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Study shows that CD28 ligation during priming endows T cells with mitochondrial capacity that is important for future T cell responses. We speculate that CD28 temporarily restricts TXNIP (show TXNIP ELISA Kits) and miR33 expression, and this leads to a transient induction of Cpt1a (show CPT1A ELISA Kits) and fatty acid oxidation, which are marked by characteristic changes in mitochondria shape and structure.
findings revealed a dual mechanism of monocyte and neutrophil recruitment by T cells relying on overlapping and nonoverlapping roles for the noninducible costimulatory receptor CD28 and the inflammatory cytokine TNF (show TNF ELISA Kits)
results are consistent with a complex pathway in which CD28 is the primary driver of Treg proliferation and CTLA-4 (show CTLA4 ELISA Kits) functions as the main brake but is also dependent on TCR signals and interactions with CD80 (show CD80 ELISA Kits)/CD86 (show CD86 ELISA Kits).
data suggest that mPEG PV1 (show PLVAP ELISA Kits)-Fab (show FANCB ELISA Kits)' acts mainly on IFN-gamma (show IFNG ELISA Kits)-producing CD4 (show CD4 ELISA Kits)+ T cells and emphasize that this specific CD28 blockade strategy is a potential specific and alternative tool for the treatment of autoimmune disorders in the eye.
the scaffolding role of RLTPR predominates during CD28 co-stimulation and underpins the similar function of RLTPR in human and mouse T cells.
BAFF (show TNFSF13B ELISA Kits) upregulates CD28/B7 and CD40 (show CD40 ELISA Kits)/CD154 (show CD40LG ELISA Kits) expression, and promotes the interactions between T and B cells in a BAFF-R (show TNFRSF13C ELISA Kits)-dependent manner
we report that cell-intrinsic deletion of CD28 after the peak of the primary response does not affect the establishment, maintenance, or recall of long-term memory. Thus, if given sufficient time, the progeny of primed CD8 (show CD8A ELISA Kits)(+) T cells adapt to the absence of this costimulator.
Deletion of CD28 co-stimulatory signals exacerbates left ventricular remodeling and increases cardiac rupture after MI through prolongation of the inflammatory period and reduction of collagen fiber in the infarct scars.
identified a new plasmacytoid dendritic cells regulatory mechanism by which the same CD28 molecule that promotes stimulation in most cells
Ndrg1 (show NDRG1 ELISA Kits) is phosphorylated and degraded by CD28 signalling in a proteasome-dependent manner.
The mutant CD28 isoforms could accelerate tumor cell growth.
CD3 (show CD3 ELISA Kits)/28-activated T cells expanded in IL-7 (show IL7 ELISA Kits) and IL-15 (show IL15 ELISA Kits) produced greater expansion of memory stem T cells and central memory T cell-derived T cells compared with IL-2 (show IL2 ELISA Kits). Our strategy provides a powerful tool to elucidate the characteristics of CAR-modified T cells, regardless of the protocol used for expansion, reveals the functional properties of each expanded T cell subset.
identified recurrent mutations in CD28 in peripheral T-cell lymphomas. Molecular modeling studies on each of these mutations suggested how these mutants result in increased affinities.
Our data show that mast cells can costimulate human CD4 (show CD4 ELISA Kits)(+) T cells to induce strong T-cell proliferation, but that therapies aiming at disrupting the interaction of CD28 and B7 molecules do not inhibit mast cell mediated T-cell activation.
High CD28 Circulating Levels are associated with Breast Cancer.
The CTLA4 (show CTLA4 ELISA Kits)-CD28 gene fusion is likely a major contributor to the pathogenesis of T-cell lymphomas and represents a potential target for anti-CTLA4 (show CTLA4 ELISA Kits) cancer immunotherapy.
Following phosphorylation of the tyrosine, the proteins growth factor receptor-bound protein 2 (Grb2 (show GRB2 ELISA Kits)), Grb2 (show GRB2 ELISA Kits)-related adaptor downstream of Shc (show SHC1 ELISA Kits) (Gads (show GRAP2 ELISA Kits)), and p85 subunit of phosphoinositide 3-kinase may bind to pYMNM (where pY is phosphotyrosine) via their Src (show SRC ELISA Kits) homology 2 (SH2) domains, leading to downstream signaling to distinct immune pathways. These three adaptor proteins bind to the same site on CD28 with variable affinity
CD28 family receptors are potential clinical indicators for the rapid monitoring of changes in T cell function during CHB treatment.
The eQTL mapping analysis revealed that the variations in CD28 and NFKB1 gene content might affect the abundance of transcripts of CD28 and Family with sequence similarity 177 member A1 (FAM177A1) genes, respectively. These results suggest that CD28 and NFKB1 gene variants may be associated with increased risks to IRM.
The protein encoded by this gene is essential for T-cell proliferation and survival, cytokine production, and T-helper type-2 development. Several alternatively spliced transcript variants encoding different isoforms have been found for this gene.
, T-cell-specific surface glycoprotein CD28
, CD28 antigen (Tp44)
, T-cell-specific surface glycoprotein CD28 homolog
, T-cell costimulatory molecule CD28
, cell surface protein
, costimulatory molecule B7 receptor CD28
, antigen CD28
, T-cell specific surface glycoprotein CD28
, CD28 precursor protein
, T-cell-specific surface glycoprotein CD28-like protein
, CD28 molecule L homeolog