Inappropriate movement of Rac1 contributes to glucotoxicity of the islet β-cell.

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

8 citing papers in PubMed.

1. Protein prenylation in islet β-cell function in health and metabolic stress.Biochemical pharmacology · 2025
   Review
2. Hyperglycemic Conditions Promote Rac1-Mediated Serine536 Phosphorylation of p65 Subunit of NFκB (RelA) in Pancreatic Beta Cells.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2022
   Article
3. Underappreciated roles for Rho GDP dissociation inhibitors (RhoGDIs) in cell function: Lessons learned from the pancreatic islet β-cell.Biochemical pharmacology · 2022
   Review
4. GPCRs, G Proteins, and Their Impact on β-cell Function.Comprehensive Physiology · 2020
   Review
5. [Effects of glycosylated hemoglobin and disease course on islet β-cell function in patients with type 2 diabetes].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019
   Article
6. RACking up ceramide-induced islet β-cell dysfunction.Biochemical pharmacology · 2018
   Review
7. The Dynamic Effects of Isosteviol on Insulin Secretion and Its Inability to Counteract the Impaired β-Cell Function during Gluco-, Lipo-, and Aminoacidotoxicity: Studies In Vitro.Nutrients · 2018
   Article
8. Glucotoxicity promotes aberrant activation and mislocalization of Ras-related C3 botulinum toxin substrate 1 [Rac1] and metabolic dysfunction in pancreatic islet β-cells: reversal of such metabolic defects by metformin.Apoptosis : an international journal on programmed cell death · 2017
   Article

Corrections and comments

• Comment on
  Exposure to chronic hyperglycemic conditions results in Ras-related C3 botulinum toxin substrate 1 (Rac1)-mediated activation of p53 and ATM kinase in pancreatic β-cells.2017

Authors and funding

1 author.

Funding

Abstract

PubMed holds no abstract for this paper.

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