Killer Cell Lectin-like Receptor Subfamily G, Member 1 Human Recombinant
Killer Cell lectin-like Receptor Subfamily F Member 1 Human Recombinant
Recombinant Human KLRF1, expressed in HEK293 cells, is a single, glycosylated polypeptide chain. It comprises 414 amino acids (60-231a.a) with a molecular weight of 47.1kDa. The protein includes a C-terminal fusion of a 242 amino acid hIgG-His-Tag and is purified using proprietary chromatographic techniques.
Killer Cell Lectin-Like Receptor Subfamily C, Member 2 Human Recombinant
Killer Cell Lectin-Like Receptor Subfamily C, Member 3 Human Recombinant
Killer Cell Lectin-Like Receptor Subfamily C, Member 1 Human Recombinant
Sf9, Baculovirus cells.
Killer Cell Lectin Like Receptor D1 Human Recombinant
Killer Cell lectin-Like Receptor Subfamily K, Member 1 Human Recombinant, Sf9
Killer Cell Lectin-Like Receptor Subfamily B, Member 1 Human Recombinant
Killer Cell Lectin-Like Receptor Subfamily B, Member 1 Human Recombinant, Sf9
Sf9, Baculovirus cells.
Killer cell lectin-like receptors (KLRs) are a family of transmembrane proteins primarily expressed on natural killer (NK) cells and subsets of T cells. They belong to the C-type lectin-like receptor (CLR) superfamily, characterized by their ability to recognize carbohydrate structures on pathogens and host cells. KLRs are classified into activating and inhibitory receptors based on their signaling motifs and functional outcomes .
Key Biological Properties: KLRs are type II transmembrane glycoproteins with an extracellular C-type lectin domain, a transmembrane domain, and a cytoplasmic tail containing signaling motifs. They can bind to various ligands, including cadherins and other cell surface molecules .
Expression Patterns: KLRs are predominantly expressed on NK cells and subsets of T cells, including CD8+ T cells, CD4+ T cells, and regulatory T cells (Tregs). Their expression can be modulated by various factors, including cytokines and cellular activation states .
Tissue Distribution: KLRs are widely distributed across various tissues, with high expression in lymphoid organs such as the spleen, lymph nodes, and bone marrow. They are also found in non-lymphoid tissues, including the liver, lungs, and intestines .
Primary Biological Functions: KLRs play crucial roles in regulating immune cell activation, proliferation, and cytotoxicity. They provide both stimulatory and inhibitory signals, balancing immune responses to self-antigens and foreign antigens .
Role in Immune Responses: KLRs are involved in the recognition and elimination of infected or transformed cells. They contribute to immune surveillance by modulating NK cell and T cell functions, including cytokine production and cytotoxic activity .
Pathogen Recognition: KLRs can recognize pathogen-associated molecular patterns (PAMPs) on the surface of microbes, facilitating the immune system’s ability to detect and respond to infections .
Mechanisms with Other Molecules and Cells: KLRs interact with various ligands, including cadherins on antigen-presenting cells (APCs) and tumor cells. These interactions trigger signaling cascades that modulate immune cell functions .
Binding Partners: KLRs bind to ligands such as E-cadherin and N-cadherin, which are expressed on epithelial and mesenchymal cells, respectively. These interactions are crucial for the regulation of immune responses .
Downstream Signaling Cascades: Upon ligand binding, KLRs initiate signaling pathways involving the phosphorylation of immunoreceptor tyrosine-based inhibitory motifs (ITIMs) or activation motifs (ITAMs). These pathways recruit phosphatases like SHIP-1 and SHP-2, leading to the modulation of immune cell activity .
Expression and Activity Control: The expression and activity of KLRs are tightly regulated by transcriptional and post-transcriptional mechanisms. Cytokines such as IL-2 and IL-15 can upregulate KLR expression, while cellular activation states can modulate their activity .
Transcriptional Regulation: KLR gene expression is controlled by transcription factors that respond to immune signals. For example, the transcription factor T-bet is known to regulate the expression of certain KLRs in NK cells .
Post-translational Modifications: KLRs undergo various post-translational modifications, including phosphorylation and glycosylation, which can influence their stability, localization, and signaling capacity .
Biomedical Research: KLRs are valuable tools in immunological research, providing insights into immune regulation and potential therapeutic targets for immune-related diseases .
Diagnostic Tools: KLR expression patterns can serve as biomarkers for immune cell activation and differentiation, aiding in the diagnosis and monitoring of immune disorders .
Therapeutic Strategies: Targeting KLRs with specific inhibitors or agonists holds promise for therapeutic interventions in cancer, autoimmune diseases, and infectious diseases. For example, blocking inhibitory KLRs can enhance anti-tumor immunity .
Development: KLRs are involved in the development and maturation of NK cells and T cells. Their expression is regulated during different stages of immune cell differentiation .
Aging: The expression and function of KLRs can change with age, potentially contributing to age-related declines in immune function. For instance, increased expression of inhibitory KLRs has been associated with reduced NK cell activity in elderly individuals .
Disease: Dysregulation of KLR expression and signaling is implicated in various diseases, including cancer, autoimmune disorders, and chronic infections. Understanding the role of KLRs in these conditions can inform the development of targeted therapies .