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we describe for the first time the clinical manifestations associated with XLP-1 based on the c.278G>A variant in the SH2D1A gene. The patient had a relatively late age of onset and presented mainly with primary HLH associated with EBV infection without a familial history of immunodeficiency.
this study shows reduced intracellular SAP (Montrer APCS Kits ELISA) expression in iNKT cells and other lymphocytes in the blood from common variable immunodeficiency
in X-linked lymphoproliferative disease patient (Montrer APCS Kits ELISA)s, SAP deficiency reduces CD74 expression, resulting in the perturbation of B cell maintenance from the naive stage
study concludes that systemic lupus erythematosus (SLE) T cells display reduced levels of the adaptor protein SAP (Montrer APCS Kits ELISA), probably as a result of continuous T cell activation and degradation by caspase-3 (Montrer CASP3 Kits ELISA). Restoration of SAP (Montrer APCS Kits ELISA) levels in SLE T cells corrects the overexcitable lupus T cell phenotype.
High LAT1 expression correlated with significantly shorter prostate specific antigen recurrence-free survival in patients receiving androgen deprivation therapy
We describe here a novel c.137+5G > A intronic mutation in the SH2D1A gene of the signaling lymphocyte activation molecule (SLAM (Montrer SLAMF1 Kits ELISA))-associated protein (SAP) in association with Epstein-Barr virus (EBV)-induced fatal infectious mononucleosis (FIM (Montrer ZMYM2 Kits ELISA)) in an 8-year-old male patient and his 3-year-old step brother. The mother and the maternal grandmother of the boys are healthy and heterozygous for this sequence variant.
In addition to their role in NK cell activation by hematopoietic cells, the SLAM-SAP-SHP1 pathways influence responsiveness toward nonhematopoietic targets by a process akin to NK cell 'education'.
The mutation c.131G>A in this patient was found in combination with a second SH2D1A mutation
Study of SAP (Montrer APCS Kits ELISA) expression is specific but may have insufficient sensitivity for screening XLP1 as a single tool; however, combination with 2B4 (Montrer CD244 Kits ELISA) functional assay allows identification of all cases
Molecular dynamics analysis revealed that mutant R32Q and T53I structures of SAP (Montrer APCS Kits ELISA) exhibited structural variation with respect to their backbone atoms before and after binding with the unphosphorylated SLAM (Montrer SLAMF1 Kits ELISA) peptide.
naive T cells regulate B cell survival in a SAP (Montrer APCS Kits ELISA)-dependent manner
SAP (Montrer APCS Kits ELISA)-dependent activating SFR signaling is essential for NKT (Montrer CTSL1 Kits ELISA) cell selection.
SAP (Montrer APCS Kits ELISA) differentially regulates the late-stage lineage decisions of iNKT cell subsets. These results also provide evidence that iNKT1, iNKT2, and iNKT17 cells are differentially regulated by SAP (Montrer APCS Kits ELISA). SAP (Montrer APCS Kits ELISA)-dependent signals are essential for the fate decisions that drive the differentiation of iNKT2 but not iNKT1 and NKT17 cells.
SAP (Montrer APCS Kits ELISA) is an essential molecule for autoimmune antibody production.
SLAM (Montrer SLAMF1 Kits ELISA)-SAP (Montrer APCS Kits ELISA) signaling promotes differentiation of IL-17 (Montrer IL17A Kits ELISA)-producing T cells and progression of experimental autoimmune encephalomyelitis.
these data suggest that SAP (Montrer APCS Kits ELISA) is critical for regulating type II NKT (Montrer CTSL1 Kits ELISA) cell responses.
functional analysis in vitro indicates that SAP-2 is a non-functional isoform due to decreased protein stability
Here we report that B cell intrinsic responses to haptenated protein antigens are impaired in SAP (Montrer APCS Kits ELISA)-/- mice and in Rag-/- mice into which B cells derived from SAP (Montrer APCS Kits ELISA)-/- mice together with wt CD4 (Montrer CD4 Kits ELISA)+ T cells had been transferred.
SAP (Montrer APCS Kits ELISA) plays an essential role in CIA (Montrer NCOA5 Kits ELISA) because of Fyn (Montrer FYN Kits ELISA)-independent and Fyn (Montrer FYN Kits ELISA)-dependent effects on TFH cells and, possibly, other T cell types.
This gene encodes a protein that plays a major role in the bidirectional stimulation of T and B cells. This protein contains an SH2 domain and a short tail. It associates with the signaling lymphocyte-activation molecule, thereby acting as an inhibitor of this transmembrane protein by blocking the recruitment of the SH2-domain-containing signal-transduction molecule SHP-2 to its docking site. This protein can also bind to other related surface molecules that are expressed on activated T, B and NK cells, thereby modifying signal transduction pathways in these cells. Mutations in this gene cause lymphoproliferative syndrome X-linked type 1 or Duncan disease, a rare immunodeficiency characterized by extreme susceptibility to infection with Epstein-Barr virus, with symptoms including severe mononucleosis and malignant lymphoma. Multiple transcript variants encoding different isoforms have been found for this gene.
Duncan disease SH2-protein
, SH2 domain-containing protein 1A
, SLAM associated protein/SH2 domain protein 1A
, SLAM-associated protein
, T cell signal transduction molecule SAP
, T-cell signal transduction molecule SAP
, signaling lymphocyte activation molecule-associated protein
, signaling lymphocytic activation molecule-associated protein
, SH2 domain protein 1A
, SH2 domain protein 1A, Duncan's disease (lymphoproliferative syndrome)
, Signaling lymphocytic activation molecule-associated protein
, Duncan disease homolog