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001-es BibID:	BIBFORM054304
035-os BibID:	PMID: 18064043
Első szerző:	Koncz Gábor (biológus, immunológus)
Cím:	Regulating Vav1 phosphorylation by the SHP-1 tyrosine phosphatase is a fine-tuning mechanism for the negative regulation of DISC formation and Fas-mediated cell death signaling / G. Koncz, K. Kerekes, K. Chakrabandhu, Anne-Odile Hueber
Dátum:	2008
ISSN:	1350-9047
Megjegyzések:	The actin cytoskeleton association is required for caspase 8-independent Fas/CD95 receptor internalization, a critical step for an optimal death-inducing signaling complex formation along the endocytic pathway, leading to efficient activation of the caspase cascade and, ultimately, cell death. However, the way in which this initiation phase of Fas receptor signaling is regulated is still unknown. We report herein that, in B cells, upon Fas engagement, the tyrosine phosphatase SHP-1-regulated Vav dephosphorylation, by downmodulating the Fas-ezrin-actin linkage is a fine-tune switch-off mechanism that the cell uses as a way to terminate the receptor internalization, controlling therefore the time and extent of the DISC formation and cell death.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Fas signaling Vav SHP-1
Megjelenés:	Cell Death and Differentiation. - 15 : 3 (2008), p. 494-503. -
További szerzők:	Kerekes Krisztina Chakrabandhu, Krittalak Hueber, Anne-Odile
Pályázati támogatás:	D48469 OTKA Magyar Allami Eotvos osztondij Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM039523
Első szerző:	Koncz Gábor (biológus, immunológus)
Cím:	Vesicles Released by Activated T Cells Induce Both Fas-Mediated RIP-Dependent Apoptotic and Fas-Independent Nonapoptotic Cell Deaths / Koncz, G., Hancz, A., Chakrabandhu, K., Gogolak, P., Kerekes, K., Rajnavolgyi, E., Hueber, Anne-Odile
Dátum:	2012
ISSN:	0022-1767
Megjegyzések:	Activated T cells secrete Fas ligand (FasL)-containing vesicles (secreted vesicles) that induce death of target cells. We provide evidence that secreted vesicles from culture supernatants (Csup) of various origins are able to generate both Fas-dependent apoptotic and Fas-independent, nonapoptotic cell death. In the absence of Fas, the nonapoptotic, Fas-independent pathway could still induce cell death. In contrast to RIP-independent classical Fas-induced cell death triggered by cross-linked or membrane-bound FasL, CSup-derived stimuli-induced apoptosis exhibited unique molecular and enzymatic characteristics. It could be partially inhibited by blocking cathepsin D enzyme activity and required the presence of RIP. Whereas stimulation with CSup, derived from both FasL-overexpressing Jurkat cells and PBMC, could induce cell death, the requirements for Fas-associated death domain protein and caspase-9 were different between the two systems. Our study highlights an important distinction between cell contact-mediated and secreted vesicle-generated activation-induced cell death and also demonstrates that the type of the secreted vesicles can also modify the cell death route. We propose that besides cell-to-cell interaction-mediated Fas triggering, stimuli induced by secreted vesicles can mediate important additional cell death signals regulating activation-induced cell death under physiological conditions.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Molekuláris Medicina
Megjelenés:	Journal Of Immunology. - 189 : 6 (2012), p. 2815-2823. -
További szerzők:	Hancz Anikó Chakrabandhu, Krittalak Gogolák Péter (1968-) (biológus, immunológus) Kerekes Krisztina Rajnavölgyi Éva (1950-) (immunológus) Hueber, Anne-Odile
Pályázati támogatás:	TÁMOP-4.2.1/B-09/1/KONV-2010-0007 TÁMOP Jelátviteli kapcsolatok ős- és dendritikus sejt altípusokban
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM086503
035-os BibID:	(WoS)000559845300001 (Scopus)85085550676
Első szerző:	Varga Zsófia (molekuláris biológus)
Cím:	Differences in the sensitivity of classically and alternatively activated macrophages to TAK1 inhibitor-induced necroptosis / Zsófia Varga, Tamás Molnár, Anett Mázló, Ramóna Kovács, Viktória Jenei, Krisztina Kerekes, Attila Bácsi, Gábor Koncz
Dátum:	2020
ISSN:	0340-7004
Megjegyzések:	Controlling the balance of pro-inflammatory M1 versus anti-inflammatory M2 macrophages may have paramount therapeutic benefit in cardiovascular diseases, infections, cancer and chronic inflammation. The targeted depletion of different macrophage populations provides a therapeutic option to regulate macrophage-mediated functions. Macrophages are highly sensitive to necroptosis, a newly described regulated cell death mediated by receptor-interacting serine/threonine-protein kinase 1 (RIPK1), RIPK3 and mixed lineage kinase domain like pseudokinase. Antagonists of inhibitors of apoptosis proteins (SMAC mimetics) block RIPK1 ubiquitination, while TGF-activated kinase 1 (TAK1) inhibitors prevent the phosphorylation of RIPK1, resulting in increased necroptosis. We compared the sensitivity of monocyte-derived human M1 and M2 cells to various apoptotic and necroptotic signals. The two cell types were equally sensitive to all investigated stimuli, but TAK1 inhibitor induced more intense necroptosis in M2 cells. Consequently, the treatment of co-cultured M1 and M2 cells with TAK1 inhibitor shifted the balance of the two populations toward M1 dominance. Blockage of either Aurora Kinase A or glycogen synthase kinase 3 beta, two newly described necroptosis inhibitors, increased the sensitivity of M1 cells to TAK1-inhibitor-induced cell death. Finally, we demonstrated that in vitro differentiated tumor-associated macrophages (TAM-like cells) were as highly sensitive to TAK1 inhibitor-induced necroptosis as M2 cells. Our results indicate that at least two different necroptotic pathways operate in macrophages and the targeted elimination of different macrophage populations by TAK1 inhibitor or SMAC mimetic may provide a therapeutic option to regulate the balance of inflammatory/anti-inflammatory macrophage functions.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Necroptosis Macrophage Infammation Cancer
Megjelenés:	Cancer Immunology Immunotherapy. - 8 (2020), p. 1-15. -
További szerzők:	Molnár Tamás (1989-) (molekuláris biológus) Türk-Mázló Anett (1989-) (molekuláris biológus) Kovács Ramóna (1991-) (biológus, okleveles klinikai laboratóriumi kutató) Jenei Viktória (1997-) (biológus) Kerekes Krisztina Bácsi Attila (1967-) (immunológus) Koncz Gábor (1970-) (biológus, immunológus)
Pályázati támogatás:	GINOP-2.3.2-15-2016-00005 GINOP NKFIH 125224 Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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