ArticlePloS one2012
Pdx1 is post-translationally modified in vivo and serine 61 is the principal site of phosphorylation.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- PDX1 phosphorylation at S61 by mTORC1 links nutrient signaling to β cell function and metabolic disease.Cell reports · 2026Article
- Post translational modification regulation of transcription factors governing pancreatic β-cell identity and functional mass.Frontiers in endocrinology · 2025Review
- Future treatment of Diabetes - Tyrosine Kinase inhibitors.Journal of diabetes and metabolic disorders · 2023Review
- The Chd4 Helicase Regulates Chromatin Accessibility and Gene Expression Critical for β-Cell Function In Vivo.Diabetes · 2023Article
- The Chd4 subunit of the NuRD complex regulates Pdx1-controlled genes involved in β-cell function.Journal of molecular endocrinology · 2022Article
- Role of nutrient-driven O-GlcNAc-post-translational modification in pancreatic exocrine and endocrine islet development.Development (Cambridge, England) · 2020Article
- Protein Kinase CK2-A Putative Target for the Therapy of Diabetes Mellitus?International journal of molecular sciences · 2019Review
- Phosphorylation of carboxypeptidase B1 protein regulates β-cell proliferation.International journal of molecular medicine · 2017Article
- Age-related accumulation of phosphorylated mitofusin 2 protein in retinal ganglion cells correlates with glaucoma progression.Experimental neurology · 2017Article
- Genome Editing of Lineage Determinants in Human Pluripotent Stem Cells Reveals Mechanisms of Pancreatic Development and Diabetes.Cell stem cell · 2016Article
- Capillary nano-immunoassays: advancing quantitative proteomics analysis, biomarker assessment, and molecular diagnostics.Journal of translational medicine · 2015Review
- Transcriptional activity of the islet β cell factor Pdx1 is augmented by lysine methylation catalyzed by the methyltransferase Set7/9.The Journal of biological chemistry · 2015Article
- MST1 is a key regulator of beta cell apoptosis and dysfunction in diabetes.Nature medicine · 2014Article
- Dietary regulation of histone acetylases and deacetylases for the prevention of metabolic diseases.Nutrients · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Maintaining sufficient levels of Pdx1 activity is a prerequisite for proper regulation of blood glucose homeostasis and beta cell function. Mice that are haploinsufficient for Pdx1 display impaired glucose tolerance and lack the ability to increase beta cell mass in response to decreased insulin signaling. Several studies have shown that post-translational modifications are regulating Pdx1 activity through intracellular localization and binding to co-factors. Understanding the signaling cues converging on Pdx1 and modulating its activity is therefore an attractive approach in diabetes treatment. We employed a novel technique called Nanofluidic Proteomic Immunoassay to characterize the post-translational profile of Pdx1. Following isoelectric focusing in nano-capillaries, this technology relies on a pan specific antibody for detection and it therefore allows the relative abundance of differently charged protein species to be examined simultaneously. In all eukaryotic cells tested we find that the Pdx1 protein separates into four distinct peaks whereas Pdx1 protein from bacteria only produces one peak. Of the four peaks in eukaryotic cells we correlate one of them to a phosphorylation Using alanine scanning and mass spectrometry we map this phosphorylation to serine 61 in both Min6 cells and in exogenous Pdx1 over-expressed in HEK293 cells. A single phosphorylation is also present in cultured islets but it remains unaffected by changes in glucose levels. It is present during embryogenesis but is not required for pancreas development.
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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.