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

In this study, we have found two peptides of Tag7 (PGLYRP1) protein-17.1A (HRDVQRT) and 17.1B (RSNYVLKG), that have different affinities to the TNFR1 receptor and the Hsp70 protein. Peptide 17.1A is able to inhibit signal transduction through the TNFR1 receptor, and peptide 17.1B can activate this r...

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Autores principales: Yurkina, Daria M., Sharapova, Tatiana N., Romanova, Elena A., Yashin, Denis V., Sashchenko, Lidia P.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10379010/
https://www.ncbi.nlm.nih.gov/pubmed/37511122
http://dx.doi.org/10.3390/ijms241411363
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author Yurkina, Daria M.
Sharapova, Tatiana N.
Romanova, Elena A.
Yashin, Denis V.
Sashchenko, Lidia P.
author_facet Yurkina, Daria M.
Sharapova, Tatiana N.
Romanova, Elena A.
Yashin, Denis V.
Sashchenko, Lidia P.
author_sort Yurkina, Daria M.
collection PubMed
description In this study, we have found two peptides of Tag7 (PGLYRP1) protein-17.1A (HRDVQRT) and 17.1B (RSNYVLKG), that have different affinities to the TNFR1 receptor and the Hsp70 protein. Peptide 17.1A is able to inhibit signal transduction through the TNFR1 receptor, and peptide 17.1B can activate this receptor in a complex with Hsp70. Thus, it is possible to modulate the activity of the TNFR1 receptor and further perform its specific inhibition or activation in the treatment of various autoimmune or oncological diseases.
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spelling pubmed-103790102023-07-29 Short Peptides of Innate Immunity Protein Tag7 (PGLYRP1) Selectively Induce Inhibition or Activation of Tumor Cell Death via TNF Receptor Yurkina, Daria M. Sharapova, Tatiana N. Romanova, Elena A. Yashin, Denis V. Sashchenko, Lidia P. Int J Mol Sci Article In this study, we have found two peptides of Tag7 (PGLYRP1) protein-17.1A (HRDVQRT) and 17.1B (RSNYVLKG), that have different affinities to the TNFR1 receptor and the Hsp70 protein. Peptide 17.1A is able to inhibit signal transduction through the TNFR1 receptor, and peptide 17.1B can activate this receptor in a complex with Hsp70. Thus, it is possible to modulate the activity of the TNFR1 receptor and further perform its specific inhibition or activation in the treatment of various autoimmune or oncological diseases. MDPI 2023-07-12 /pmc/articles/PMC10379010/ /pubmed/37511122 http://dx.doi.org/10.3390/ijms241411363 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Yurkina, Daria M.
Sharapova, Tatiana N.
Romanova, Elena A.
Yashin, Denis V.
Sashchenko, Lidia P.
Short Peptides of Innate Immunity Protein Tag7 (PGLYRP1) Selectively Induce Inhibition or Activation of Tumor Cell Death via TNF Receptor
title Short Peptides of Innate Immunity Protein Tag7 (PGLYRP1) Selectively Induce Inhibition or Activation of Tumor Cell Death via TNF Receptor
title_full Short Peptides of Innate Immunity Protein Tag7 (PGLYRP1) Selectively Induce Inhibition or Activation of Tumor Cell Death via TNF Receptor
title_fullStr Short Peptides of Innate Immunity Protein Tag7 (PGLYRP1) Selectively Induce Inhibition or Activation of Tumor Cell Death via TNF Receptor
title_full_unstemmed Short Peptides of Innate Immunity Protein Tag7 (PGLYRP1) Selectively Induce Inhibition or Activation of Tumor Cell Death via TNF Receptor
title_short Short Peptides of Innate Immunity Protein Tag7 (PGLYRP1) Selectively Induce Inhibition or Activation of Tumor Cell Death via TNF Receptor
title_sort short peptides of innate immunity protein tag7 (pglyrp1) selectively induce inhibition or activation of tumor cell death via tnf receptor
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10379010/
https://www.ncbi.nlm.nih.gov/pubmed/37511122
http://dx.doi.org/10.3390/ijms241411363
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