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CD5-Mediated Negative Regulation of Antigen Receptor-Induced Growth Signals in B-1 B Cells
TLDR
In CD5-deficient mice, B-1 cells responded to mIgM crosslinking by developing a resistance to apoptosis and entering the cell cycle, indicating the B cell receptor-mediated signaling is negatively regulated by CD5 in normal B- 1 cells.
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Negative regulation of antigen receptor‐mediated signaling by constitutive asociation of CD5 with the SHP‐1 protein tyrosine phosphatase in B‐1 B cells
TLDR
Prior cross‐linking of CD5 restores a normal calcium mobilization response as well as NF‐κB activation in B‐1 cells, which support a model whereby CD5 negatively regulates antigen receptor‐mediated growth signals by recruiting SHP‐1 into the BCR complex in B-1 cells.
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Molecular basis of age‐associated cytokine dysregulation in LPS‐stimulated macrophages
TLDR
Low doses of a p38 MAPK inhibitor enhanced proinflammatory cytokine production by MΦ and reduced IL‐10 levels, indicating that increased p38MAPK activity has a role in cytokine dysregulation in the aged mouse M Φ.
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The unresponsiveness of aged mice to polysaccharide antigens is a result of a defect in macrophage function
TLDR
It is shown that aged mice are profoundly hyporesponsive to these TI Ag vaccines, and the inability of aged MΦ to help the B cell response appears to be caused by an excess of IL‐10.
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Defective macrophage function in neonates and its impact on unresponsiveness of neonates to polysaccharide antigens
TLDR
Neonates do not respond to thymus‐independent (TI) antigens (Ag) as a result of the inability of neonatal MΦ to secrete cytokines, such as IL‐1β and IL‐6, probably as a consequence of an excess production of IL‐10.
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Milk-derived exosomes for oral delivery of paclitaxel.
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Curcumin causes the growth arrest and apoptosis of B cell lymphoma by downregulation of egr-1, c-myc, bcl-XL, NF-kappa B, and p53.
TLDR
Evidence is presented to show that curcumin inhibited proliferation of a variety of B lymphoma cells and caused the growth arrest and apoptosis of BKS-2 immature B cell lymphoma by downregulation of growth and survival promoting genes.
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c-Jun N-terminal kinase (JNK) is required for survival and proliferation of B-lymphoma cells.
TLDR
Several primary murine and human B lymphomas and cell lines were found to constitutively express high levels of the activated form of c-jun N-terminal kinase (JNK), a member of the mitogen-activated protein (MAP) kinase family, which appears to have a unique prosurvival role in the B-lymphoma model.
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Redox proteomic identification of HNE-bound mitochondrial proteins in cardiac tissues reveals a systemic effect on energy metabolism after doxorubicin treatment.
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Identification of a Gal/GalNAc Lectin in the Protozoan Hartmannella vermiformis as a Potential Receptor for Attachment and Invasion by the Legionnaires' Disease Bacterium
TLDR
It is concluded that attachment of L. pneumophila to the H. vermiformis 170-kD lectin is required for invasion and is associated with tyrosine dephosphorylation of the Gal lectin and other host proteins, the first demonstration of a potential receptor used by L. pneumoniae to invade protozoa.
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