Transferrin Receptor contributes to PANoptosis in thyroid cancer
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ABSTRACT:
PROVIDER: PRJNA1176525 | ENA |
REPOSITORIES: ENA
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Project description:PANoptosis is a novel type of cell death triggered by the cross-talk of three types of cell death (necrosis, apoptosis, and pyroptosis). Nevertheless, the molecular mechanisms associated with PANoptosis in thyroid cancer (TC) remain uncharted. Therefore, this study explored the effect of TFRC on PANoptosis in TC cells in vitro.
2025-08-31 | GSE280138 | GEO
Project description:UBE2N deficiency contributes to MASH development via p62-regulated mitophagy and PANoptosis
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Project description:Metabolomics dataset of serum from T3-treated dams. Related to following publication by Oelkrug et al: "Maternal thyroid hormone receptor beta activation sparks brown fat thermogenesis in the offspring"
2023-01-11 | MSV000091042 | GNPS
Project description:Thyroid hormones are important for homeostatic control of energy metabolism and body temperature. Although skeletal muscle is considered an important site for thyroid action, the contribution of thyroid hormone receptor signaling, in muscle, to whole-body energy metabolism and body temperature has not been resolved. Here, we show that thyroid hormone-induced increase in energy expenditure requires thyroid hormone receptor alpha 1 (TRa1) in skeletal muscle, but that thyroid hormone induced elevation in body temperature is independent of muscle-TRa1. In slow-twitch soleus muscle, ablation of TRa1 leads to an altered fiber type composition toward a more oxidative phenotype, which, however, does not influence running capacity or motivation to voluntary running. RNA-sequencing of soleus muscle from WT mice and TRaHSACre mice revealed differentiated transcriptional regulation of genes associated with muscle thermogenesis, such as sarcolipin and UCP3, thus providing molecular clues pertaining to the mechanistic underpinnings of TRa1-linked control of whole-body metabolic rate. Together, this work establishes a fundamental role for skeletal muscle in thyroid hormone-stimulated increase in whole-body energy expenditure.
2020-09-21 | GSE146336 | GEO
Project description:Cell death provides host defense and maintains homeostasis. Zα-containing molecules are essential for these processes. ZBP1 activates inflammatory cell death, PANoptosis, while ADAR1 serves as an RNA editor to maintain homeostasis. Here, we identify and characterize ADAR1’s interaction with ZBP1, defining its role in cell death regulation and tumorigenesis. Combining IFNs and nuclear export inhibitors (NEIs) activates ZBP1–dependent PANoptosis. ADAR1 suppresses PANoptosis by interacting with the Zα2 domain of ZBP1 to limit ZBP1 and RIPK3 interactions. Adar1fl/flLysMcre mice are resistant to development of colorectal cancer and melanoma, but deletion of the ZBP1 Zα2 domain restores tumorigenesis in these mice. In addition, treating wildtype mice with IFN-γ and the NEI KPT-330 regresses melanoma in a ZBP1–dependent manner. Our findings suggest that ADAR1 suppresses ZBP1–mediated PANoptosis, promoting tumorigenesis. Defining the functions of ADAR1 and ZBP1 in cell death is fundamental to inform therapeutic strategies for cancer and other diseases.
