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001-es BibID:	BIBFORM112979
035-os BibID:	(cikkazonosító)10938 (WoS)001028670900001 (Scopus)85165107467
Első szerző:	Jambrovics Károly (biológus, gyógyszer-biotechnológus)
Cím:	ATO Increases ROS Production and Apoptosis of Cells by Enhancing Calpain-Mediated Degradation of the Cancer Survival Protein TG2 / Károly Jambrovics, Szilárd Póliska, Beáta Scholtz, Iván P. Uray, Zoltán Balajthy
Dátum:	2023
ISSN:	1422-0067
Megjegyzések:	Transglutaminase 2 (TG2) is a critical cancer cell survival factor that activates several signalling pathways to foster drug resistance, cancer stem cell survival, metastasis, inflammation, epithelial-mesenchymal transition, and angiogenesis. All-trans retinoic acid (ATRA) and chemotherapy have been the standard treatments for acute promyelocytic leukaemia (APL), but clinical studies have shown that arsenic trioxide (ATO), alone or in combination with ATRA, can improve outcomes. ATO exerts cytotoxic effects in a variety of ways by inducing oxidative stress, genotoxicity, altered signal transduction, and/or epigenetic modification. In the present study, we showed that ATO increased ROS production and apoptosis ratios in ATRA-differentiated NB4 leukaemia cells, and that these responses were enhanced when TG2 was deleted. The combined ATRA + ATO treatment also increased the amount of nuclear factor erythroid 2-related factor 2 (NRF2) transcription factor, an adaptive regulator of the cellular oxidative stress response, and calpain proteolytic activity, resulting in TG2 degradation and the reduced survival of WT leukaemia cells. We further showed that the induced TG2 protein expression was degraded in the MCF-7 epithelial cell line and primary peripheral blood mononuclear cells upon ATO treatment, thereby sensitising these cell types to apoptotic signals.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	International Journal Of Molecular Sciences. - 24 : 13 (2023), p. 1-11. -
További szerzők:	Póliska Szilárd (1978-) (biológus) Scholtz Beáta (1967-) (biokémikus, molekuláris biológus) Uray Iván Péter (1970-) (kutatóorvos) Balajthy Zoltán (1957-) (biokémikus, sejtbiológus)
Pályázati támogatás:	129139 OTKA
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM087859
035-os BibID:	(cikkazonosító)6640 (scopus)85090621567 (wos)000580228400001
Első szerző:	Szatmári-Tóth Mária (molekuláris biológus)
Cím:	Thermogenic Activation Downregulates High Mitophagy Rate in Human Masked and Mature Beige Adipocytes / Mária Szatmári-Tóth, Abhirup Shaw, István Csomós, Gábor Mocsár, Pamela Fischer-Posovszky, Martin Wabitsch, Zoltán Balajthy, Cecília Lányi, Ferenc Győry, Endre Kristóf, László Fésüs
Dátum:	2020
ISSN:	1661-6596 1422-0067
Megjegyzések:	Thermogenic brown and beige adipocytes oxidize metabolic substrates producing heat, mainly by the mitochondrial uncoupling protein UCP1, and can thus counteract obesity. Masked beige adipocytes possess white adipocyte-like morphology, but can be made thermogenic by adrenergic stimuli. We investigated the regulation of mitophagy upon thermogenic activation of human masked and mature beige adipocytes. Human primary abdominal subcutaneous adipose-derived stromal cells (hASCs) and SGBS preadipocytes were differentiated to white and beige adipocytes, then their cAMP-induced thermogenic potential was assessed by detecting increased expressions of UCP1, mitochondrial DNA content and respiratory chain complex subunits. cAMP increased the thermogenic potential of white adipocytes similarly to beige ones, indicating the presence of a masked beige population. In unstimulated conditions, a high autophagic flux and mitophagy rates (demonstrated by LC3 punctae and TOM20 co-immunostaining) were observed in white adipocytes, while these were lower in beige adipocytes. Silencing and gene expression experiments showed that the ongoing mitophagy was Parkin-independent. cAMP treatment led to the downregulation of mitophagy through PKA in both types of adipocytes, resulting in more fragmented mitochondria and increased UCP1 levels. Our data indicates that mitophagy is repressed upon encountering a short-term adrenergic stimulus, as a fast regulatory mechanism to provide high mitochondrial content for thermogenesis.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	International Journal of Molecular Sciences. - 21 : 18 (2020), p. 1-21. -
További szerzők:	Shaw, Abhirup (1992-) Csomós István (1983-) (molekuláris biológus) Mocsár Gábor (1981-) (biofizikus) Fischer-Posovszky Pamela Wabitsch, Martin Balajthy Zoltán (1957-) (biokémikus, sejtbiológus) Lányi Cecília Győry Ferenc (1964-) (sebész) Kristóf Endre (1987-) (általános orvos) Fésüs László (1947-) (orvos biokémikus)
Pályázati támogatás:	GINOP-2.3.2-15-2016-00006 GINOP FK131424 OTKA K129139 OTKA ÚNKP-20-5-DE-12 Egyéb
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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