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HBS1 like translational GTPase is a protein encoded by the HBS1L gene in humans and acts as a GTPase component of the Pelota-HBS1L complex, which is essential for recognizing stalled ribosomes and initiating the No-Go Decay (NGD) pathway for ribosome rescue and RNA quality control[1][4]. It is also a member of the GTP-binding elongation factor family involved in protein synthesis regulation, with its highest expression in heart and skeletal muscle[1]. The intergenic region between HBS1L and MYB genes acts as a quantitative trait locus affecting fetal hemoglobin levels, erythrocyte and platelet production, and is implicated in the severity and clinical course of hemoglobinopathies such as sickle cell disease and beta-thalassemia[1][3]. Polymorphisms in the HBS1L region are associated with these hematologic traits and disease phenotypes.
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