ArticlePloS one2014
Protein tyrosine phosphatase-1B modulates pancreatic β-cell mass.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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
14 citing papers in PubMed, 34 citations in OpenAlex.
- Modern Approaches to Diabetes: The Role of Phytochemicals in Targeting Molecular Receptors.Current topics in medicinal chemistry · 2025Review
- The role of protein tyrosine phosphatase 1B (PTP1B) in the pathogenesis of type 2 diabetes mellitus and its complications.Journal of physiology and biochemistry · 2022Review
- Exploring New Drug Targets for Type 2 Diabetes: Success, Challenges and Opportunities.Biomedicines · 2022Review
- Consolidation of network and experimental pharmacology to divulge the antidiabetic action of3 Biotech · 2021Article
- Integration of in silico, in vitro and ex vivo pharmacology to decode the anti-diabetic action ofJournal of diabetes and metabolic disorders · 2020Article
- Design and synthesis of tricyclic terpenoid derivatives as novel PTP1B inhibitors with improved pharmacological property andJournal of enzyme inhibition and medicinal chemistry · 2020Article
- Antidiabetic activity in vitro and in vivo of BDB, a selective inhibitor of protein tyrosine phosphatase 1B, from Rhodomela confervoides.British journal of pharmacology · 2020Article
- Research of anti-GAD and anti-IA2 autoantibodies by ELISA test in a series of Moroccan pediatric patients with diabetes type 1.African health sciences · 2020Article
- Hypoglycemic activity of extracts ofJournal of traditional and complementary medicine · 2020Article
- Impact of global PTP1B deficiency on the gut barrier permeability during NASH in mice.Molecular metabolism · 2020Article
- The down regulation of PTP1B expression and attenuation of disturbed glucose and lipid metabolism usingSaudi journal of biological sciences · 2020Article
- Article
- The protein tyrosine phosphatase 1B inhibitor MSI-1436 stimulates regeneration of heart and multiple other tissues.NPJ Regenerative medicine · 2017Article
- Genetic models rule out a major role of beta cell glycogen in the control of glucose homeostasis.Diabetologia · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein tyrosine phosphatase 1B (PTP1B) is a negative regulator of the insulin signalling pathway. It has been demonstrated that PTP1B deletion protects against the development of obesity and Type 2 Diabetes, mainly through its action on peripheral tissues. However, little attention has been paid to the role of PTP1B in β-cells. Therefore, our aim was to study the role of PTP1B in pancreatic β-cells. Silencing of PTP1B expression in a pancreatic β-cell line (MIN6 cells) reveals the significance of this endoplasmic reticulum bound phosphatase in the regulation of cell proliferation and apoptosis. Furthermore, the ablation of PTP1B is able to regulate key proteins involved in the proliferation and/or apoptosis pathways, such as STAT3, AKT, ERK1/2 and p53 in isolated islets from PTP1B knockout (PTP1B (-)/(-)) mice. Morphometric analysis of pancreatic islets from PTP1B (-)/(-) mice showed a higher β-cell area, concomitantly with higher β-cell proliferation and a lower β-cell apoptosis when compared to islets from their respective wild type (WT) littermates. At a functional level, isolated islets from 8 weeks old PTP1B (-)/(-) mice exhibit enhanced glucose-stimulated insulin secretion. Moreover, PTP1B (-)/(-) mice were able to partially reverse streptozotocin-induced β-cell loss. Together, our data highlight for the first time the involvement of PTP1B in β-cell physiology, reinforcing the potential of this phosphatase as a therapeutical target for the treatment of β-cell failure, a central aspect in the pathogenesis of Type 2 Diabetes.
Indexed as
Identifiers
What OpenQuestion holds
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.