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A caspase-2-RFXANK interaction and its implication for MHC class II expression
Stockholms universitet, Naturvetenskapliga fakulteten, Institutionen för biokemi och biofysik.
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Rekke forfattare: 72018 (engelsk)Inngår i: Cell Death and Disease, ISSN 2041-4889, E-ISSN 2041-4889, Vol. 9, artikkel-id 80Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Despite recent achievements implicating caspase-2 in tumor suppression, the enzyme stands out from the apoptotic caspase family as a factor whose function requires further clarification. To specify enzyme characteristics through the definition of interacting proteins in apoptotic or non-apoptotic settings, a yeast 2-hybrid (Y2H) screen was performed using the full-length protein as bait. The current report describes the analysis of a captured prey and putative novel caspase-2 interacting factor, the regulatory factor X-associated ankyrin-containing protein (RFXANK), previously associated with CIITA, the transactivator regulating cell-type specificity and inducibility of MHC class II gene expression. The interaction between caspase-2 and RFXANK was verified by co-immunoprecipitations using both exogenous and endogenous proteins, where the latter approach suggested that binding of the components occurs in the cytoplasm. Cellular co-localization was confirmed by transfection of fluorescently conjugated proteins. Enhanced caspase-2 processing in RFXANK-overexpressing HEK293T cells treated with chemotherapeutic agents further supported Y2H data. Yet, no distinct differences with respect to MHC class II expression were observed in plasma membranes of antigen-presenting cells derived from wild type and caspase-2(-/-) mice. In contrast, increased levels of the total MHC class II protein was evident in protein lysates from caspase-2 RNAi-silenced leukemia cell lines and B-cells isolated from gene-targeted mice. Together, these data identify a novel caspase-2-interacting factor, RFXANK, and indicate a potential non-apoptotic role for the enzyme in the control of MHC class II gene regulation.

sted, utgiver, år, opplag, sider
2018. Vol. 9, artikkel-id 80
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Identifikatorer
URN: urn:nbn:se:su:diva-154660DOI: 10.1038/s41419-017-0144-yISI: 000427384500006PubMedID: 29362422OAI: oai:DiVA.org:su-154660DiVA, id: diva2:1202094
Tilgjengelig fra: 2018-04-27 Laget: 2018-04-27 Sist oppdatert: 2018-04-27bibliografisk kontrollert

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