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the upregulation of others syncytial molecules, including LAG3 (show LAG3 ELISA Kits), CTLA4 (show CTLA4 ELISA Kits), CD28 and CD3 (show CD3 ELISA Kits), assisting the formation of syncytia with APC (show APC ELISA Kits) cells.
our data provide the first evidence of a strict link between the absence of CD28 and the expression of perforin (show PRF1 ELISA Kits), which is likewise enhanced by the expression of NKG2D (show KLRK1 ELISA Kits), within selected CD4 (show CD4 ELISA Kits)(+) T cells from cervical cancer patients.
Mutation of the basic clusters in the CD28 cytoplasmic domain reduced the recruitment to the CD28-Lck (show LCK ELISA Kits) complex of protein kinase (show CDK7 ELISA Kits) Ctheta; (PKCtheta (show PRKCQ ELISA Kits);), which serves as a key effector kinase in the CD28 signaling pathway.
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.
the scaffolding role of RLTPR predominates during CD28 co-stimulation and underpins the similar function of RLTPR in human and mouse T cells.
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.
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.
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
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