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Proteome profile of Traf6-OE OT-I T cells

ABSTRACT: Proteome profile of Traf6-OE OT-I T cells and EV OT-I cells after viral transfection

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): T Cell, Cell Culture

DISEASE(S): Cardiovascular System Disease

SUBMITTER: shuan ran

LAB HEAD: yu jizhang

PROVIDER: PXD039327 | Pride | 2025-05-06

REPOSITORIES: Pride

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	WD089TQ_1.raw	Raw
	WD089TQ_2.raw	Raw
	WD089TQ_3.raw	Raw
	WD089TQ_4.raw	Raw
	WD089TQ_5.raw	Raw

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Publications

The OX40-TRAF6 axis promotes CTLA-4 degradation to augment antitumor CD8<sup>+</sup> T-cell immunity.

Yu Jizhang J Cui Jikai J Zhang Xi X Xu Heng H Chen Zhang Z Li Yuan Y Niu Yuqing Y Wang Song S Ran Shuan S Zou Yanqiang Y Ye Weicong W Zhang Dan D Zhou Cheng C Xia Jiahong J Wu Jie J

Cellular & molecular immunology 20231107 12

Immune checkpoint blockade (ICB), including anti-cytotoxic T-lymphocyte associated protein 4 (CTLA-4), benefits only a limited number of patients with cancer. Understanding the in-depth regulatory mechanism of CTLA-4 protein stability and its functional significance may help identify ICB resistance mechanisms and assist in the development of novel immunotherapeutic modalities to improve ICB efficacy. Here, we identified that TNF receptor-associated factor 6 (TRAF6) mediates Lys63-linked ubiquiti ...[more]

PMID: 37932534

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Differentially activated CD8 T cells in liver and gut

Project description:NaM-CM-/ve, liver- and gut-activated CD8 OT-I T cells show differential migration behaviour. To analyze which genes could be responsible for different migration patterns, naM-CM-/ve, liver-activated and gut-activated CD8 T cells were isolated and compared for their gene expression profile. Gene expression profiles of naM-CM-/ve CD8 OT-I T cells versus liver-activated T cells and gut-activated T cells, respectively. NaM-CM-/ve CD8 OT-I T cells were isolated from lymph nodes and spleens of OT-I mice. CD8 OT-I T cells activated by liver-derived and gut-derived antigen for three days in vivo, positive for CFSE were sorted from livers of TF-OVA mice or from mesenteric lymph nodes of iFABP-OVA mice. After total RNA extraction, reverse transcription, cDNA extraction, the biotinylated cRNA was transcribed, fragmented, and 15 M-BM-5g cRNA hybridized in duplicates for each of the three groups to the GeneChip arrays. Group1: naM-CM-/ve, Group2: liver-activated Group3: gut-activated. Lists of differentially regulated genes were created using High Performance Chip Data Analysis (HPCDA) with Bioretis database (http://www.bioretis-analysis.de). Worldwide data sharing is possible via Bioretis, please ask the authors.

2014-02-25 | E-GEOD-39449 | biostudies-arrayexpress

Transcription profiling of mouse splenocytes from OT-1 TCR transgenic mice to assess the effect of IL-12 on CTL gene expression

Project description:The goal was to determine how IL-12 affects gene expression by murine CTL. Experiment Overall Design: Following RBC lysis, splenocytes from OT-1 TCR transgenic mice (5 million/ml) were cultured in six well-plates (5-6ml/well) in IMDM supplemented with 10% FCS and 55Î¼M 2-ME with 1Î¼M SIINFEKL. After 4 days, the cells were harvested by purification with Ficoll-Paque PLUS and placed in fresh medium containing 0 or 20ng/ml rmIL-12. Twenty-four hours later the cells were harvested and used in experiments. The live cells harvested were >98% CD8+VÎ±2+ (OT-1).

