ArticleJournal of hepatology2012
It's not all in the cilium, but on the road to it: genetic interaction network in polycystic kidney and liver diseases and how trafficking and quality control matter.
Article in Journal of hepatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Polycystic kidney disease.Nature reviews. Disease primers · 2018Review
- knnAUC: an open-source R package for detecting nonlinear dependence between one continuous variable and one binary variable.BMC bioinformatics · 2018Article
- Bagging Nearest-Neighbor Prediction independence Test: an efficient method for nonlinear dependence of two continuous variables.Scientific reports · 2017Article
- Genetics of Autosomal Recessive Polycystic Kidney Disease and Its Differential Diagnoses.Frontiers in pediatrics · 2017Review
- Polarity gene alterations in pure invasive micropapillary carcinomas of the breast.Breast cancer research : BCR · 2014Article
- Polycystin-1: a master regulator of intersecting cystic pathways.Trends in molecular medicine · 2014Review
- Diagnosis and management of polycystic liver disease.Nature reviews. Gastroenterology & hepatology · 2013Review
- Loss of cilia causes embryonic lung hypoplasia, liver fibrosis, and cholestasis in the talpid3 ciliopathy mutant.OrganogenesisArticle
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autosomal dominant polycystic liver disease results from mutations in PRKCSH or SEC63. The respective gene products, glucosidase IIb and SEC63p, function in protein translocation and quality control pathways in the endoplasmic reticulum. Here we show that glucosidase IIb and Sec63p are required in mice for adequate expression of a functional complex of the polycystic kidney disease gene products, polycystin-1 and polycystin-2. We find that polycystin-1 is the rate-limiting component of this complex and that there is a dose–response relationship between cystic dilation and levels of functional polycystin-1 following mutation of Prkcsh or Sec63.Reduced expression of polycystin-1 also serves to sensitize the kidney to cyst formation resulting from mutations in Pkhd1, the recessive polycystic kidney disease gene. Finally, we show that proteasome inhibition increases steady-state levels of polycystin-1 in cells lacking glucosidase IIb and that treatment with a proteasome inhibit or reduces cystic disease in orthologous gene models of human autosomal dominant polycystic liver.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.