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Mirc11 selectively regulates inflammatory responses of NK cells by targeting ubiquitin modifiers and TRAF6-dependent NF-kB and AP1 activation (RNA-seq: IL-2_expanded_NKG2D_stimulation)

ABSTRACT: Mirc11 selectively regulates inflammatory responses of NK cells by targeting ubiquitin modifiers and TRAF6-dependent NF-kB and AP1 activation (RNA-seq: IL-2_expanded_NKG2D_stimulation)

PROVIDER: PRJNA560941 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10004300.fastq.gz	Fastqsanger.gz
	SRR10004301.fastq.gz	Fastqsanger.gz
	SRR10004302.fastq.gz	Fastqsanger.gz
	SRR10004303.fastq.gz	Fastqsanger.gz
	SRR10004304.fastq.gz	Fastqsanger.gz

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Mirc11 selectively regulates inflammatory responses of NK cells by targeting ubiquitin modifiers and TRAF6-dependent NF-kB and AP1 activation (RNA-seq: Listeria_challenge)

Project description:Lack of Mirc11 significantly reduces NK cell-mediated cytokine production in vivo Mirc11 cluster targets NF-kB and AP-1-mediated gene transcriptions

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Mirc11 selectively regulates inflammatory responses of NK cells by targeting ubiquitin modifiers and TRAF6-dependent NF-kB and AP1 activation

Project description:Mirc11 selectively regulates inflammatory responses of NK cells by targeting ubiquitin modifiers and TRAF6-dependent NF-kB and AP1 activation

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Mirc11 selectively regulates inflammatory responses of NK cells by targeting ubiquitin modifiers and TRAF6-dependent NF-kB and AP1 activation (RNA-seq: IL-2_expanded_NKG2D_stimulation)

Project description:Lack of Mirc11 significantly reduces NK cell-mediated cytokine production in vivo Mirc11 cluster targets NF-kB and AP-1-mediated gene transcriptions

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Mirc11 selectively regulates inflammatory responses of NK cells by targeting ubiquitin modifiers and TRAF6-dependent NF-kB and AP1 activation (RNA-seq: Listeria_challenge)

Project description:Mirc11 selectively regulates inflammatory responses of NK cells by targeting ubiquitin modifiers and TRAF6-dependent NF-kB and AP1 activation (RNA-seq: Listeria_challenge)

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Mirc11 selectively regulates inflammatory responses of NK cells by targeting ubiquitin modifiers and TRAF6-dependent NF-kB and AP1 activation

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Gene expression of Mirc11-/- hematopoietic myeloid progenitors

Project description:Compared gene expression between Lin-Sca1-cKit+ myeloid progenitors isolated from the bone marrow of 6-8 week old wildtype and Mirc11-/- mice. Previously observed that overexpression of Mirc11 in hematopoietic progenitors increased myeloid differentiation whereas loss of Mirc11 decreased myeloid differentiation. Performed RNA-seq to identify potential genes involved in myeloid differentiation regulated by Mirc11. Gene expression analysis of Mirc11 deficient myeloid progenitors revealed a decrease in Toll like receptor and interferon signaling. This anti-inflammatory phenotype was further observed in mature cells as Mirc11-/- bone marrow derived macrophages (BMDMs) have an attenuated response to inflammatory lip-opolysaccharide (LPS).

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Misfolded SOD1 binds the ubiquitin ligase TRAF6

Project description:Amyotrophic lateral sclerosis (ALS) is a fatal disease, characterized by the selective loss of motor neurons. Mutations in Cu/Zn superoxide dismutase (SOD1) are the second most common cause of ALS and it is now well accepted that they result in a gain of toxicity due to protein misfolding. We previously demonstrated in the SOD1G93A rat model that misfolded SOD1 exists as distinct conformers and deposits on mitochondrial subpopulations. Here, using SOD1G93A rats coupled with conformation-restricted antibodies for misfolded SOD1 (AMF7-63 and B8H10), we identified the interactomes of the mitochondrial pools of misfolded SOD1. This strategy identified binding partners that uniquely interacted with either AMF7-63- or B8H10-reactive SOD1 conformers as well as a high proportion of interactors common to both conformers. Of this latter set, we identified the E3 ubiquitin ligase TNF receptor-associated factor 6 (TRAF6) and determined that exposure of the SOD1 functional loops facilitates this interaction. However, this conformational criterion is not universally fulfilled by all SOD1 mutants and differentiates TRAF6-interacting from non-interacting SOD1 mutants. Functionally, TRAF6 stimulates mutant SOD1 polyubiquitination and aggregation. While TRAF6 E3 ubiquitin ligase activity is required for the former, it is dispensable for the latter, indicating that the polyubiquitination and aggregation of mutant SOD1 mediated by TRAF6 are independent events. We propose that misfolded SOD1 binding to TRAF6 may be relevant to ALS disease.

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