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TYROBP

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All listed services and products are For Research Use Only. Do Not use in any diagnostic or therapeutic applications.

Background

Transmembrane immune signaling adaptor TYROBP (DAP12) is a short transmembrane signaling subunit encoded by TYROBP gene, selectively expressed in myeloid and innate lymphoid cell subsets, localized exclusively to plasma membrane lipid bilayers. Distinct from standalone immune receptors, TYROBP associates non-covalently with multiple myeloid surface receptors via charged transmembrane residues, delivering intracellular ITAM-based phosphorylation signals to trigger downstream inflammatory and phagocytic cascades. Under resting immune states, minimal TYROBP-receptor complexes exist to avoid spontaneous immune activation. Upon ligand crosslinking of paired surface receptors, TYROBP cytoplasmic ITAM motifs undergo phosphorylation to recruit cytoplasmic tyrosine kinases, amplifying antimicrobial and pro-inflammatory cytokine secretion programs. Unlike universal signaling adaptors with broad cell distribution, TYROBP carries myeloid-restricted innate immune amplification functions that cannot be fully compensated by other ITAM-bearing subunits, linking surface receptor ligation to myeloid effector activation pathways. Loss of functional TYROBP ablates multiple myeloid receptor signaling and weakens host anti-pathogen defense, while sustained TYROBP-dependent signaling drives exaggerated tissue inflammation, establishing TYROBP as a core research target for immune adaptor biology and anti-inflammatory compound screening.

TYROBP executes ITAM-mediated signal adaptor function embedded within myeloid cell surface bilayers, utilizing conserved cytoplasmic immunoreceptor tyrosine-based activation motifs to mediate kinase recruitment after receptor clustering. Conserved transmembrane charged residues exclusively mediate pairing with myeloid sensor receptors, separating its binding spectrum from lymphocyte-specific signaling adaptors. TYROBP-mediated signal transduction bridges extracellular ligand detection and intracellular myeloid effector transcription programs, balancing inflammatory response magnitude relative to pathogen stimulus intensity. TYROBP participates in myeloid phagocytosis, microbial pattern sensing and innate cytokine production. Deficient TYROBP expression disrupts myeloid receptor signal transduction and impairs systemic innate immune surveillance. Therefore, TYROBP represents a pivotal research target for ITAM adaptor study and myeloid immune modulator screening.

Fig. 1 Structural and signaling core diagram of TYROBP adaptor protein: domain annotation, cross-species sequence alignment and complete Src-Syk-PI3K/ERK/PLCγ innate immune transduction pathway. (OA Literature)Fig. 1 Full schematic of TYROBP (DAP12) homodimer protein architecture, human/mouse sequence conservation, canonical ITAM phosphorylation signaling cascade and three downstream effector axes governing myeloid cell proliferation, cytokine secretion and phagocytosis.1

TYROBP Protein Function: Core Roles in ITAM Signaling and Myeloid Innate Immune Tuning

The biological functions of TYROBP are focused on receptor co-association, ITAM phosphorylation and myeloid effector signal control:

  • Myeloid Receptor Co-Pairing: Associates with multiple cell-surface innate receptors via transmembrane electrostatic interactions.
  • ITAM-Dependent Signal Initiation: ITAM motifs are phosphorylated by Src-family kinases following receptor activation, enabling recruitment of downstream kinases such as SYK.
  • Resting Immune Homeostasis: Maintains low-level uncomplexed adaptor pools to prevent spontaneous inflammatory signaling.
  • Innate Immune Amplification: Adjusts magnitude of phagocytic and cytokine responses upon microbial ligand exposure.
  • Disease Relevance: TYROBP loss blunts myeloid anti-pathogen immunity, while persistent signaling drives chronic inflammatory pathology.

TYROBP Protein Product

Creative Biolabs offers high-quality TYROBP proteins through optimized expression systems, including full-length transmembrane adaptor constructs and isolated cytoplasmic ITAM reagents. Full-length constructs are suitable for receptor-pairing studies, while phosphorylated or non-phosphorylated ITAM reagents support kinase and SH2-domain binding studies. All TYROBP proteins undergo strict quality control to ensure consistent performance across research applications.

TYROBP Protein Product

Not finding the membrane protein product you need? Contact us to start your one-stop custom service!

TYROBP Stable Cell Line Product

Creative Biolabs provides custom-engineered TYROBP stable cell lines, including overexpression and blank control models. These cell lines are optimized for immune adaptor expression profiling and ITAM signal functional analysis. Each cell line undergoes stringent validation to ensure stable expression profiles and consistent functional performance in diverse experimental contexts.

TYROBP Stable Cell Line Product

Not finding the stable cell line product you need? Contact us to start your one-stop custom service!

TYROBP Recombinant Antibody Product

High-specificity recombinant antibodies targeting TYROBP are developed via advanced antibody engineering technologies. These antibodies are validated for plasma membrane localization detection and myeloid tissue expression profiling, and can be combined with paired myeloid receptor detection reagents to analyze complete receptor-adaptor signaling complexes in primary myeloid cell models.

TYROBP Recombinant Antibody Product

Not finding the recombinant antibody product you need? Contact us to start your one-stop custom service!

Product Features

  • Native Receptor Pairing & ITAM Signaling Activity: Preserves intact adaptor-receptor association capacity for myeloid innate immune research.
  • TYROBP Isoform Specificity: Eliminates non-specific cross-recognition of unrelated ITAM signaling adaptors.
  • Myeloid Immunology Compatibility: Optimized reagent series for innate inflammatory signaling and anti-inflammatory compound screening workflows.
  • Comprehensive Customization Support: Facilitates end-to-end development of customized proteins, antibodies and stable cell lines to address immune adaptor research demands.

Custom TYROBP Research Services

Beyond catalog products, Creative Biolabs offers specialized custom services for TYROBP research:

  • Custom TYROBP Protein Production: Tailored expression of mutant and tagged TYROBP constructs for receptor-adaptor binding interaction analysis.
  • Custom Antibody Development: Generation of TYROBP-specific antibodies for plasma membrane immunostaining in myeloid cell populations.
  • Stable Cell Line Engineering: Construction of TYROBP-modified cell models for ITAM inflammatory signaling research.
  • Functional Assay Development: Custom design of receptor co-association and cytokine secretion detection workflows.

Frequently Asked Questions (FAQ)

  1. What is the primary function of TYROBP?

    TYROBP is a transmembrane ITAM adaptor that complexes with myeloid surface receptors to transmit phosphorylation signals driving innate immune activation.

  2. Why is TYROBP a significant research target?

    TYROBP acts as a critical link between myeloid microbial sensor receptors and intracellular inflammatory effector programs, governing anti-pathogen innate immunity.

  3. Are Creative Biolabs' TYROBP products suitable for clinical use?

    No, all TYROBP products and services are strictly for research use only, not intended for clinical diagnosis or treatment.

  4. What types of TYROBP products does Creative Biolabs offer?

    Offerings include full-length TYROBP signaling adaptors, isoform-specific detection antibodies and custom stable cell lines for myeloid innate immune research.

  5. How are TYROBP proteins validated for activity?

    TYROBP proteins are validated via receptor co-association and ITAM phosphorylation functional testing.

Reference
  1. Haure-Mirande, Jean-Vianney, et al. "Microglial TYROBP/DAP12 in Alzheimer's disease: Transduction of physiological and pathological signals across TREM2." Molecular neurodegeneration 17.1 (2022): 55. Under Open Access license CC BY 4.0, without modification. https://doi.org/10.1186/s13024-022-00552-w
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