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629 results on '"Prabhakar, Bellur S"'

153. Transfusion of Nonobese Diabetic Mice with Allogeneic Newborn Blood Ameliorates Autoimmune Diabetes and Modifies the Expression of Selected Immune Response Genes

Author

Jayaraman, Sundararajan, primary, Patel, Tejas, additional, Patel, Vasu, additional, Ajani, Shahnaz, additional, Garza, Rebecca, additional, Jayaraman, Arathi, additional, Kwon, Sung, additional, Singh, Rajvir, additional, Rondelli, Damiano, additional, Prabhakar, Bellur S., additional, and Holterman, Mark, additional

Published
2010
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158. Structure-Based Design, Synthesis, and Biological Evaluation of a Series of Novel and Reversible Inhibitors for the Severe Acute Respiratory Syndrome−Coronavirus Papain-Like Protease

Author

Ghosh, Arun K., primary, Takayama, Jun, additional, Aubin, Yoann, additional, Ratia, Kiira, additional, Chaudhuri, Rima, additional, Baez, Yahira, additional, Sleeman, Katrina, additional, Coughlin, Melissa, additional, Nichols, Daniel B., additional, Mulhearn, Debbie C., additional, Prabhakar, Bellur S., additional, Baker, Susan C., additional, Johnson, Michael E., additional, and Mesecar, Andrew D., additional

Published
2009
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184. IG20/MADD Plays a Critical Role in Glucose-Induced Insulin Secretion.

Author

Liang-cheng Li, Yong Wang, Carr, Ryan, Haddad, Christine Samir, Ze Li, Lixia Qian, Oberholzer, Jose, Maker, Ajay V., Qian Wang, and Prabhakar, Bellur S.

Subjects
ANTISENSE DNA, PANCREATIC beta cells, HYPERGLYCEMIA, GLUCOSE, INSULIN research, TYPE 2 diabetes, SINGLE nucleotide polymorphisms
Abstract

Pancreatic β-cell dysfunction is a common feature of type 2 diabetes. Earlier, we had cloned IG20 cDNA from a human insulinoma and had shown that IG20/MADD can encode six different splice isoforms that are differentially expressed and have unique functions, but its role in β-cell function was unexplored. To investigate the role of IG20/MADD in β-cell function, we generated conditional knockout (KMA1ko) mice. Deletion of IG20/MADD in β-cells resulted in hyperglycemia and glucose intolerance associated with reduced and delayed glucose-induced insulin production. KMA1ko β-cells were able to process insulin normally but had increased insulin accumulation and showed a severe defect in glucose-induced insulin release. These findings indicated that IG20/MADD plays a critical role in glucose-induced insulin release from β-cells and that its functional disruption can cause type 2 diabetes. The clinical relevance of these findings is highlighted by recent reports of very strong association of the rs7944584 single nucleotide polymorphism (SNP) of IG20/MADD with fasting hyperglycemia/diabetes. Thus, IG20/MADD could be a therapeutic target for type 2 diabetes, particularly in those with the rs7944584 SNP. [ABSTRACT FROM AUTHOR]

Published
2014
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200. MADD Knock-Down Enhances Doxorubicin and TRAIL Induced Apoptosis in Breast Cancer Cells.

Author

Turner, Andrea, Li, Liang-Cheng, Pilli, Tania, Qian, Lixia, Wiley, Elizabeth Louise, Setty, Suman, Christov, Konstantin, Ganesh, Lakshmy, Maker, Ajay V., Li, Peifeng, Kanteti, Prasad, Das Gupta, Tapas K., and Prabhakar, Bellur S.

Subjects
DOXORUBICIN, APOPTOSIS, MITOGEN-activated protein kinases, BREAST cancer, CANCER cells, GENE expression, CELL lines, CYTOLOGY
Abstract

The Map kinase Activating Death Domain containing protein (MADD) isoform of the IG20 gene is over-expressed in different types of cancer tissues and cell lines and it functions as a negative regulator of apoptosis. Therefore, we speculated that MADD might be over-expressed in human breast cancer tissues and that MADD knock-down might synergize with chemotherapeutic or TRAIL-induced apoptosis of breast cancer cells. Analyses of breast tissue microarrays revealed over-expression of MADD in ductal and invasive carcinomas relative to benign tissues. MADD knockdown resulted in enhanced spontaneous apoptosis in human breast cancer cell lines. Moreover, MADD knockdown followed by treatment with TRAIL or doxorubicin resulted in increased cell death compared to either treatment alone. Enhanced cell death was found to be secondary to increased caspase-8 activation. These data indicate that strategies to decrease MADD expression or function in breast cancer may be utilized to increase tumor cell sensitivity to TRAIL and doxorubicin induced apoptosis. [ABSTRACT FROM AUTHOR]

Published
2013
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