PTPRJ is a negative regulator of insulin signaling in neuronal cells, impacting protein biosynthesis, and neurite outgrowth


Here are the PTPRJ is a negative regulator of insulin signaling in neuronal cells, impacting protein biosynthesis, and neurite outgrowth journals presenting the latest research across various disciplines. From social sciences to technology, each article is expected to provide valuable insights to our readers.

Ptprj is a negative regulator of inflammation, ptprj is a negative number, ptprj is a negative regulator of insulin signaling in cardiomyocytes, ptprj is a negative p/e, ptprj is a negative regulator of insulin signaling definition, ptprj is a negative regulator of insulin signaling diagram, ptprj is a negative regulator of insulin signaling is an example.

PTPRJ is a negative regulator of insulin signaling in neuronal cells, impacting protein biosynthesis, and neurite outgrowth

Central insulin resistance has been linked to the development of neurodegenerative diseases and mood disorders. Various proteins belonging to the enzyme family of protein tyrosine phosphatases (PTPs) act as inhibitors of insulin signaling. Protein tyrosine phosphatase receptor type J (PTPRJ) has been identified as a negative regulator in insulin signaling in the periphery. However, the impact of PTPRJ on insulin signaling and its functional role in neuronal cells is largely unknown. Therefore, we generated a Ptprj knockout (KO) cell model in the murine neuroblast cell line Neuro2a by CRISPR-Cas9 gene editing. Ptprj KO cells displayed enhanced insulin signaling, as shown by increased phosphorylation of the insulin receptor (INSR), IRS-1, AKT, and ERK1/2. Further, proximity ligation assays (PLA) revealed both direct interaction of PTPRJ with the INSR and recruitment of this phosphatase to the receptor upon insulin stimulation. By RNA sequencing gene expression analysis, we iden tified multiple gene clusters responsible for glucose uptake and metabolism, and genes involved in the synthesis of various lipids being mainly upregulated under PTPRJ deficiency. Furthermore, multiple Ca2+ transporters were differentially expressed along with decreased protein biosynthesis. This was accompanied by an increase in endoplasmic reticulum (ER) stress markers. On a functional level, PTPRJ deficiency compromised cell differentiation and neurite outgrowth, suggesting a role in nervous system development. Taken together, PTPRJ emerges as a negative regulator of central insulin signaling, impacting neuronal metabolism and neurite outgrowth. © 2024 The Author(s). Journal of Neuroendocrinology published by John Wiley & Sons Ltd on behalf of British Society for Neuroendocrinology.

Authors : Ulke J.; Chopra S.; Kadiri O.L.-J.; Geserick P.; Stein V.; Cheshmeh S.; Kleinridders A.; Kappert K.

Source : John Wiley and Sons Inc

Article Information

Year 2024
Type Article
DOI 10.1111/jne.13446
ISSN 09538194
Volume 36

You can download the article here


If You have any problem, contact us here


Support Us:

Download Now Buy me a coffee Request Paper Here