Zobrazeno 1 - 10
of 10
pro vyhledávání: '"Kyril Turpaev"'
Publikováno v:
PLoS ONE, Vol 8, Iss 4, p e61828 (2013)
PURPOSE: Transplantation of pancreatic islets to Type 1 diabetes patients is hampered by inflammatory reactions at the transplantation site leading to dysfunction and death of insulin producing beta-cells. Recently we have shown that co-transplantati
Externí odkaz:
https://doaj.org/article/02c7642460734d328ce114680bedfe22
Publikováno v:
Aarhus University
Turpaev, K, Hartmann, R & Justesen, J 1999, ' 2′-Adenylated derivatives of Ap3A activate RNase L ', F E B S Letters, vol. 457, pp. 9-12 .
Turpaev, K, Hartmann, R & Justesen, J 1999, ' 2′-Adenylated derivatives of Ap3A activate RNase L ', F E B S Letters, vol. 457, pp. 9-12 .
The exact physiological function of Ap 3 A (A5′ppp5″A, 5′5″ diadenosine triphosphate) remains unclear. Previously we have demonstrated that the human p46 2-5A synthetase (OAS1) efficiently utilises Ap 3 A as an acceptor substrate for oligoade
Publikováno v:
FEBS Letters. 408:177-181
The biological role of Ap3A synthesized in cells by tryptophanyl-tRNA synthetase (WRS) is unknown. Previously we have demonstrated that the cellular level of Ap3A significantly increases after interferon treatment. Here we show that the human 46 kDa
Publikováno v:
Biochemical Pharmacology
Biochemical Pharmacology, Elsevier, 2011, 82 (5), pp.535. ⟨10.1016/j.bcp.2011.05.028⟩
Biochemical Pharmacology, Elsevier, 2011, 82 (5), pp.535-547. ⟨10.1016/j.bcp.2011.05.028⟩
Biochemical Pharmacology, Elsevier, 2011, 82 (5), pp.535. ⟨10.1016/j.bcp.2011.05.028⟩
Biochemical Pharmacology, Elsevier, 2011, 82 (5), pp.535-547. ⟨10.1016/j.bcp.2011.05.028⟩
International audience; Benzylidenemalononitrile (BMN) tyrphostins are well known as potent tyrosine kinase inhibitors. Moreover, in recent years it has been recognized that members of the tyrphostin family possess additional biological activities in
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f90be814254a217d832128e76833bc80
https://hal.archives-ouvertes.fr/hal-00721650/file/PEER_stage2_10.1016%2Fj.bcp.2011.05.028.pdf
https://hal.archives-ouvertes.fr/hal-00721650/file/PEER_stage2_10.1016%2Fj.bcp.2011.05.028.pdf
Publikováno v:
Free Radical Biology and Medicine
Free Radical Biology and Medicine, Elsevier, 2010, 48 (2), pp.298-305. ⟨10.1016/j.freeradbiomed.2009.10.054⟩
Free Radical Biology and Medicine, Elsevier, 2010, 48 (2), pp.298-305. ⟨10.1016/j.freeradbiomed.2009.10.054⟩
International audience; We examined early and late alterations in gene expression patterns and phosphorylation levels of key regulators of selected signaling pathways in U937 cells exposed to various (.)NO fluxes. cDNA microarray analysis and real-ti
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e9336a3ee4c003f97e639bc08205d8a7
https://hal.archives-ouvertes.fr/hal-00450886
https://hal.archives-ouvertes.fr/hal-00450886
Autor:
Jean-Claude Drapier, Kyril Turpaev
Publikováno v:
European Journal of Pharmacology
European Journal of Pharmacology, Elsevier, 2009, 606 (1-3), pp.1-8. ⟨10.1016/j.ejphar.2009.01.015⟩
European Journal of Pharmacology, Elsevier, 2009, 606 (1-3), pp.1-8. ⟨10.1016/j.ejphar.2009.01.015⟩
Tyrphostins are well-established selective inhibitors of protein tyrosine kinase activity of EGF receptor and other growth factor receptors. Unexpectedly, we found that, in U-937 monocytic cells, tyrphostin AG-126 augments the sensitivity of the corr
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4a643bef7b497da25f1c39905fd2936e
https://hal.archives-ouvertes.fr/hal-00369133
https://hal.archives-ouvertes.fr/hal-00369133
Publikováno v:
Free radical biologymedicine. 38(10)
In this study we examined the gene expression pattern of *NO-dependent genes in U937 and Mono Mac 6 monocytes exposed to the synthetic NO-donor DPTA-NO using microarray technology. cDNA microarray data were validated by Northern blot analysis and qua
Publikováno v:
Biochemistry. 43(33)
In living cells, NO signaling is mediated by NO-derived metabolites and is therefore dependent on the rate of formation of these so-called reactive nitrogen intermediates (RNIs). We have examined the effects of NO-oxidizing agents, the nitronyl nitro
Publikováno v:
Turpaev, K, Litvinov, D & Justesen, J 2003, ' Redox modulation of NO-dependent induction of interleukin 8 gene in monocytic U937 cells ', Cytokine, vol. 23, pp. 15-22 .
We have examined the effects of various antioxidants and inhibitors of redox-sensitive signal transduction pathways on induction of interleukin 8 (IL-8) gene by NO in monocytic U937 cells. We have observed that nitrosoglutathione or another NO-genera
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3a8182f2397dcaba2cde6f6f4b91bd72
https://pure.au.dk/portal/da/publications/redox-modulation-of-nodependent-induction-of-interleukin-8-gene-in-monocytic-u937-cells(ac4be650-8577-11dc-bee9-02004c4f4f50).html
https://pure.au.dk/portal/da/publications/redox-modulation-of-nodependent-induction-of-interleukin-8-gene-in-monocytic-u937-cells(ac4be650-8577-11dc-bee9-02004c4f4f50).html
Publikováno v:
Aarhus University
Turpaev, K, Hartmann, R, Kisselev, L & Justesen, J 1997, ' Ap 3 A and Ap 4 A is primers for oligoadenylate synthesis catalyzed by interferon-inducible 2-5A synthetase. ', F E B S Letters, vol. 408, pp. 177-181 .
Turpaev, K, Hartmann, R, Kisselev, L & Justesen, J 1997, ' Ap 3 A and Ap 4 A is primers for oligoadenylate synthesis catalyzed by interferon-inducible 2-5A synthetase. ', F E B S Letters, vol. 408, pp. 177-181 .
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=dedup_wf_001::93035395e1c40bea309f581ca7665402
http://pure.au.dk/portal/en/publications/ap3a-and-ap4a-is-primers-for-oligoadenylate-synthesis-catalyzed-by-interferoninducible-25a-synthetase(8762dac0-c54c-11da-bee9-02004c4f4f50).html
http://pure.au.dk/portal/en/publications/ap3a-and-ap4a-is-primers-for-oligoadenylate-synthesis-catalyzed-by-interferoninducible-25a-synthetase(8762dac0-c54c-11da-bee9-02004c4f4f50).html