. 14, 2618-2622, 2000
28. 2000 The role of the Pleckstrin Homology (PH) domain in membrane-targeting and activation of phospholipase Cb1. J.Biol.Chem. 275, 14873-14881, 2000
29. 1998 Activation of the c-fos serum response element by phosphatidylinositol 3-kinase and rho pathways in HeLa cells Cell Growth & Diff. 9, 513-522, 1998.
30. 1998 Signalling activities of glycerophosphoinositols. Anticancer Res.(1998), 18 (6C), 4847
31. 1998 Promiscuity and specificity in pleckstrin homology (PH) domain binding to phosphoinositides J. Biol. Chem. 273, 30497-30508, 1998
32. 1998 Activation of phospholipase Cg1 by PI3-kinase induced PH domain mediated membrane targeting EMBO J. 17, 414-422, 1998.
33. 1998 Release of the mitogen Lysophosphatidylinositol from H-ras transformed fibrblasts: a possible mechanism of autocrine control of cell proliferation Oncogene. 16, 2357-2365, 1998
34. 1997 Regulatory recruitment of signalling molecules to the cell membrane by pleckstrin-homology domains Trends Cell Biol. 7, 237-242, 1997.
35. 1997 Fast receptor-induced formation of glycerophosphoinositol-4-phosphate, a putative novel intracellular messenger in the ras pathway. Mol. Biol. Cell. 8, 443-453, 1997
36. 1997 Phosphatidylinositol 3-kinase mediates EGF-induced activation of the c-Jun N-terminal kinase signaling pathway Mol. Cell. Biol. 17, 5784-5790, 1997
37. 1996 Glycerophosphoinositols as potential markers of ras-induced transformation and novel second messengers Anticancer Res. 16, 1341-1350, 1996
38. 1996 Corda. Changes in the levels of glycerophosphoinositols during differentiation of hepatic and neuronal cells Eur. J. Biochem. 241, 386-392, 1996
39. 1996 Glycerophosphoinositol-4-phosphate in intracellular signalling "Frontiers in bioactive lipids". Ed. Vanderhoek, Plenum Press, New York, 1996.
40. 1995 Ramakrishna and D. Corda. Signalling pathways involved in the mitogenic action of lysophosphatidylinositol Oncogene 10, 2113-2124, 1995
41. 1995 Physiological concentrations of thyrotropin increase cytosolic calcium levels in primary cultures of human thyroid cells J. Clin. Endocrinol. Metab. 80, 1136-1143, 1995
42. 1994 G-protein-dependent modulation of phospholipase C and phospholipase A2. “Biomembranes” Vol. 3, Shinitzky M. (ed. ) Balaban & VCH Publishers Weinheim Publishers, 283-317, 1994
43. 1994 Elevated levels and mitogenic activity of lysophosphatidylinositol in k-ras transformed epithelial cells Eur. J. Bioch. 221, 383-389, 1994
44. 1994 Novel cellular activities of phosphoinositide metabolites originated by the action of phospholipase A2. GTPase-controlled molecular machines” D. Corda, H. Hamm, A. Luini (eds). 79-91, 1994.
45. 1993 Accumulation and mitogenic activity of lysophosphatidylinositol in k-ras transformed thyroid cells “Molecular oncology and clinical applications”, A. Cittadini, R. Baserga, H. Pinedo, T. Galeotti, D. Corda (eds) MCBU, Birkhauser Verlag, Basel ,165-171, 1993
46. 1993 Glycerophosphoinositol-4-phosphate: a putative endogenous inhibitor of adenylyl cyclase J. Biol. Chem. 268, 20402-20407, 1993.
47. 1992 Food restriction in female Wistar rats: V. Lipid peroxidation and antioxidant enzymes in the liver. Arch. Gerontol Geriat. 14, 93-99, 1992.
48. 1992 Diet restriction: a tool to prolong the lifespan of experimental animals. Model and current hypothesis of action. Comp. Biochem. Physiol. 103 (3), 551-554, 1992.
