ArticleHistochemistry and cell biology2007
Expression of mutant Ins2C96Y results in enhanced tubule formation causing enlargement of pre-Golgi intermediates of CHO cells.
Article in Histochemistry and cell biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Golgi tubules: their structure, formation and role in intra-Golgi transport.Histochemistry and cell biology · 2013Review
- Mutant proinsulin proteins associated with neonatal diabetes are retained in the endoplasmic reticulum and not efficiently secreted.Biochemical and biophysical research communications · 2010Article
- State-of-the-art technologies, current opinions and developments, and novel findings: news from the field of histochemistry and cell biology.Histochemistry and cell biology · 2008Review
- Protein quality control: the who's who, the where's and therapeutic escapes.Histochemistry and cell biology · 2008Review
- Protein quality control in the early secretory pathway.The EMBO journal · 2008Review
- Recent progress in histochemistry.Histochemistry and cell biology · 2007Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Misfolded proteins are recognized by the protein quality control and eventually degraded by the ubiquitin-proteasome system. Previously, we demonstrated accumulation of a misfolded non-glycosylated protein, namely proinsulin, in enlarged pre-Golgi intermediates and dilated rough endoplasmic reticulum (ER) domains in pancreatic beta-cells of Akita mice. In order to exclude effects possibly due to coexisting wild type and mutant proinsulin in pancreatic beta-cells, CHO cells expressing singly wild type or mutant C96Y proinsulin 2 were now analyzed by electron microscopic morphometry and immunogold labeling as well as serial section 3D analysis. We found a significant increase in volume density of pre-Golgi intermediates in CHO Ins2(C96Y) cells which was principally due to an increase of its tubular elements, and no significant changes of the ER. The average diameter of the pre-Golgi intermediates of CHO Ins2(C96Y) cells was about twice that of CHO Ins2(wt) cells. The enlarged pre-Golgi intermediates and the ER of CHO Ins2(C96Y) cells were positive for proinsulin, which was not detectable in the significantly enlarged Golgi cisternal stack. Treatment of CHO Ins2(C96Y) cells with proteasome inhibitors resulted in the formation of proinsulin-containing aggresomes. We conclude that misfolded proinsulin causes enlargement of pre-Golgi intermediates which indicates their involvement in protein quality control.
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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.