ArticleCellular and molecular biology (Noisy-le-Grand, France)2022
The role of the Siglec-G ITIM domain during bacterial infection.
Article in Cellular and molecular biology (Noisy-le-Grand, France), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 4 citations in OpenAlex.
- GDI2 protein: research progress and its mechanisms in diseases.Frontiers in cell and developmental biology · 2026Review
- Chimerolectins: Classification, structural architecture, and functional perspectives.Protein science : a publication of the Protein Society · 2025Review
- Membrane Trafficking-Related Genes Predict Tumor Immune Microenvironment and Prognosis in Colorectal Cancer.Biochemical genetics · 2024Article
- The Novel Role of GDI2: A Mini-Review.Annals of medicine and medical research · 2024Article
- Article
- Targeted disruption of Rab1a causes early embryonic lethality.International journal of molecular medicine · 2022Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Siglecs, membrane-bound lectins of the sialic acid-binding immunoglobulin superfamily, inhibit immune responses by recruiting tyrosine phosphatases (e.g., SHP-1 and SHP-2) through their cytoplasmic immunoreceptor tyrosine-based inhibition motif (ITIM) domain. The role of Siglecs in infection has been extensively studied, but downstream signaling through the ITIM domain remains unclear. Here, we used a GST pull-down assay to identify additional proteins associated with the ITIM domain during bacterial infection. Gdi2 bound to ITIM under normal homeostasis, but Rab1a was recruited to ITIM during bacterial infection. Western blot analysis confirmed the presence of SHP-1 and SHP-2 in eluted ITIM-associated proteins under normal homeostasis. We confirmed the association of ITIM with Gdi2 or Rab1a by transfection of corresponding expression vectors in 293T cells followed by immunoprecipitation-western blot assay. Thus, ITIM's role in the inhibition of the immune response during bacterial infection may be regulated by interaction with Gdi2 and Rab1a in addition to SHP-1 and SHP-2.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.