SRGN antibody
- Known as:
- SRGN (anti-)
- Catalog number:
- orb101744
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- SRGN antibody
Related genes to: SRGN antibody
- Gene:
- SRGN NIH gene
- Name:
- serglycin
- Previous symbol:
- PRG, PRG1
- Synonyms:
- PPG
- Chromosome:
- 10q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1988-07-22
- Date modifiied:
- 2014-11-18
Related products to: SRGN antibody
Related articles to: SRGN antibody
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Publication date: 2026/07/23
Su WenyaWu YudiHe QianZhou LinZhou Jun - Glutamine-Fructose-6-Phosphate Transaminase 1 (GFPT1), the rate-limiting enzyme of the hexosamine biosynthetic pathway (HBP), provides the UDP-N-acetylglucosamine (UDP-GlcNAc) required for protein glycosylation. Biallelic mutations in cause congenital myasthenic syndromes (-CMS), yet the molecular mechanisms linking impaired glycosylation to skeletal muscle dysfunction remain incompletely understood. Here, we combine cellular models of inducible knockdown and a skeletal muscle-specific knockout mouse () with whole-cell proteomics, immunoblot studies and secretomics to define glycosylation-dependent defects in intracellular trafficking, ER stress signaling and autophagy. Global proteomic profiling of -deficient myoblasts revealed marked downregulation of protein trafficking pathways and impaired secretion of key muscle cargo proteins, including serglycin (Srgn). Loss of GFPT1 reduced both high-molecular-weight glycosylated serglycin and its core protein, accompanied by intracellular retention and decreased secretion. These trafficking defects coincide with robust activation of the unfolded protein response (UPR), evidenced by increased expression and accumulation of spliced Xbp1s across pharmacologic, cellular, and mouse models of deficiency. Converging evidence from proteomics, immunoblotting, and immunofluorescence demonstrated impaired autophagy, including increased LC3-II accumulation, elevated p62/Sqstm1 levels, and enhanced p62-positive puncta in both -deficient C2C12 myoblasts and skeletal muscle. Soluble/insoluble fractionation further confirmed p62 accumulation, indicating defective autophagic flux and buildup of aggregated cargo. Together, these findings identify a glycosylation-dependent failure in protein trafficking that triggers ER stress, UPR activation, and autophagy impairment in -deficient skeletal muscle. This mechanistic cascade provides a unifying explanation for muscle pathology in -CMS and suggests that restoring glycosylation or improving proteostasis may represent viable therapeutic approaches. - Source: PubMed
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