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Validated All-in-One™ qPCR Primer for CD244(NM_001166663.2) Search again
Product ID:
HQP175807
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
2B4, NAIL, NKR2B4, Nmrk, SLAMF4
Gene Description:
CD244 molecule
Target Gene Accession:
NM_001166663.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
Natural killer (NK) cells express both activating and inhibitory cell surface receptors. Inhibitory signaling receptors all possess cytoplasmic immunoreceptor tyrosine-based inhibitory motifs, or ITIMs, whereas the activating receptors lack ITIMs and associate with DAP12 (TYROBP; MIM 604142), which contains an immunoreceptor tyrosine-based activation motif, or ITAM. Killer cell immunoglobulin (Ig)-like receptors, or KIRs (see KIR2DL1; MIM 604936), and other NK cell receptors interact with major histocompatibility complex (MHC) molecules (see MIM 142800).
Gene References into function
- Up-regulation of the activatory receptor 2B4 by CD8+ alpha beta T cells in vivo correlates with the acquisition of effector cell properties such as granzyme B and perforin expression, IFN-gamma production, and down-regulation of chemokine receptor CCR7.
- 2B4-mediated activation of natural killer cells involves the complex interactions of LAT, Ras, Raf, ERK and p38 kinase in the regulation of lytic function and cytokine production.
- X-linked lymphoproliferative disease causes impaired 2b4 function in NK cells.
- expressed on CD3+/CD56+ large granular lymphocytes proliferating in response to a tumor-expressed activating ligand (CD48) and killing autologous leukemia cells by a novel mechanism in a patient with acute myeloid leukemia.
- Natural killer cell inhibitory receptors block actin cytoskeleton-dependent recruitment of 2B4 (CD244) to lipid rafts.
- engagement of 2B4 on NK cells triggered a tyrosine phosphorylation signal
- expression significantly up-regulated on CD4 and CD8 T cells during infectious mononucleosis, and significantly more lymphocytes expressing CD8 and CD244/CD8 in patients with severe sore throat.
- The function of 2B4 as an adhesion molecule is underscored and a relevant role is suggested in the initial binding, scanning of target cells, and formation of cytotoxic natural killer cell immune synapse.
- the SAP/2B4 pathway plays a key role in CTL lytic activity against EBV-positive targets by promoting the polarization of the lytic machinery
- analysis of the molecular basis for the different signals generated by 2B4
- Functional analysis indicates that Lys-68 and Glu-70 in the extracellular domain of human 2B4 play a key role in the activation of human natural killer (NK) cells through 2B4/CD48 interaction.
- Review of recent studies suggests an important role for interactions between 2B4 and CD48 in the course of T cell activation and proliferation
- CD244-3BP2 association regulates cytolytic function but not IFN-gamma release
- blocking the engagement of 2B4, NTB-A and CRACC has no effect on the proliferation or development of the cytotoxic potential of NK cells but triggering by their physiological ligands on MHC class I-negative target cells induces potent NK cell cytotoxicit
- 2B4 (CD244) can stimulate NK cell cytotoxicity and cytokine production by interacting with NK cell expressed CD48 and adds CD48 to the growing number of activating NK cell receptors
- REVIEW: different functions of the murine and human 2B4 (CD244) receptor on NK cells
- CD48 is a CD2 and CD244 (2B4)-binding protein
- The lower surface expression of 2B4 after ligand-induced down-modulation results in reduced 2B4-mediated NK cell activation and cytotoxicity.
- The triggering of 2B4 (CD244) alone is sufficient to induce natural killer (NK) cell cytotoxicity in IL-2-activated NK cells with high SLAM-associated protein expression.
- stimulation of natural killer cells through surface 2B4 (CD244) down-regulates its own expression due to a reduction in the promoter activity at the Ets element
- the mechanism of signal transduction by CD244 is to regulate FYN kinase recruitment and/or activity and the outcome of CD48/CD244 interactions is determined by which other receptors are engaged.
- HTLV-1-infected CD4+ T cells did not express ligands for NK cell activating receptors, NCR and NKG2D, although they did express ligands for NK cell coactivating receptors, NTB-A and 2B4.
- 2B4, NTB-A and CRACC have roles in the regulation of Natural Killer cell function [review]
- 3BP2 acts downstream of SAP, increases CD244 phosphorylation and links the receptor with PI3K, Vav, PLC gamma, and PKC downstream events in order to achieve maximum natural killer cell killing function.
- Studies under identical and controlled conditions reveal that both human and mouse 2B4 can activate or inhibit natural killer (NK) cells.
- Single nucleotide polymorphism in CD244 gene is asociated with rheumatoid arthritis.