2021-10-19 | GSE184323 | GEO
Project description:Thyroid hormone receptor a in skeletal muscle is essential for thyroid thermogenesis
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Project description:The extensive crosstalk between pyroptosis, apoptosis, and necroptosis suggests that inhibiting one of them can lead to compensating for the other, thereby reducing therapeutic efficacy. Here, we identify Prussian blue (PB) nanoparticle as an effective PANoptosis inhibitor that binds to key proteins (RIPK1, ZBP1, and AIM2) to regulate multiple PANoptosomes, thereby comprehensively inhibiting pyroptosis, apoptosis, and necroptosis and blocking their crosstalk in myocardial ischemia-reperfusion injury (MIRI) therapy. This PANoptosis inhibitor significantly alleviated MIRI-induced cardiac functional impairment and adverse ventricular remodeling, promoted extracellular matrix repair and neovascularization, and prevented cardiomyocyte hypertrophy. Furthermore, it modulated mitochondrial metabolism and immune-inflammatory homeostasis, helping to block the crosstalk within PANoptosis. Specifically, single-nuclear transcriptome sequencing of human heart samples, molecular dynamics simulations, transcriptome sequencing analysis, medical imaging technology, and molecular biological methods comprehensively elucidated the role of PB as a PANoptosis inhibitor in MIRI therapy. This study provides a reference paradigm for exploring the role of PANoptosis in other diseases and a framework for studying nanobiological interactions to uncover broader nanomaterial mechanisms.
2026-02-10 | GSE298751 | GEO
Project description:Plasmacytoid dendritic cells (pDCs) are critical antiviral sentinels known for rapid type I interferon (IFN-I) production. However, their proteomic profile and nutrient dependencies are not well understood. Here, we used absolute quantitative proteomics of ex vivo murine splenic pDCs to characterize their protein landscape. Cross-species comparison with human blood pDCs revealed strong conservation but some differences in metabolic machinery. The transferrin receptor, responsible for transferrin-iron uptake, is the most abundant nutrient transporter in both species with 40,000 copies per murine pDC, and is significantly enriched compared to conventional dendritic cells. Despite pDCs showing constitutive transferrin-iron uptake they have low expression of iron storage proteins and a modest repertoire of iron-dependent enzymes. Also, pDC do not have an increase in iron atoms per cell compared to cDC, which suggests that pDC export excess iron through ferroportin and argue that Tfrc may have iron-independent roles. Indeed, iron chelation did not affect pDC production of type I interferon. These data suggest that Tfrc supports noncanonical functions in pDC biology, possibly related to antigen uptake. This work provides new insights into pDC metabolism and iron biology, advancing understanding of their specialized immune roles. Plasmacytoid dendritic cells (pDCs) are specialized antiviral sentinels defined by rapid type I interferon (IFN‑I) production, yet their metabolic organization and metal‑ion handling remain poorly understood. Here, we establish a high‑confidence, absolute quantitative proteome of murine splenic pDCs directly ex vivo and compare it with conventional dendritic cell subsets and human pDCs. Cross‑species proteomic analysis reveals strong conservation of pDC identity alongside divergence in metabolic pathway usage. pDCs display exceptionally high expression of the transferrin receptor (TFRC) and robust transferrin uptake compared with other immune cells; however, quantitative ironome analysis demonstrates that total cellular iron content is equivalent across dendritic cell subsets. Instead, iron is differentially allocated, with pDCs enriched for iron-sulfur cluster assembly proteins, cDC1s for heme‑binding proteins, and cDC2s for non‑heme iron enzymes. Despite elevated transferrin uptake, pDCs do not accumulate intracellular iron, coincident with expression of the iron exporter ferroportin, suggesting active iron efflux. Functionally, acute chelation or supplementation of extracellular iron does not affect CpG‑A plus IFNα-induced IFNα or TNFα production by pDCs. Together, these data demonstrate that pDCs uncouple surface transferrin receptor abundance from intracellular iron accumulation and effector cytokine production, revealing a distinct organization of iron handling that may support specialized trafficking or sensing functions rather than metabolic iron demand.
2026-06-29 | PXD079623 | Pride
Project description:Using tadpoles mutant for thyroid hormone receptor alpha (thra), we show that TRa is required for thyroid hormone (T3) induction of cell proliferation in the brain. RNA-sequencing showed that the TRa is required for 95% of the gene regulation responses to T3.
2019-05-13 | GSE130816 | GEO
Project description:Thyroid Hormone Receptor Beta Induces a Tumor Suppressive Program in Anaplastic Thyroid Cancer
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