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Human Monoclonal SH2D1A Primary Antibody for ELISA, WB - ABIN561703
Ma, Suryani, Avery, Chan, Nanan, Santner-Nanan, Deenick, Tangye: Early commitment of naïve human CD4(+) T cells to the T follicular helper (T(FH)) cell lineage is induced by IL-12. in Immunology and cell biology 2009
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Human Polyclonal SH2D1A Primary Antibody for WB - ABIN1881802
Snow, Marsh, Krummey, Roehrs, Young, Zhang, van Hoff, Dhar, Nichols, Filipovich, Su, Bleesing, Lenardo: Restimulation-induced apoptosis of T cells is impaired in patients with X-linked lymphoproliferative disease caused by SAP deficiency. in The Journal of clinical investigation 2009
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Human Polyclonal SH2D1A Primary Antibody for IP, WB - ABIN4369745
Sayos, Wu, Morra, Wang, Zhang, Allen, van Schaik, Notarangelo, Geha, Roncarolo, Oettgen, De Vries, Aversa, Terhorst: The X-linked lymphoproliferative-disease gene product SAP regulates signals induced through the co-receptor SLAM. in Nature 1998
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Human Polyclonal SH2D1A Primary Antibody for ELISA, WB - ABIN250561
Mikhalap, Shlapatska, Yurchenko, Yurchenko, Berdova, Nichols, Clark, Sidorenko: The adaptor protein SH2D1A regulates signaling through CD150 (SLAM) in B cells. in Blood 2004
Human Polyclonal SH2D1A Primary Antibody for ELISA, WB - ABIN251451
Romero, Benítez, March, Vilella, Miralpeix, Engel: Differential expression of SAP and EAT-2-binding leukocyte cell-surface molecules CD84, CD150 (SLAM), CD229 (Ly9) and CD244 (2B4). in Tissue antigens 2004
The nonsense mutation in SH2D1A (NM_002351.4:c.300T>A) was reported for the first time in a case of X-linked lymphoproliferative syndrome type 1 (XLP1) and was considered to be likely pathogenic based on the truncation of the mRNA sequence. This finding expands the spectrum of known XLP-related mutations in Chinese patients.
miR-126 inhibits the migration of malignant glioma cells by inhibiting MTCP1.
these results showed that the NTB-A/SAP pathway regulates T-cell activation and restimulation-induced cell death during human tuberculosis
this paper shows that the X-linked lymphoproliferative disease gene product SAP regulates signals induced through the co-receptor SLAM
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 expression in iNKT cells and other lymphocytes in the blood from common variable immunodeficiency
in X-linked lymphoproliferative disease patients, 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, probably as a result of continuous T cell activation and degradation by caspase-3. Restoration of SAP 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)-associated protein (SAP) in association with Epstein-Barr virus (EBV)-induced fatal infectious mononucleosis (FIM) 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.
no association between genetic polymorphism and X-linked lymphoproliferative disease in pediatric patients in Iran
novel missense mutation in Australian patient with cerebral vasculitis in X-linked lymphoproliferative disease
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 expression is specific but may have insufficient sensitivity for screening XLP1 as a single tool; however, combination with 2B4 functional assay allows identification of all cases
Molecular dynamics analysis revealed that mutant R32Q and T53I structures of SAP exhibited structural variation with respect to their backbone atoms before and after binding with the unphosphorylated SLAM peptide.
Signaling lymphocytic activation molecule (SLAM)/SLAM-associated protein pathway regulates human B-cell tolerance.
In patients suffering from X-linked lymphoproliferative disease (XLP1), SAP is nonfunctional, not only abolishing the activating function of 2B4, but rendering this receptor inhibitory.
our data reveal how SAP nucleates a previously unknown signaling complex involving NTB-A and LCK to potentiate restimulation-induced cell death of activated human T cells.
SAP is a new actor downstream of PECAM-1 and its binding regulates PECAM-1 mediated cell adhesion.
naive T cells regulate B cell survival in a SAP-dependent manner
SAP-dependent activating SFR signaling is essential for NKT cell selection.
SAP 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. SAP-dependent signals are essential for the fate decisions that drive the differentiation of iNKT2 but not iNKT1 and NKT17 cells.
SAP is an essential molecule for autoimmune antibody production.
SLAM-SAP signaling promotes differentiation of IL-17-producing T cells and progression of experimental autoimmune encephalomyelitis.
these data suggest that SAP is critical for regulating type II NKT 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-/- mice and in Rag-/- mice into which B cells derived from SAP-/- mice together with wt CD4+ T cells had been transferred.
SAP plays an essential role in CIA because of Fyn-independent and Fyn-dependent effects on TFH cells and, possibly, other T cell types.
SAP was required not only for the initiation but also for the progression of primary T cell-driven B cell responses to haptens.
Loss of SAP expression is associated with invariant NKT cell cytotoxicity and defective lytic synapse formation.
SAP is required for the development of innate phenotype in H2-M3--restricted Cd8(+) T cells.
In the absence of SAP, several routes of natural killer cell-mediated antibody production are still accessible.
SAP(-) cytotoxic lymphocytes had defects in synapse organization with B-cell & low-avidity T-cell targets. SAP & SLAM receptors regulate positive & negative signals for synapse organization & cytotoxicity thresholds for distinct targets.
SAP secures NK cell activation in 2 ways. It couples SLAM receptors to Fyn, triggering Vav-1. It coupled SLAM family receptors to the kinase Fyn, which triggered the exchange factor Vav-1 and augmented NK cell activation.
Overexpression of SAP in T cells increases and sustains protein kinase C-theta recruitment to the immune synapse and elevated IL-4 production, in response to T cell receptor (TCR)- plus SLAM-mediated stimulation.
showed that Id3(-/-) CD8(+) T cells had an innate-like phenotype and required SAP for their development
SAP is not required for T follicular helper (TFH) cell differentiation but is required for germinal center TFH cell differentiation and the resultant interleukin (IL)-4 production.
PLZF acts independently of SAP- and Fyn-mediated signaling pathways.
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