Target intelligence / Profile preview

Myosin IG (MYO1G)

Target
MYO1G
Molecular classification
Class I unconventional myosin (cytoskeletal motor protein), Actin-binding protein, Minor histocompatibility antigen (as source of antigenic peptide HA-2)
01

Overview

Myosin IG (MYO1G) is a member of the class I unconventional myosin family, encoded by the *MYO1G* gene. It is a plasma membrane-associated, actin-binding cytoskeletal motor protein highly expressed in hematopoietic cells, especially T and B lymphocytes and mast cells. MYO1G regulates immune cell migration, membrane elasticity, and adhesion through modulation of actin-plasma membrane interactions. It is uniquely involved in the immune response by generating membrane tension to facilitate lymphocyte surveillance for rare antigens. As a source of the minor histocompatibility antigen HA-2, MYO1G-derived peptides, when presented by MHC class I molecules (notably HLA-A*0201), can stimulate T cell responses that are implicated in graft-versus-host disease and potentially in immune-mediated therapies against hematologic malignancies. Variants in MYO1G alter the immunogenic peptide, impacting transplant outcomes and immune surveillance. If more information is needed for druggability, crystal structures, or more specific ligand interactions, a deeper search in structural biology or immunotherapy databases would be required.

Other names
MYO1GMyosin IGUnconventional myosin-IgMinor histocompatibility antigen HA-2HA2HLA-HA2MHAGmHag HA-2
02

Mechanism of action

Immunologic recognition: Peptides from MYO1G can be presented by MHC class I (e.g., HLA-A*0201) and recognized by T cells. Cell migration modulation: Not targeted directly but indirectly involved in therapies modifying T/B lymphocyte function via antigen presentation.

03

Biological functions

Regulation of T-cell migration (by generating plasma membrane tension; enhances surveillance and detection of rare antigen-presenting cells)Regulation of cell elasticity and adhesion in T and B lymphocytesFc-gamma receptor-mediated phagocytosis in immune cellsCell motility and shape control by coupling plasma membrane and actin filamentsRegulation of immune response, specifically lymphocyte migration and tissue homingAs a source of minor histocompatibility antigen HA-2, implicated in graft-versus-host responses
04

Disease associations

Graft-versus-host disease (GVHD) via presentation of minor histocompatibility antigen HA-2Hematologic cancer (not specified if causal, but associated via antigenic context)Transplant rejection (via minor histocompatibility response)Potential role in autoimmunity and immunotherapy (by selective targeting of leukemic cells via T cell recognition of minor antigens)
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Safety considerations

Expression of minor histocompatibility antigen HA-2 from MYO1G increases risk of GVHD, even in HLA-matched transplantsImmunogenicity can lead to unwanted transplant rejection or autoimmunity if not properly accounted for in donor-recipient matchingNo small molecule inhibitors listed; main concern is immune recognition and subsequent tissue damage or systemic immune activation
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Interacting drugs

T cell-mediated therapies (immunotherapy) via recognition of HA-2
07

Biomarkers

Presentation of the HA-2 peptide (sequence YIGEVLVSV) for patient selection in hematopoietic stem cell transplantation and early detection of GVHD riskPolymorphic variants of MYO1G may be monitored post-transplantation as biomarkers for antigen mismatches

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