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results of this study indicate that a novel T cell adaptor protein, activation-dependent, raft-recruited ADAP-like phosphoprotein (ARAP (Montrer MDK Protéines)), plays a unique role in T cells as a part of both the proximal activation signaling and inside-out signaling pathways that result in integrin activation and T cell adhesion
Ubc9 is an essential regulator of ADAP where it is required for TCR-induced membrane recruitment of the small GTPase Rap1 and its effector protein RapL and for activation of the small GTPase Rac1 in T cell adhesion.
Current knowledge of the functions of the adapter protein ADAP in T cell signaling with a focus on the role of individual phosphotyrosine (pY) motifs for SH2 domain mediated interactions is presented.
A distinct set of proteins interaction partners required for chemokine (Montrer CCL1 Protéines)-directed T cell migration is attracted by phosphotyrosine 571 of ADAP, including ZAP70 (Montrer ZAP70 Protéines).
Data strongly suggest that chemokine-stimulated associations between Vav1, SLP-76, and ADAP facilitate Rac1 activation and alpha4beta1-mediated adhesion, whereas Pyk2 opposes this adhesion by limiting Rac1 activation.
FYB nonsense mutations in humans causing small-platelet thrombocytopenia and a significant bleeding tendency.
Data (including data from studies in knockout/transgenic mice) suggest that ADAP regulates positive feedback loop of TGFbeta1 (Montrer TGFB1 Protéines) production and TGFbeta1 (Montrer TGFB1 Protéines)-induced CD103 (Montrer ITGAE Protéines) expression in CD8 (Montrer CD8A Protéines)+ T-lymphocytes and protects against influenza H5N1 virus infection.
The aim of this study was to perform an association study between seven Fyn-binding protein gene (FYB)-tag single nucleotide polymorphisms (SNPs) and type I diabetes mellitus (T1DM), as well as with disease age of onset.
The autosomal recessive bleeding phenotype seen in several members of this highly consanguineous family included petechial rash, mild epistaxis and thrombocytopenia with some decrease in platelet volume. These clinical findings, together with the results of exome sequencing pointed to only one strong candidate gene, the FYB gene.
ADAP interacts with talin and kindlin-3 to promote platelet Integrin alphaIIbbeta3 activation and stable fibrinogen binding.
ADAP (Montrer APP Protéines) fulfills different functions in CD4 (Montrer CD4 Protéines)(+) and CD8 (Montrer CD8A Protéines)(+) T cells, with CD8 (Montrer CD8A Protéines)(+) T cells being less dependent on ADAP (Montrer APP Protéines).
ADAP (Montrer APP Protéines) regulates CD8 (Montrer CD8A Protéines) T cell differentiation events following acute pathogen challenge that are critical for the formation and selected functions of TRM cells in nonlymphoid tissues.
Data (including data from studies in knockout/transgenic mice) suggest that ADAP (Montrer APP Protéines) regulates positive feedback loop of TGFbeta1 (Montrer TGFB1 Protéines) production and TGFbeta1 (Montrer TGFB1 Protéines)-induced CD103 (Montrer ITGAE Protéines) expression in CD8 (Montrer CD8A Protéines)+ T-lymphocytes and protects against influenza H5N1 virus infection.
The results indicate that ADAP (Montrer APP Protéines) dampens naive CD8 (Montrer CD8A Protéines) T cell responses to lymphopenia and IL-15 (Montrer IL15 Protéines), and they demonstrate a novel Ag-independent function for ADAP (Montrer APP Protéines) in the suppression of memory phenotype CD8 (Montrer CD8A Protéines) T cell generation.
provide evidence that CD28 (Montrer CD28 Protéines) and the TCR complex regulate NF-kappaB (Montrer NFKB1 Protéines) via different signaling modules of GRB-2 (Montrer GRB2 Protéines)/VAV1 (Montrer VAV1 Protéines) and LAT (Montrer LAT Protéines)/ADAP (Montrer APP Protéines) pathways respectively.
we demonstrate that loss of ADAP (Montrer APP Protéines) promotes resistance of experimental autoimmune encephalomyelitis in mice, likely by trapping encephalitogenic T cells in the peripheral lymph nodes on LYVE-1 (Montrer LYVE1 Protéines)+ lymphatic structures.
Signaling by Fyn (Montrer FYN Protéines)-ADAP (Montrer APP Protéines) via the Carma1 (Montrer CARD11 Protéines)-Bcl-10 (Montrer BCL10 Protéines)-MAP3K7 (Montrer MAP3K7 Protéines) signalosome exclusively regulates inflammatory cytokine production in NK cells.
integrin activation by the ADAP (Montrer APP Protéines)-SKAP55 (Montrer SKAP1 Protéines)-signaling module controls the stability and duration of T cell-dendritic cell contacts during the progressive phases necessary for optimal T cell activation.
ADAP (Montrer APP Protéines) coordinates distinct CARMA1 (Montrer CARD11 Protéines)-dependent control of key cell cycle proteins in T cells
The protein encoded by this gene is an adapter for the FYN protein and LCP2 signaling cascades in T-cells. The encoded protein is involved in platelet activation and controls the expression of interleukin-2. Three transcript variants encoding different isoforms have been found for this gene.
, FYN-T-binding protein
, SLP-76-associated phosphoprotein
, adhesion and degranulation-promoting adaptor protein
, FYN binding protein FYB-130
, adhesion and degranulation promoting adaptor protein
, FYN binding protein (FYB-120/130)