Gyula Hoffka
Postdoctoral fellow
Phosphorylation of ITIM motifs drives the structural transition of indoleamine 2,3-dioxygenase 1 between enzymatic and non-enzymatic states
Author
Summary, in English
Indoleamine 2,3-dioxygenase 1 (IDO1) is the rate-limiting enzyme in tryptophan metabolism that plays a central role in immune regulation across a range of diseases, including cancer. Beyond its enzymatic role, IDO1 has a non-enzymatic function that remains poorly understood. This study explores how phosphorylation of immunoreceptor tyrosine-based inhibitory motifs (ITIMs) modulates IDO1's structural dynamics and functional states. Using molecular dynamics simulations and structural analysis, we show that phosphorylation acts as a molecular switch, inducing conformational changes that regulate heme-binding, remodel specific loop regions, and govern protein–protein interactions with SHP1, SHP2, and SOCS3. Notably, Tyr249 phosphorylation inhibits enzymatic activity by compacting the heme-binding pocket, creating steric hindrance that prevents cofactor binding. In contrast, Tyr111 phosphorylation enhances interactions with SHP1 or SHP2 proteins by embedding their C-terminal regions into the heme-binding pocket, also obstructing heme binding. Furthermore, Tyr249 phosphorylation promotes SOCS3 binding through the formation of a unique loop structure near the phosphorylation site. These findings provide a detailed mechanistic framework for understanding how ITIM phosphorylation orchestrates IDO1's functional transitions, effectively balancing its enzymatic and non-enzymatic functions.
Department/s
- Computational Chemistry
Publishing year
2025-06
Language
English
Publication/Series
Protein Science
Volume
34
Issue
6
Document type
Journal article
Publisher
The Protein Society
Topic
- Cell and Molecular Biology
- Theoretical Chemistry (including Computational Chemistry)
Keywords
- heme binding
- IDO1
- immune modulation
- immunoreceptor tyrosine-based inhibitory motifs (ITIMs)
- indoleamine 2,3-dioxygenase 1
- molecular dynamics
- SHP1
- SHP2
- SOCS3
Status
Published
ISBN/ISSN/Other
- ISSN: 0961-8368