49. 1992 Aging impairs membrane potential responsiveness as well as opening of voltage and ligand gated Na+ channels in human lymphocytes. Arch. Gerontol. Ger. 14, 145-154, 1992
50. 1992 Lipid peroxidation causes an increase of lipid order and a decrease of 5’- Nucleotidase activity in the liver plasma membrane Cell. Mol. Biol. 38, 4, 437-442, 1992
51. 1992 Adenosine Deaminase from bovine brain: purification and partial caracterization. Biochem. Int. 26, 6, 1053-1063, 1992
52. 1992 Adenosine Deaminase from Saccharomyces Cerevisiae: kinetics and interaction with transition ground state inhibitor Bioch. Biophys. Acta 1122, 311-316, 1992
53. 1992 A sodium channel opener inhibits stimulation of human peripheral T-lymphocytes. Mol. Immunol. 29, 4, 517-524, 1992.
54. 1992 Diet restriction preserves the physochemical properties of cell membranes from the age-dependent alterations Mod. of the rate of aging Eds. A. Ruiz-Torres/ G. Hofecker 213-217, 1992.
55. 1992 Cholesterol rich rabbit serum modulates ß-adrenergic receptor density of human lymphocytes: a possible role of LDL-cholesterol. Ann. N.Y. Acad. Sci. 650, 239-244, 1992.
56. 1992 Bretylium-induced voltage-gated sodium current in human lymphocytes Bioch. Biophys. Acta 1137, 143-147, 1992
57. 1991 Parameters to monitor aging with a possible prospective for intervention. An immunological approach Arch. Gerontol. Geriat. 12, 231-238, 1991.
58. 1991 Diet restriction, body temperature and physicochemical properties of cell membranes. Arch. Gerontol. Geriat. 12, 179-185, 1991.
59. 1991 Food restriction in female Wistar rats: IV. Morphometric parameters of cerebellar synapses. Arch. Gerontol. Geriat. 13, 161-166, 1991.
60. 1991 Modulation of 5’-Nucleotidase activity by lipid peroxidation Topics in aging research 16, 181-190, 1991
61. 1991 Studies on the cell membrane properties in food restricted rats Aging 3, 4, 401-403, 1991
62. 1991 Influence of membrane fluidity on 5’ Nucleotidase activity in isolated hepatocytes plasma membrane Biochem. Int. 25, 631-638, 1991
63. 1990 Food restriction in female Wistar rats: III. Microviscosity and 5’-Nucleotidase activity of liver plasma membranes Arch. Gerontol. Geriat. 11, 117-124, 1990.
64. 1990 Food restriction in female Wistar rats: II. B- adrenoceptor density in the cerebellum and in the splenic lymphocytes. Arch. Gerontol. Geriat., 11, 109-115, 1990.
65. 1990 Food restriction in female Wistar rats: I. survival characteristics, membrane microviscosity and proliferative response in lymphocytes. Arch. Gerontol. Geriat. 11, 99-108, 1990.
