Member SpotlightsAn Interview with SAB Steering Committee Member G.D. Heda, Ph.D. G.D. Heda, Ph.D. A Science Advisory Board Member Since 2002 & Current SAB Steering Committee Member G.D. Heda, Ph.D, is currently an Assistant Professor of Biology at the Mississippi University for Women. Previously, Heda was a Research Biologist at the V.A. Medical Center, and was a joint faculty appointment with the department of medicine at the University of Tenneesee Health Sciences Center. Heda's research career spans over 25 years of working in academic, industrial, and government settings. After completing his Ph.D. in plant genetics from Osmania University, India, he pursued a Post-doctoral fellowship at Northwestern University Medical School. He joined the microbiology department of Southern Illinois University in 1984 to work on enzymology and protein biochemistry using thermophylic bacterial systems. In 1987, he moved to the Temple University School of Medicine, as a Research Assistant Professor working on the aspects of thrombosis. In 1992, Heda moved to Memphis, TN to head the Molecular Biology Group of the Skin Biology Department of Schering-Plough Health Care Products, Inc. This was his first experience working in an industrial setting, where he devised a molecular assay to screen keratolytic agents. In 1995, he joined the V.A. Medical Center, Memphis, and has since then worked on the aspects of cystic fibrosis (CF). In summary, Heda has worked with several human diseases such as cystic fibrosis, cancer, thrombosis and skin disorders. Research Interests My current areas of research and interests include the trafficking and function of two membrane proteins, viz., CFTR and NPC1. Both of these proteins are misfolded with cholesterol imbalance in their endocytic vesicles that alters the normal trafficking of these proteins to the plasma membrane. Proper protein folding and cholesterol trafficking are essential for the normal activity and function of proteins within a cell. Currently, I am working on CFTR. My role includes the writing of proposals for funding to execution of the project. What motivated you to pursue this research? What changed your interests from plant genetics to animal models? My Ph.D. degree is in genetics with a major in plant genetics. After submitted my thesis, I arrived in the United States in 1982. After 3 months of intense searching, I found my first post-doctoral position at Northwestern University Medical School at Chicago to work on characterizing α-amylase in pancreatic acinar cells obtained from rats. I visualized more prospects for mammalian biology in the US than in plant biology, and hence made this switch. Looking back, is your current career path what you expected it would be? When I look at the current unstable research funding situation, I wish I had switched to teaching with a part-time research option during the early part of my career. I rather chose full-time research. My advice to younger scientists would be to secure their career path by obtaining a hard-money position within first 2-3 years or as soon as possible after obtaining a Ph.D. degree. Further, they should take control of their career rather than expecting special favors from their mentors. What would you like to achieve with your research in the future? My career goal is to teach at the graduate and undergraduate levels and continue research in the area of cystic fibrosis and other misfolded proteins that play a role in genetic diseases. What are your other hobbies and interests? Social service, reading history books, nature walks, spending quality time with family members. What research strategies are you currently utilizing to target cystic fibrosis? I am using a 'discovery science approach' to achieve goals of my current research project. This is a non-hypothesis driven approach where new discoveries are made using modern approaches such as 'proteomics'. Goals of my ongoing research project are to identify differential protein expressions and protein modifications (e.g., phosphorylation, ubiquitination) in sorting endosomes of wild-type and mutated CFTR expressing cells. CFTR is a protein product of a gene that when mutated causes the genetic disease cystic fibrosis. Are you directly involved in the drug discovery process, and if so, what stage does your research contribute to? My current research is based on using fundamental biological concepts to identify proteins involved in causing the disease cystic fibrosis, and hence not directly involved in the drug discovery process. However, at my previous assignment with a pharmaceutical drug company (Schering-Plough) while working with its’ foot care division, I was involved with drug discovery of products for removal of hyperkeratotic skin. One of your primary areas of concern lies in the lack of funding, lack of interest, and hence, the decline of science education in the US. Do you believe this applies to CFTR as well? CFTR is a protein product of a gene that when defective causes the disease cystic fibrosis (CF). This is a highly competitive area. In the United States, the Cystic Fibrosis Foundation (CFF) is the only private foundation that provides initial funding and helps establish young and new investigators in this area, so that they can apply for larger grants to major funding agencies such as NIH. Unfortunately, the new direction for CFF is primarily to fund clinical research oriented grants. In the absence of such support, it is becoming more and more difficult for new investigators to get their foot in basic research in the CF area. National funding agencies such as NIH do not look favorably to those CF research proposals that do not have a track record of initial support from agencies such as CFF. This trend is very discouraging and more or less true with other areas of research. As a result it