ArticleThe Journal of biological chemistry2014
N-glycosylation determines the abundance of the transient receptor potential channel TRPP2.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 45 citations in OpenAlex.
- Deep learning-supported image quantification of epithelial cell shapes and its application to polycystic kidney disease.PLoS computational biology · 2026Article
- Physiological functions and pharmacological targeting of transient receptor potential channels.Pharmacological reviews · 2025Review
- Glycosylation in kidney diseases.Precision clinical medicine · 2025Review
- Identification of polycystin 2 missense mutants targeted for endoplasmic reticulum-associated degradation.American journal of physiology. Cell physiology · 2025Article
- Polycystin Channel Complexes.Annual review of physiology · 2023Review
- Wildtype heterogeneity contributes to clonal variability in genome edited cells.Scientific reports · 2022Article
- Hyperinsulinemic Hypoglycemia Due toPediatric reports · 2022Article
- Monoallelic pathogenic ALG5 variants cause atypical polycystic kidney disease and interstitial fibrosis.American journal of human genetics · 2022Article
- Identification of pathological transcription in autosomal dominant polycystic kidney disease epithelia.Scientific reports · 2021Article
- Novel GANAB variants associated with polycystic liver disease.Orphanet journal of rare diseases · 2020Article
- Polycystin 2: A calcium channel, channel partner, and regulator of calcium homeostasis in ADPKD.Cellular signalling · 2020Review
- Polycystin 2 is increased in disease to protect against stress-induced cell death.Scientific reports · 2020Article
- Ciliary exclusion of Polycystin-2 promotes kidney cystogenesis in an autosomal dominant polycystic kidney disease model.Nature communications · 2019Article
- Structure and function of polycystins: insights into polycystic kidney disease.Nature reviews. Nephrology · 2019Review
- The mitochondrial transporter SLC25A25 links ciliary TRPP2 signaling and cellular metabolism.PLoS biology · 2018Article
- Charge and Polarity Preferences forFrontiers in oncology · 2018Article
- Cryo-EM structures of the mammalian endo-lysosomal TRPML1 channel elucidate the combined regulation mechanism.Protein & cell · 2017Article
- Polycystic Kidney Disease with Hyperinsulinemic Hypoglycemia Caused by a Promoter Mutation in Phosphomannomutase 2.Journal of the American Society of Nephrology : JASN · 2017Article
- Isolated polycystic liver disease genes define effectors of polycystin-1 function.The Journal of clinical investigation · 2017Article
- Efficient genome editing of differentiated renal epithelial cells.Pflugers Archiv : European journal of physiology · 2017Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Glycosylation plays a critical role in the biogenesis and function of membrane proteins. Transient receptor potential channel TRPP2 is a nonselective cation channel that is mutated in autosomal dominant polycystic kidney disease. TRPP2 has been shown to be heavily N-glycosylated, but the glycosylation sites and the biological role of N-linked glycosylation have not been investigated. Here we show, using a combination of mass spectrometry and biochemical approaches, that native TRPP2 is glycosylated at five asparagines in the first extracellular loop. Glycosylation is required for the efficient biogenesis of TRPP2 because mutations of the glycosylated asparagines result in strongly decreased protein expression of the ion channel. Wild-type and N-glycosylation-deficient TRPP2 is degraded in lysosomes, as shown by increased TRPP2 protein levels upon chemical inhibition of lysosomal degradation. In addition, using pharmacological and genetic approaches, we demonstrate that glucosidase II (GII) mediates glycan trimming of TRPP2. The non-catalytic β subunit of glucosidase II (GIIβ) is encoded by PRKCSH, one of the genes causing autosomal dominant polycystic liver disease (ADPLD). The impaired GIIβ-dependent glucose trimming of TRPP2 glycosylation in ADPLD may explain the decreased TRPP2 protein expression in Prkcsh(-/-) mice and the genetic interaction observed between TRPP2 and PRKCSH in ADPLD. These results highlight the biological importance of N-linked glycosylation and GII-mediated glycan trimming in the control of biogenesis and stability of TRPP2.
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