2018 International Conference on Applied Biochemistry and Biotechnology (ABB 2018)
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Bhumi Nath Tripathi, Professor & Head, Department of Biotechnology; Dean, Faculty of Earth Sciences, Indira Gandhi National Tribal University, Amarkantak, 484887, Madhya Pradesh, India
Bhumi Nath Tripathi, PhD from Banaras Hindu University, India, works as Professor and Head, Department of Biotechnology and as Dean, Faculty of Earth Sciences at Indira Gandhi National Tribal University (A Central University), Amarkantak, India. The research works of Professor Tripathi is focused on Redox Homeostasis in Plants during Stress Conditions and also Molecular Biology of Abiotic Stress Responses in Plants. He has also worked at Bielefeld University, Germany, Okayama University, Japan, University of Leeds, UK and Korea Atomic Energy Research Institute, South Korea. Professor Tripathi has published more than 50 good quality research papers in journals of International repute and also written four books on Stress Metabolism, Biotechnology, Molecular Biology and Algal Biotechnology. He is recipient several awards and academic fellowships and several research grants. |
Speech Title: Characterization of the structural/functional switching of the redox protein and its significance in improving stress tolerance Abstract: Alkyl hydroperoxide reductase subunit C (AhpC) is a member of the 2-Cys peroxiredoxin family. The present work demonstrated the peroxidase and molecular chaperone functions of AhpC of Pseudomonas using a site-directed mutagenesis approach by substitution of Ser and Thr residues located between two catalytic cysteines. Substitution of Ser with Cys enhanced the chaperone activity of the mutant by approximately 9-fold compared to wild-type protein (WT-PaAhpC). The increased chaperone activity was linked with increase in the high-molecular-weight (HMW) fraction of mutant protein. In silico modeling showed that mutation of Ser to Cys between two catalytic cysteines resulted in a more compact decameric structure than wild type and decreased the atomic distance between the two neighboring sulfur atoms of Cys in the dimer-dimer interface of mutant AhpC, was perhaps responsible for the enhanced hydrophobic interaction at the dimer-dimer interface. Moreover, complementation assays showed that mutant AhpC significantly improved heat tolerance under thermal stress. This work has modulated the mechanism of structural and functional switching of AhpC of Pseudomonas. |
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Richard H. Finnell, Professor, Departments of Molecular and Cellular Biology and Medicine, Baylor College of Medicine, Houston, Texas, USA.
Dr. Richard H. Finnell is a Professor in the Center for Precision Environmental Health in the Department of Molecular and Cell Biology and in the Department of Medicine at Baylor College of Medicine. He is also a Changjiang Scholar Professor at Fudan University, an Adjunct Professor in the Shanghai Institute of Medical Genetics of Jiaotong University, and in the Institute for Reproductive and Child Health at Peking University. A pediatric geneticist, he has been involved in investigating genetic susceptibility to environmentally induced birth defects, applying stem cell technology to the detection of potential teratogenic compounds in efforts to prevent these birth defects, developing mouse models to understand the pathogenesis of the defects, and using highly innovative approaches to treating these disabilities. Professor Finnell has authored over 350 publications in journals such as Science, Nature Genetics, Nature Cell Biology, PNAS and Developmental Cell. |
Speech Title: Embryonic Consequences of Abnormal Folate Transport During Development Abstract: The presentation will cover two disorders linked to the human folate receptor alpha protein. The first portion of the presentation will focus on the role of preconceptional folic acid supplementation in reducing the occurrence of complex congenital defects in humans. Specifically, we will focus on the role of folic acid in the prevention of neural tube defects. To better understand the mechanisms underlying theses beneficial effects, we developed a variety of genetically modified mice whose folate transport systems have been ablated. Administration of exogenous one-carbon sources partially rescues the nullizygous embryos; although they present with a low prevalence of malformations involving the neural tube, craniofacies, heart, eyes and abdominal wall. Inadequate maternal folate causes notable changes in the Folr1 mutant embryos at the molecular and cellular levels, clearly indicating the importance of folate homeostasis during early mammalian development. The second part of the talk will focus on the cerebral folate deficiency (CFD) syndrome, which is characterized by very low concentration of 5-methyltetrahydrofolate (5-MTHF) in cerebrospinal fluid, while folate levels in plasma and red blood cells are normal. CFD patients present with symptoms including: developmental delay, ataxia, dyskinesias, spasticity, speech difficulties and epilepsy. Previously, mutations in several folate pathway genes, including hFRa (folate receptor alpha), DHFR (dihydrofolate reductase), PCFT (proton coupled folate transporter) and MTHFS (methenyltetrahydrofolate synthetase) have been identified in CFD patients. In an effort to identify causal mutations for CFD, we performed whole exome sequencing analysis of DNA samples collected from CFD patients, developed mouse models to test hypotheses which was published in the April 2017 issue of Nature Genetics. |
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