Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2023 Apr 1;14(4):233. doi: 10.1038/s41419-023-05752-w

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Fig. 2 — A Co-IP analysis of protein interaction between endogenous RIP3 and PRMT methyltransferases (PRMT1, PRMT2, PRMT4) in HT29 cells. B The methylation of stable overexpressed RIP3 and RIP3^R486 in HT29 cells with or without PRMT1 overexpression was analyzed by immunoprecipitation and immunoblot. C The methylation of endogenous RIP3 in the control and PRMT1 stable knockdown HT29 cells was analyzed by immunoprecipitation and immunoblot. D In vitro methylation of commercial recombinant RIP3 by PRMT1. E In vitro methylation of purified RIP3 and RIP3^R486 by PRMT1. F The methylation of endogenous RIP3 in the HT29 cells treated with or without PRMT1 inhibitor C-7280948 (100 nM) for 6 h was analyzed by immunoprecipitation and immunoblot. G The methylation of endogenous RIP3 in HT29 cells treated with or without PRMT1 inhibitor TC-E 5003 (25 nM) for 6 h was analyzed by immunoprecipitation and immunoblot.