Stanford University Affiliated VA Palo Alto Health Care System.
Amar Bahadur Singh
Office of Research and Development,
3801 Miranda Ave, Bldg. 4, C-311,
Palo Alto, California 94304,
Hypercholesterolemia, Diabetes, Diabetic Cardiomyopathy, Molecular Biology, Transcription regulation, Post-transcriptional regulation of LDLR, New drug discovery R&D on Diabetes, Dyslipidemia and Cardiovascular diseases.
- Stanford Affiliated VA Palo Alto Health Care System, Palo Alto, California, (Research advisor: Dr. Jingwen Liu).
My current focus research:
- Characterization of cellular genes that are regulated by diets, natural lipid lowering compounds, and cytokines in liver tissues, primary hepatocytes, and liver cell lines.
- Promoter analysis to identify critical cis-acting elements and trans-acting factors that play important roles in PPAR gene expression and regulation in liver cells.
- Regulation of LDLR mRNA levels and PPARs in hepatic lipid metabolism.
2012-2014 Postdoctoral Research:
- Division of Endocrinology, Gerontology & Metabolism, Stanford University, (Research advisor: Prof. Fredric B. Kraemer).
- Project was focus on regulation of LDLR mRNA by Berberine. we have generated a Luc-UTR in vivo model to study the regulation of LDLR mRNA stability in liver tissue of living mice, and by using this model we established inverse relationship between hnRNPD abundance and LDLR mRNA levels after BBR treatment of Alb-Luc-UTR mice Amar Bahadur Singh, Ph.D. suggests a critical function of hnRNPD in mediating hepatic LDLR mRNA degradation.
- We have also identified a novel posttranscriptional regulatory mechanism by which dietary cholesterol inhibits liver LDLR expression via inducing hnRNPD to accelerate LDLR mRNA degradation.
2009-2011 Postdoctoral Research:
- Molecular Cardiology, Cardiovascular Research Institute, Texas A&M Health Science Center, (Research advisor: Prof. Kenneth M. Baker).
- Project was focus on molecular mechanisms of RA-mediated signaling in hyperglycemia-induced cardiac remodeling, Using neonatal rat cardiomyocytes, we have demonstrated that hyperglycemia (HG)-induced oxidative stress and activation of the JNK pathway negatively regulated expression/activation of RAR and RXR.
- The impaired RAR/RXR signaling and oxidative stress/JNK pathway forms a vicious circle, which significantly contributes to hyperglycemia induced cardiomyocyte apoptosis.
2004-2009 Doctoral Research:
- Biochemistry Division, Central Drug Research Institute, Lucknow, (Research advisor: Dr. Arvind K Srivastava).
- My doctoral research was to focus on identification of new anti-diabetic and anti-dyslipidemic lead molecules from different source of compounds & exploration of their mechanism of action (s).
- I was also working on nuclear receptors that are mainly involved in regulation of glucose, cholesterol and lipid metabolism like PPAR, RAR, RXR, LXR and FXR.
- Simultaneously, I was also screened the new agonists /antagonist ligand molecules from different series of compounds synthesized by medicinal chemistry division of our Institute and are exploring the relevance of these ligands for therapeutics in pathophysiological conditions such as diabetes, dyslipidemia and atherosclerosis.
- 2010-Present - American Heart Association