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001-es BibID:	BIBFORM098738
035-os BibID:	(cikkazonosító)630569 (WoS)000627757800001 (Scopus)85102440838
Első szerző:	Alatshan, Ahmad (immunológus)
Cím:	Nuclear Receptors as Multiple Regulators of NLRP3 Inflammasome Function / Alatshan Ahmad, Benkő Szilvia
Dátum:	2021
ISSN:	1664-3224
Megjegyzések:	Nuclear receptors are important bridges between lipid signaling molecules and transcription responses. Beside their role in several developmental and physiological processes, many of these receptors have been shown to regulate and determine the fate of immune cells, and the outcome of immune responses under physiological and pathological conditions. While NLRP3 inflammasome is assumed as key regulator for innate and adaptive immune responses, and has been associated with various pathological events, the precise impact of the nuclear receptors on the function of inflammasome is hardly investigated. A wide variety of factors and conditions have been identified as modulators of NLRP3 inflammasome activation, and at the same time, many of the nuclear receptors are known to regulate, and interact with these factors, including cellular metabolism and various signaling pathways. Nuclear receptors are in the focus of many researches, as these receptors are easy to manipulate by lipid soluble molecules. Importantly, nuclear receptors mediate regulatory mechanisms at multiple levels: not only at transcription level, but also in the cytosol via non-genomic effects. Their importance is also reflected by the numerous approved drugs that have been developed in the past decade to specifically target nuclear receptors subtypes. Researches aiming to delineate mechanisms that regulate NLRP3 inflammasome activation draw a wide range of attention due to their unquestionable importance in infectious and sterile inflammatory conditions. In this review, we provide an overview of current reports and knowledge about NLRP3 inflammasome regulation from the perspective of nuclear receptors, in order to bring new insight to the potentially therapeutic aspect in targeting NLRP3 inflammasome and NLRP3 inflammasome-associated diseases.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk inflammasome NLRP3 IL-1 signaling PPAR LXR PXR metabolism
Megjelenés:	Frontiers in Immunology. - 12 (2021), p. 630569. -
További szerzők:	Benkő Szilvia (1973-) (molekuláris biológus)
Pályázati támogatás:	K131844 OTKA
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM081504
035-os BibID:	(PMID)31134061 (cikkazonosító)937 (WoS)000466465900001 (Scopus)85067055685
Első szerző:	Csete Dániel
Cím:	Hematopoietic or Osteoclast-Specific Deletion of Syk Leads to Increased Bone Mass in Experimental Mice / Dániel Csete, Edina Simon, Ahmad Alatshan, Petra Aradi, Csaba Dobó-Nagy, Zoltán Jakus, Szilvia Benkő, Dávid S. Győri, Attila Mócsai
Dátum:	2019
ISSN:	1664-3224
Megjegyzések:	Syk is a non-receptor tyrosine kinase critically involved in signaling by various immunoreceptors including B-cell-receptors and activating Fc-receptors. We have previously shown that Syk also mediates immunoreceptor-like signals required for the in vitro development and function of osteoclasts. However, the perinatal lethality of Syk -/- mice precluded the analysis of the role of Syk in in vivo bone metabolism. To overcome that problem, we generated mice with osteoclast-specific (Syk ?OC ) or hematopoietic (Syk ?Haemo ) Syk deficiency by conditional deletion of Syk using Cre recombinase expressed under the control of the Ctsk or Vav1 promoter, respectively. Micro-CT analysis revealed increased bone trabecular density in both Syk ?OC and Syk ?Haemo mice, although hematopoietic Syk deficiency caused a more severe phenotype than osteoclast-specific Syk deficiency. Osteoclast-specific Syk deficiency reduced, whereas hematopoietic Syk deficiency completely blocked in vitro development of osteoclasts. Both interventions inhibited the resorptive activity of osteoclasts and osteoclast-specific gene expression. Kinetic analysis of Syk protein levels, Cre expression and the genomic deletion of the Syk flox allele revealed complete and early deletion of Syk from Syk ?Haemo osteoclasts whereas Syk was incompletely deleted at a later stage of osteoclast development from Syk ?OC cultures. Those results provide an explanation for the in vivo and in vitro difference between the Syk ?OC and Syk ?Haemo mutant strains and suggest late activation of, and incomplete target gene deletion upon, osteoclast-specific Cre expression driven by the Ctsk promoter. Taken together, our results indicate that Syk plays an indispensable role in osteoclast-mediated in vivo bone resorption and suggest that Syk-specific inhibitors may provide therapeutic benefit in inflammatory and other diseases characterized by excessive osteoclast-mediated bone resorption.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Cre-Lox SYK (spleen tyrosine kinase) in vivo mice osteoclasts tyrosine kinase
Megjelenés:	Frontiers in Immunology. - 10 (2019), p. 937. -
További szerzők:	Simon Edina (1981-) (ökológus) Alatshan, Ahmad (1984-) (immunológus) Aradi Petra Dobó Nagy Csaba (1961-) (fogszakorvos) Jakus Zoltán Benkő Szilvia (1973-) (molekuláris biológus) Győri Dávid Mócsai Attila
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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