is very difficult to convince students to further their career in basic science research which is essential if we have to embark for a better tomorrow. I am afraid that this trend in the US may effect negatively to its' current superiority in basic science research in the world. More and more youngsters in the US, in my opinion, are deviating from choosing a research based career. You have experience working in academia, industry, and government research; where have you witnessed the greatest decline in funding for research? Each one of these sectors has their own strength and weaknesses. In terms of most declines in funding for research, I would say it is in government funded research. This decline is mainly due to ongoing conflicts on the foreign soil and political agenda of the government in Washington DC. The government funded research (e.g., NIH, NSF, VA etc.) has direct implicationd on academic research. As far as industrial research is concerned, it always depends on the economic situation at a given time. The scenario of basic research in today’s date is not gloomy with any of these sectors. Having said this, under normal political and peace situations funded research is more or less similar in all the sectors. What programs or strategies should be implemented to increase funding and job security in scientific careers in the US? Should we look to other countries for a good model of science education and subsequent career paths that are secure? Being from and educated in India, trained in the USA, and having visited different parts of the world, I can say that security of scientists is at the lowest in the United States. I can comment on one country’s policies over the other, in terms of support to scientific research. Productivity is a key to remain employed and funded in the USA and as a result the best science is produced. So this is a give and take situation. Security of Ph.D. scientists on the research track whose jobs depend on funded grants need to be addressed. I have witnessed many of my qualified friends, colleagues, even a former mentor on the research track retiring pre-maturely from science and choosing other professions (from personal business to non-science jobs) due to lack of financial support. Some sort of national policy is required to protect careers of scientists who are on the research track. For example 2-3 years of bridge funding from national agencies (e.g. NIH) may help protect this highly talented pool from becoming extinct. Another option that is not competitive enough and can be heavily debated, is to allow only individuals with a research degree (e.g., Ph.D., M.D.Ph.D., not M.D. alone) to compete for federal research dollars. Ph.D.'s on tenure track (mainly teaching) and M.D.s', who can always go back to the clinic, is not that much of a concern. This particular topic of 'job security of scientists' is shied from being discussed and needs attention. If you'd like to comment on this article, or join in discussion on other topics with SAB members, please visit our community forums. Web Resources G.D. Heda’s Professional Profile Publications Heda, GD and Roberts LK. Tissue type plasminogen activator is a potential mediator of salicylic acid induced sloughing of human corn tissue. J Am Podiatr Med Assoc (JAPMA), 98, 345-352, 2008. Norez C, Heda GD Jensen T. Ilana Kogan I, Hughes LK, Auzanneau C, Dérand R, Bulteau- Pignoux L, Li C, Ramjeesingh M, Li H, Sheppard DN, Bear CE, Riordan JR, Becq F. Determination of CFTR chloride channel activity and pharmacology using radiotracer flux methods. J Cystic Fibrosis, 3, 119-121, 2004. Roxo-Rosa M, Davezac N, Bensalem N, Majumdar M, Heda GD, Simas A, Penque D, Amaral MD, Lukacs GL, Edelman A. Proteomics techniques for cystic fibrosis research. J Cystic Fibrosis, 3, 85-89, 2004. Farinha, CM, Penque D, Roxo-Rosa M, Lukacs G, Dormer R, McPherson M, Pereira M, Bot AGM, Jorna H, Willemsen R, DeJonge H, Heda GD, et al. Biochemical methods to assess CFTR expression and membrane localization. J Cystic Fibrosis, 3, 73-77, 2004. Mendes, F, Farinha M, Roxo-Rosa M, Fanen P, Edelman A, Dormer R, McPherson M, Davidson H, Puchelle E, De Jonge H, Heda GD, et al. Antibodies for CFTR studies. J Cystic Fibrosis, 3, 69-72, 2004. Ann E, Farinha CM, Heda GD, Harris A, Amaral MD, Mouchel N. Non-PCR methods for the analysis of CFTR transcripts. J Cystic Fibrosis, 3, 25-28, 2004. Anabela S, Ramalho, AS, Beck S, Carlos M. Farinha CM, Clarke LA, Heda GD, Steiner B, Sanz J, Sabina G, Amaral MD, Harris A, Tzetis M. Methods for RNA extraction, cDNA preparation and analysis of CFTR transcripts. J Cystic Fibrosis, 3, 11-15, 2004. Yoshimura K, Anzai C, Iizuka S, Eto Y, Heda GD. Molecular biological study of action mechanism of macrolide antibiotics on CFTR. Jpn J Antibiot. 2003, 56 Suppl A: 117-20. Naren AP, Cobb B., Li C, Roy K, Nelson D, Heda GD, Lion J, Kirk KL, Sorscher EJ, Hanrahan J, Clancy JP, A macromolecular complex of 2 adrenergic receptor, CFTR, and ezrin/radixin/moesin-binding phosphoprotein 50 is regulated by PKA, Proc of Natl Acad Sci USA, 100(1), 342-346, 2003. Heda GD, Tanwani M, Marino CR: The ΔF508 mutation shortens the biochemical half-life of plasma Membrane CFTR in polarized epithelial cells. Am J Physiol Cell Physiol 280, C166- C174, 2001. Mahan, JT, Heda GD, Rao RH, Mansbach, II CM: The intestine expresses pancreatic triacylglycerol lipase: Regulation by dietary lipid. Am J Physiol Gastrointest Liver Physiol, 280, G1187-G1196, 2001. Heda GD and Marino CR: Surface expression of the cystic fibrosis transmembrane conductance regulator mutant, F508, is markedly upregulated by combination treatment with sodium butyrate and low temperature. Biochemi Biophysi Res Comm, 271, 659-664, 2000. ### << Previous Next >> [ View All Member Spotlights ] |
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