Share This Author
CD5-Mediated Negative Regulation of Antigen Receptor-Induced Growth Signals in B-1 B Cells
- G. Bikah, J. Carey, J. Ciallella, A. Tarakhovsky, S. Bondada
- Biology, MedicineScience
- 13 December 1996
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.
Negative regulation of antigen receptor‐mediated signaling by constitutive asociation of CD5 with the SHP‐1 protein tyrosine phosphatase in B‐1 B cells
- G. Sen, G. Bikah, C. Venkataraman, S. Bondada
- Biology, MedicineEuropean journal of immunology
- 1 October 1999
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.
Molecular basis of age‐associated cytokine dysregulation in LPS‐stimulated macrophages
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.
The unresponsiveness of aged mice to polysaccharide antigens is a result of a defect in macrophage function
- R. Chelvarajan, Sarah M. Collins, J. Van Willigen, S. Bondada
- Biology, MedicineJournal of leukocyte biology
- 1 April 2005
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.
Defective macrophage function in neonates and its impact on unresponsiveness of neonates to polysaccharide antigens
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.
Milk-derived exosomes for oral delivery of paclitaxel.
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.
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.
c-Jun N-terminal kinase (JNK) is required for survival and proliferation of B-lymphoma cells.
- M. Gururajan, Roger G. Chui, A. K. Karuppannan, J. Ke, C. D. Jennings, S. Bondada
- 15 August 2005
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.
Redox proteomic identification of HNE-bound mitochondrial proteins in cardiac tissues reveals a systemic effect on energy metabolism after doxorubicin treatment.
Identification of a Gal/GalNAc Lectin in the Protozoan Hartmannella vermiformis as a Potential Receptor for Attachment and Invasion by the Legionnaires' Disease Bacterium
- C. Venkataraman, B. J. Haack, S. Bondada, Y. Kwaik
- BiologyThe Journal of experimental medicine
- 18 August 1997
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.