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High-affinity self-ligand important in bidirectional T- cell to B-cell stimulation. Additionally we are shipping SLAMF1 Antibodies (308) and SLAMF1 Proteins (20) and many more products for this protein.
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the Slam locus has an overall inhibitory role during NK cell activation that is solely dependent on 2B4 (show CD244 ELISA Kits). This effect is influenced by cytokines and leads to suppression of LFA-1 (show ITGAL ELISA Kits) activity.
CRISPR-Mediated Slamf1Delta/Delta Slamf5Delta/Delta Slamf6Delta/Delta Triple Gene Disruption Reveals NKT (show CTSL1 ELISA Kits) Cell Defects but Not T Follicular Helper Cell Defects.
We demonstrated that Bacille Calmette-Guerin infection significantly upregulated SLAMF1, which enhanced inflammatory response by activating the NF-kappaB (show NFKB1 ELISA Kits) signaling pathway and facilitated bacterial clearance in BCG (show SLC11A1 ELISA Kits)-infected RAW264.7 cells and mice.
Slamf1 and Slamf8 (show SLAMF8 ELISA Kits) govern ROS (show ROS1 ELISA Kits)-dependent innate immune responses of myeloid cells.
The combined effects of RIIB deletion and pathogenic SLAM can lead to severe lupus nephritis in the B6 genetic background.
SLAM-SAP (show APCS ELISA Kits) signaling promotes differentiation of IL-17 (show IL17A ELISA Kits)-producing T cells and progression of experimental autoimmune encephalomyelitis.
The goal of the current study was to determine whether Slam haplotype affected NKT (show CTSL1 ELISA Kits) and Vgamma4+ T-cell responses subsequent to coxsackievirus b3 infection.
Signaling lymphocyte activation molecule regulates development of colitis in mice.
Slamf1, which controls phagosomal/lysosomal fusion and phagosomal NADPH-oxidase (show NOX1 ELISA Kits) activity, is required for T.cruzi replication in macrophages and dendritic cells, but not in other cells, which do not express the receptor.
conclude that Slamf1 recruits a subset of Vps34 (show PIK3C3 ELISA Kits)-associated proteins, which is involved in membrane fusion and NOX2 (show CYBB ELISA Kits) regulation
CD150 and CD180 (show CD180 ELISA Kits) receptors may modulate transcriptional program in lymphocytic leukemia cells by regulating the transcription factor expression levels
this paper shows that the X-linked lymphoproliferative disease gene product SAP (show APCS ELISA Kits) regulates signals induced through the co-receptor SLAM
combination of signals via CD150 and CD180 (show CD180 ELISA Kits) leads to blocking of pro-survival pathways that may be a restraining factor for neoplastic CLL B cells propagation in more than 50% of CLL cases where these receptors are coexpressed
EBF1 is critical for transcriptional control of SLAMF1 gene in human B cells.
MeV can hijack SLAMF1 to drive endocytosis using a complex pathway that shares features with canonical viral macropinocytosis, phagocytosis, and mechanotransduction. This uptake pathway is specific to SLAMF1-positive cells and occurs within 60 min of viral attachment.
Malignant B-cell lines at the different stages of maturation only partially resemble their normal counterparts by CD150 expression. In malignant B-cell lines, CD150 expression on mRNA level is much broader than on protein level. CD150 isoforms are differentially expressed in normal and malignant B cells with predominant expression of mCD150 isoform.
Data suggest that SLAMF1 is another significant piece in the intricate defective immune-regulatory function of patients with SLE.
results indicate that loss of SLAMF1 expression in chronic lymphocytic leukemia modulates genetic pathways
Upstream open reading frames regulate translation of the long isoform of SLAMF1 mRNA that encodes costimulatory receptor CD150
Molecular dynamics analysis revealed that mutant R32Q and T53I structures of SAP (show APCS ELISA Kits) exhibited structural variation with respect to their backbone atoms before and after binding with the unphosphorylated SLAM peptide.
High-affinity self-ligand important in bidirectional T- cell to B-cell stimulation. SLAM-induced signal-transduction events in T-lymphocytes are different from those in B-cells. Two inhibitor SH2D1A acts as a negative regulator and another in which protein-tyrosine phosphatase 2C (PTPN11)-dependent signal transduction operates.
signaling lymphocyte activation molecule
, signaling lymphocytic activation molecule
, signaling lymphocytic activation molecule family member 1