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Transferrin Receptor contributes to PANoptosis in thyroid cancer

ABSTRACT: Transferrin Receptor contributes to PANoptosis in thyroid cancer

PROVIDER: PRJNA1176525 | ENA |

REPOSITORIES: ENA

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Transferrin Receptor contributes to PANoptosis in thyroid cancer

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

GNPS - Maternal thyroid hormone receptor beta activation sparks brown fat thermogenesis in the offspring

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

ADAR1 restricts ZBP1–mediated immune response and PANoptosis to promote tumorigenesis

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

Thyroid hormone receptor a in skeletal muscle is essential for thyroid thermogenesis

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

Thyroid hormone receptor a in skeletal muscle is essential for thyroid thermogenesis

Project description:Thyroid hormone receptor a in skeletal muscle is essential for thyroid thermogenesis

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NINJ1 mediates inflammatory cell death, PANoptosis, and drives lethality during heat stress

Project description:Innate immunity provides the first line of defense through key mechanisms, including pyrogen and cytokine production and cell death. While elevated body temperature during infection is beneficial, heat stress (HS) can lead to inflammation and pathology. Links between HS, cytokine release, and inflammation have been observed, but fundamental innate immune mechanisms driving pathology during HS remain unclear. Here, we use diverse genetic approaches to elucidate innate immune pathways in HS. Our results show that bacteria and LPS robustly increase inflammatory cell death, PANoptosis, during HS. NINJ1 is the key executioner of this cell death to release inflammatory molecules, independent of other pore-forming executioners. In an in vivo HS model, mortality is reduced by deleting NINJ1 and fully rescued by deleting key PANoptosis molecules. Our findings suggest that therapeutic strategies blocking NINJ1 or its upstream regulators to prevent PANoptosis may reduce the release of inflammatory mediators and benefit patients experiencing HS.

2024-01-05 | GSE252609 | GEO

Thyroid hormone receptor alpha is required for thyroid hormone-dependent neural cell proliferation during tadpole metamorphosis

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

Microarray analysis of mice with thyroid hormone receptor and RAS mutations.

Project description:Affymetrix GeneChip Mouse Gene 1.0 ST Array was used to study gene expression profiles in three groups of mice: with thyroid hormone receptor ThrbPV (ThrbPV/PV) mutation only, with RAS mutation (KrasG12D) only, and with both ThrbPV/PV and KrasG12D mutations. Three groups mice: with thyroid hormone receptor ThrbPV (ThrbPV/PV) mutation only, with RAS mutation (KrasG12D) only, and with both ThrbPV/PV and KrasG12D mutations. Each group has three biological replicates.

2015-09-22 | E-GEOD-61652 | biostudies-arrayexpress

Conditional knock-out of Transferrin receptor 1 in Alb-cre H11-myc mice

Project description:Conditional knock-out of Transferrin receptor 1 in Alb-cre H11-myc mice

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Thyroid Hormone Receptor Beta Induces a Tumor Suppressive Program in Anaplastic Thyroid Cancer

Project description:Thyroid Hormone Receptor Beta Induces a Tumor Suppressive Program in Anaplastic Thyroid Cancer

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