Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Short Peptides of Innate Immunity Protein Tag7 (PGLYRP1) Selectively Induce Inhibition or Activation of Tumor Cell Death via TNF Receptor

Version 1 : Received: 23 June 2023 / Approved: 23 June 2023 / Online: 23 June 2023 (15:06:46 CEST)

A peer-reviewed article of this Preprint also exists.

Yurkina, D.M.; Sharapova, T.N.; Romanova, E.A.; Yashin, D.V.; Sashchenko, L.P. Short Peptides of Innate Immunity Protein Tag7 (PGLYRP1) Selectively Induce Inhibition or Activation of Tumor Cell Death via TNF Receptor. Int. J. Mol. Sci. 2023, 24, 11363. Yurkina, D.M.; Sharapova, T.N.; Romanova, E.A.; Yashin, D.V.; Sashchenko, L.P. Short Peptides of Innate Immunity Protein Tag7 (PGLYRP1) Selectively Induce Inhibition or Activation of Tumor Cell Death via TNF Receptor. Int. J. Mol. Sci. 2023, 24, 11363.

Abstract

TNF cytokine receptor TNFR1 protein plays an important role in immune response and autoimmune diseases. Previously, we demonstrated that the peptide of the innate immunity protein Tag7 (PGLYRP1), designated as 17.1, is able to perform the functions of a full-size Tag7 protein, namely, to inhibit the transmission of a signal through the TNFR1 receptor and activate this receptor in complex with the major heat shock protein Hsp70. In this study, we show that two peptides derived from 17.1 – 17.1A and 17.1B have different affinities to the TNFR1 receptor and the Hsp70 protein, and each of them is able to perform only one of the above functions: peptide 17.1A is only able to inhibit signal conduction through the TNFR1 receptor, and peptide 17.1B can only activate this receptor is in complex with Hsp70. Thus, it is possible to modulate the activity of TNFR1 receptor and further perform its specific inhibition or activation in the treatment of various autoimmune or oncological diseases.

Keywords

Tag7; Hsp70; TNFR1, signal transduction, cytotoxity, short peptides.

Subject

Biology and Life Sciences, Biochemistry and Molecular Biology

Comments (0)

We encourage comments and feedback from a broad range of readers. See criteria for comments and our Diversity statement.

Leave a public comment
Send a private comment to the author(s)
* All users must log in before leaving a comment
Views 0
Downloads 0
Comments 0
Metrics 0


×
Alerts
Notify me about updates to this article or when a peer-reviewed version is published.
We use cookies on our website to ensure you get the best experience.
Read more about our cookies here.