66. 1990 Antioxidant enzymes in erythrocytes from old and diet restricted old rats Boll. Soc. It. Biol. Sper. 10, vol.LXVI, 909-914, 1990
67. The majority of cancer-associated mortality results from the ability of tumour cells to metastasise leading to multifunctional organ failure and death. Pubmed The majority of cancer-associated mortality results from the ability of tumour cells to metastasise leading to multifunctional organ failure and death. Disseminated tumour cells in the blood circulation are faced with major challenges such as rheological shear stresses and cell-mediated cytotoxicity mediated by natural killer cells. Nevertheless, circulating tumour cells with metastatic ability appear equipped to exploit host cells to aid their survival. Despite the long interest in targeting tumour-associated host cells such as platelets for cancer treatment, the clinical benefit of this strategy is still under question. In this review, we provide a summary of the latest mechanistic and clinical evidence to evaluate the validity of targeting platelets in cancer. antiplatelet; cancer; cancer therapy; platelet
68. The efficacy of chemotherapy is one of the main challenges in cancer treatment and one of the major obstacles to overcome in achieving lasting remission and a definitive cure in patients with cancer is the emergence of cancer resistance. Pubmed The efficacy of chemotherapy is one of the main challenges in cancer treatment and one of the major obstacles to overcome in achieving lasting remission and a definitive cure in patients with cancer is the emergence of cancer resistance. Indeed, drug resistance is ultimately accountable for poor treatment outcomes and tumour relapse. There are various molecular mechanisms involved in multidrug resistance, such as the change in the activity of membrane transporters primarily belonging to the ATP binding cassette (ABC) transporter family. In addition, it has been proposed that this common feature could be attributed to a subpopulation of slow-cycling cancer stem cells (CSCs), endowed with enhanced tumorigenic potential and multidrug resistance. CSCs are characterized by the overexpression of specific surface markers that vary in different cancer cell types. Overexpression of ABC transporters has been reported in several cancers and more predominantly in CSCs. While the major focus on the role played by ABC transporters in cancer is polarized by their involvement in chemoresistance, emerging evidence supports a more active role of these proteins, in which they release specific bioactive molecules in the extracellular milieu. This review will outline our current understanding of the role played by ABC transporters in CSCs, how their expression is regulated and how they support the malignant metabolic phenotype. To summarize, we suggest that the increased expression of ABC transporters in CSCs may have precise functional roles and provide the opportunity to target, particularly these cells, by using specific ABC transporter inhibitors. ABC transporters; cancer stem cells; cell signalling; chemoresistance
69. Despite the rapid development in the field of oncology, cancer remains the second cause of mortality worldwide, with the number of new cases expected to more than double in the coming years. Pubmed Despite the rapid development in the field of oncology, cancer remains the second cause of mortality worldwide, with the number of new cases expected to more than double in the coming years. Chemotherapy is widely used to decelerate or stop tumour development in combination with surgery or radiation therapy when appropriate, and in many cases this improves the symptomatology of the disease. Unfortunately though, chemotherapy is not applicable to all patients and even when it is, there are many cases where a successful initial treatment period is followed by chemotherapeutic drug resistance. This is caused by a number of reasons, ranging from the genetic background of the patient (innate resistance) to the formation of tumour-initiating cells (acquired resistance). In this review, we discuss the potential role of PDK1 in the development of chemoresistance in different types of malignancy, and the design and application of potent inhibitors which can promote chemosensitization. PDK1; PI3K; chemoresistance; chemotherapy; phosphoinositides
70. Platelets have been demonstrated to be vital in cancer epithelial-mesenchymal transition (EMT), an important step in metastasis. Pubmed Platelets have been demonstrated to be vital in cancer epithelial-mesenchymal transition (EMT), an important step in metastasis. Markers of EMT are associated with chemotherapy resistance. However, the association between the development of chemoresistance, EMT, and the contribution of platelets to the process, is still unclear. Here we report that platelets regulate the expression of (1) human equilibrative nucleoside transporter 1 (hENT1) and (2) cytidine deaminase (CDD), markers of gemcitabine resistance in pancreatic cancer. Human ENT1 (hENT1) is known to enable cellular uptake of gemcitabine while CDD deactivates gemcitabine. Knockdown experiments demonstrate that Slug, a mesenchymal transcriptional factor known to be upregulated during EMT, regulates the expression of hENT1 and CDD. Furthermore, we demonstrate that platelet-derived ADP and ATP regulate Slug and CDD expression in pancreatic cancer cells. Finally, we demonstrate that pancreatic cancer cells express the purinergic receptor P2Y12, an ADP receptor found mainly on platelets. Thus ticagrelor, a P2Y12 inhibitor, was used to examine the potential therapeutic effect of an ADP receptor antagonist on cancer cells. Our data indicate that ticagrelor negated the survival signals initiated in cancer cells by platelet-derived ADP and ATP. In conclusion, our results demonstrate a novel role of platelets in modulating chemoresistance in pancreatic cancer. Moreover, we propose ADP/ATP receptors as additional potential drug targets for treatment of pancreatic cancer. ADP; ATP; gemcitabine; pancreatic cancer; platelets


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