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Downregulation of Human-Specific lncRNA TMEM9B-AS1 in Skeletal Muscle of People with Type 2 Diabetes Impacts Ribosomal Biogenesis

ABSTRACT: Long non-coding RNAs (lncRNAs) are important regulators of skeletal muscle physiology, with altered expression noted in several human diseases including type 2 diabetes. Here we report downregulation of TMEM9B-AS1, a previously uncharacterized lncRNA, in skeletal muscle of men with type 2 diabetes. We demonstrate that loss of TMEM9B-AS1 in primary human myotubes leads to reduction in protein synthesis, concomitant with reduced phosphorylation of ribosomal protein S6, downstream of ERK and mTOR pathways. Moreover, we show that TMEM9B-AS1 plays a pivotal role in the regulation of ribosomal biogenesis by facilitating mRNA stabilization of the transcription factor MYC through a direct physical interaction with the RNA-binding protein IGF2BP1. Disrupted ribosomal biogenesis resulting from downregulation of TMEM9B-AS1 links to the decrease in skeletal muscle mass observed in individuals with type 2 diabetes, shedding new light on the molecular mechanisms underlying this metabolic disorder.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Primary Cell, Skeletal Muscle Cell

SUBMITTER: Ilke Sen

LAB HEAD: Anna Krook

PROVIDER: PXD053490 | Pride | 2025-04-22

REPOSITORIES: Pride

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			Action	DRS
	20221004_RNA_Pulldown_TMEM9B-AS1_Rep_1.raw	Raw
	20221013_RNA_Pulldown_Negative_Control_Rep_1.raw	Raw
	20221108_RNA_Pulldown_Negative_Control_Rep_2.raw	Raw
	20221108_RNA_Pulldown_Negative_Control_Rep_3.raw	Raw
	20221108_RNA_Pulldown_TMEM9B-AS1_Rep_2.raw	Raw

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