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Bone marrow macrophage derived GPNMB protein binds to orphan receptor GPR39 and plays a critical role in cardiac repair

ABSTRACT: Bone marrow macrophage derived GPNMB protein binds to orphan receptor GPR39 and plays a critical role in cardiac repair

PROVIDER: PRJNA1160704 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30656002_1.fastq.gz	Fastqsanger.gz
	SRR30656002_2.fastq.gz	Fastqsanger.gz
	SRR30656003_1.fastq.gz	Fastqsanger.gz
	SRR30656003_2.fastq.gz	Fastqsanger.gz
	SRR30656004_1.fastq.gz	Fastqsanger.gz

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Bone marrow macrophage derived GPNMB protein binds to orphan receptor GPR39 and plays a critical role in cardiac repair

Project description:Levels of Glyco Protein Non-metastatic Melanoma protein B (GPNMB), a type I transmembrane protein, originally identified in non-metastatic melanomas has been shown to be strongly associated with human heart failure. However, the role of GPNMB in modulation of cardiac injury and cardiac function remains unclear. We analyzed human cardiac global gene expression data sets and observed increased GPNMB expression in failing hearts. In murine hearts after myocardial infarction (MI), we showed that GPNMB expression increased by an order of magnitude. Lineage tracing and bone marrow transplantation experiments demonstrated that bone marrow macrophages were the primary source of GPNMB in the injured heart. Using genetic loss of function approaches, we demonstrate that animals deficient in GPNMB exhibited significantly higher mortality, cardiac rupture and developed rapid post infarct LV dysfunction. Conversely gain of function approaches by increasing circulating GPNMB levels by viral delivery led to augmentation of post MI heart function. Single cell transcriptomics demonstrated pleiotropic effects of GPNMB on gene expression of myocytes and non-myocytes leading to enhanced myocyte contraction and decreased fibroblast activation. Using chemical cross-linking studies and immunoprecipitation studies, we identified the orphan receptor GPR39 as a receptor for circulating GPNMB. In animals deficient in GPR39, GPNMB failed to deliver beneficial effects on post infarct heart function. Taken together, these observations demonstrate that bone marrow macrophage derived GPNMB plays a pivotal role in cardiac repair following myocardial infarction, by mediating its pleiotropic effects in part via the orphan receptor GPR39

2024-09-17 | GSE277086 | GEO

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Chaperone-like protein DAY plays critical roles in photomorphogenesis

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Orphan quality control shapes network dynamics and gene expression

Project description:All eukaryotes require intricate protein networks to translate developmental signals into accurate cell fate decisions. Mutations that disturb interactions between network components often result in disease, but how composition and dynamics of complex networks are established remains poorly understood. Here, we identify the E3 ligase UBR5 as a signaling hub that helps degrade unpaired subunits of multiple transcriptional regulators that act within a network centered on the c-MYC oncoprotein. Biochemical and structural analyses show that UBR5 binds motifs that only become available upon complex dissociation. By rapidly turning over orphan transcription factor subunits, UBR5 establishes dynamic interactions between transcriptional regulators that allow cells to effectively execute gene expression, while remaining receptive to environmental signals. We conclude that orphan quality control plays an essential role in establishing dynamic protein networks, which may explain the conserved need for protein degradation during transcription and offers unique opportunities to modulate gene expression in disease. Crosslinking mass spec experiment with UBR5 HECT domain STREP-SUMO-MCRS1 and DSSO.

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Orphan quality control shapes network dynamics and gene expression

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