2009-02-08 | E-GEOD-13173 | biostudies-arrayexpress

Cytotoxic effects of Bortezomib in Myelodysplastic syndrome/Acute Myeloid Leukemia depend on autophagy-mediated lysosomal degradation of TRAF6 and repression of PSMA1

Project description:Bortezomib (VelcadeM-BM-)) is widely used for the treatment of various human cancers, however, its mechanisms of action are not fully understood, particularly in myeloid malignancies. Bortezomib is a selective and reversible inhibitor of the proteasome. Paradoxically, we find that Bortezomib induces proteasome-independent degradation of TRAF6 protein, but not mRNA, in Myelodysplastic syndrome (MDS) and Acute Myeloid Leukemia (AML) cell lines and primary cells. The reduction in TRAF6 protein coincides with Bortezomib-induced autophagy, and subsequently with apoptosis in MDS/AML cells. RNAi-mediated knockdown of TRAF6 sensitized Bortezomib-sensitive and -resistant cell lines, underscoring the importance of TRAF6 in Bortezomib-induced cytotoxicity. Bortezomib-resistant cells expressing an shRNA targeting TRAF6 were resensitized to the cytotoxic effects of Bortezomib due to down-regulation of the proteasomal subunit alpha-1 (PSMA1). To uncover the molecular consequences following loss of TRAF6 in MDS/AML cells, we applied gene expression profiling and identified an apoptosis gene signature. Knockdown of TRAF6 in MDS/AML cell lines or patient samples resulted in rapid apoptosis and impaired malignant hematopoietic stem/progenitor function. In summary, we describe novel mechanisms by which TRAF6 is regulated through Bortezomib/autophagy-mediated degradation and by which it alters MDS/AML sensitivity to Bortezomib by controlling PSMA1 expression. TF-1 cells were transduced with lentivirus encoding shRNA targeting human TRAF6 and a negative control (pLKO) for 2.5 days. GFP positive cells were sorted for RNA exctration, labeling, and hybridization. A total of four samples were included, and two groups are assigned. Two replicates are for each group. Comparison comprises mRNA expression profile of TRAF6 knockdown (shT6) v.s. control vector (pLKO).

2012-06-14 | E-GEOD-38519 | biostudies-arrayexpress

Microarray analysis of WT and Tfap4-KO CD8 T cells during early activation

Project description:Gene expression of Tfap4â/â and WT CD8+ T cells were compared after activation with anti-CD3 and anti-CD28 antibodies in vitro or with Listeria monocytogenes infection in vivo For in vitro activation, naive CD8+ T cells were purified from WT and Tfap4â/â mice and activated with anti-CD3 and anti-CD28 antibodies for 72 hours. For in vivo activation, naive CD8+ T cells from Tfap4â/â OT-I or control WT OT-I TCR transgenice mice were adoptively transferred to congenic host mice that were subsequently infected with Listeria mnocytogenes expression ovalbumin. Activated OT-I cells were harvested 48 hours after infection.

2014-07-13 | E-GEOD-58078 | biostudies-arrayexpress

The effect of TRAF6 loss on the gene expression profiles in leukemia cells II

Project description:Although altered TRAF6 expression is observed in human acute myeloid leukemia (AML), its role in the AML pathogenesis remains elusive. In this study, we showed that the loss of TRAF6 in AML cells significantly impairs leukemic function in vitro and in vivo, indicating its functional importance in AML subsets. Loss of TRAF6 induces metabolic alterations, such as changes in glycolysis as well as impaired mitochondrial membrane potential and respiratory capacity. The restoration of growth capacity and metabolic activity in leukemic cells with TRAF6 loss, achieved through either forced expression of OGT or pharmacological inhibition of O-GlcNAcase (OGA) that removes O-GlcNAc, indicates the significant role of O-GlcNAc modification in the TRAF6-related cellular and metabolic dynamics. Our findings highlight the oncogenic function of TRAF6 in leukemia and illuminate the novel TRAF6/OGT/O-GlcNAc axis as a potential regulator of metabolic reprogramming in leukemogenesis.

2024-05-15 | GSE254615 | GEO

The effect of TRAF6 loss on the gene expression profiles in leukemia cells I

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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.

2020-02-24 | PXD015279 | Pride

TRAF6, a master activator of p53 transactivation, suppresses mitochondrial p53 and apoptosis

Project description:TRAF6 -/- thymi display defects in IR-induced p53 target gene expression and attenuate further enhancement of apoptosis upon IR treatment. TRAF6-mediated K63-linked ubiquitination of p53 at K24

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Traf6 function in the innate immune response of zebrafish embryos

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