Alexander G. Obukhov

Alexander G. Obukhov, Ph.D.
Alma materBogomoletz Institute of Physiology (PhD)
Known forCationic channels activated by extracellular ATP in rat sensory neurons

Direct activation of human TRPC6 and TRPC3 channels by diacylglycerol

Receptor-mediated Regulation of the Nonselective Cation Channels TRPC4 and TRPC5*

Cloning and Functional Expression of a Human Ca2+-Permeable Cation Channel Activated by Calcium Store Depletion

Expression of TRPC3 in Chinese Hamster Ovary Cells Results in Calcium-activated Cation Currents Not Related to Store Depletion
Scientific career
FieldsIon Channels, Neurophysiology, voltage-gated calcium channels, Atherosclerosis, Vascular disease, TRPC channels
Academic advisorsAlexander Krayevsky, Oleg Krishtal, Günter Schultz
Websitehttps://medicine.iu.edu/faculty/17979/obukhov-alexander

Alexander G. Obukhov is an American researcher, who specializes in ion channels, molecular physiology, and vascular biology.[1] Since 1986, Obukhov published research articles, with the most notable ones published in academic journals such as Nature,[2] Journal of Biological Chemistry,[3] EMBO Journal,[4] Journal of Cell Biology,[5] Proceedings of the National Academy of Sciences of the United States of America,[6] and Neuron.[7] Obukhov's research later evolved to feature multiple fields including neurophysiology, traumatic brain injury, pain, and atherosclerosis.

Education

Obukhov obtained a Degree of Chemist from Samara State University (Samara, USSR) in 1983. He then studied Electrophysiology at the Bogomoletz Institute of Physiology (Kyiv, Ukraine) and earned a Ph.D. Degree in 1988. Obukhov later pursued Fellowships in Electrophysiology and Molecular Biology at Bogomoletz Institute of Physiology and later at Institut für Pharmakologie, Freie Universität Berlin (Berlin, Germany).[8]

Career

Obukhov started his research career in 1983 in the laboratory of Dr. Alexander A. Krayevsky at the Institute of Molecular Biology of Academy of Sciences of Soviet Union (Moscow, USSR) where he was involved in the chemical synthesis of unnatural nucleoside triphosphates.[9] In 1985, he joined the laboratory of Dr. Oleg A. Krishtal at Bogomoletz Institute of Physiology where he learned the advanced electrophysiological patch clamp technique and started investigating the physiological effects of adenosine triphosphate (ATP) analogs synthesized by him on the activity of sensory nodose ganglion (a vagus nerve ganglion) neurons, which express P2X receptor-channels activated by ATP. While working in the Krishtal's laboratory, Obukhov characterized the single-channel properties of an individual neuronal ATP-gated (P2X) receptor channel protein in sensory neurons[10] and determined the pharmacological properties of the neuronal ATP-gated (P2X) receptor channel.[11] After earning his PhD degree in 1988, he continued his work at Bogomoletz Institute of Physiology until 1992. In 1992, he was awarded the Humboldt Research Fellowship[12] from the Alexander von Humboldt Foundation (Bonn, Germany) to conduct research at a German University, and this allowed him to join the laboratory of Dr. Günter Schultz at the Institut für Pharmakologie of Freien Universität Berlin (Berlin, Germany) where he studied the biophysical properties of just cloned Transient Receptor Potential (TRP) Channels. In the laboratory of Dr. Schultz, Obukhov continued mastering his skills as an electrophysiologist and also started learning Pharmacology and Molecular Biology. After completing the Humboldt Fellowship at the end of 1994, Obukhov continued his research of TRP channels in the laboratory of Dr. Schultz until 1999. While working in the Schultz laboratory, Obukhov with his colleagues provided first evidence that TRP proteins are ion channels by recording their single-channels activity.[4] During this period, Obukhov published four of his most cited academic publications.[2][5][7][13] In 1999, Dr. Obukhov moved to the USA where he initially worked at New Jersey Medical School of the University of Medicine and Dentistry of NJ (Newark, NJ) as an Instructor and then as a Research Assistant Professor.[14] In 2006, Obukhov moved to Indianapolis, Indiana, USA to work for the Indiana University School of Medicine - Indianapolis as an Assistant Professor and then as an Associate Professor.[15] The laboratory of Dr. Obukhov continues investigating the molecular physiology of TRP channels.[3] Additionally, Dr. Obukhov studies the mechanisms of metabolic syndrome-associated atherosclerosis progression.[16]

Teaching

Obukhov teaches Physiology and Electrophysiology-related topics at the Indiana University School of Medicine.[15]

Professional affiliations

Obukhov is a professional member of the American Heart Association.[15]

References

  1. ^ "Alexander G. Obukhov". scholar.google.com. Retrieved 2024-03-30.
  2. ^ a b Hofmann, Thomas; Obukhov, Alexander G.; Schaefer, Michael; Harteneck, Christian; Gudermann, Thomas; Schultz, Günter (January 14, 1999). "Direct activation of human TRPC6 and TRPC3 channels by diacylglycerol". Nature. 397 (6716): 259–263. Bibcode:1999Natur.397..259H. doi:10.1038/16711. PMID 9930701 – via www.nature.com.
  3. ^ a b "Molecular Determinants of the Sensitivity to Gq/11-Phospholipase C-dependent Gating, Gd3+ Potentiation, and Ca2+ Permeability in the Transient Receptor Potential Canonical Type 5 (TRPC5) Channel* - Journal of Biological Chemistry".
  4. ^ a b Obukhov, A. G.; Harteneck, C.; Zobel, A.; Harhammer, R.; Kalkbrenner, F.; Leopoldt, D.; Lückhoff, A.; Nürnberg, B.; Schultz, G. (November 14, 1996). "Direct activation of trpl cation channels by G alpha11 subunits". The EMBO Journal. 15 (21): 5833–5838. doi:10.1002/j.1460-2075.1996.tb00970.x. PMC 452331. PMID 8918461.
  5. ^ a b Zitt C, Obukhov AG, Strübing C, Zobel A, Kalkbrenner F, Lückhoff A, Schultz G. Expression of TRPC3 in Chinese hamster ovary cells results in calcium-activated cation currents not related to store depletion. J Cell Biol. 1997;138(6): 1333-1341.
  6. ^ Luo, Na; Conwell, Michael D.; Chen, Xingjuan; Kettenhofen, Christine Insinna; Westlake, Christopher J.; Cantor, Louis B.; Wells, Clark D.; Weinreb, Robert N.; Corson, Timothy W.; Spandau, Dan F.; Joos, Karen M.; Iomini, Carlo; Obukhov, Alexander G.; Sun, Yang (September 2, 2014). "Primary cilia signaling mediates intraocular pressure sensation". Proceedings of the National Academy of Sciences. 111 (35): 12871–12876. Bibcode:2014PNAS..11112871L. doi:10.1073/pnas.1323292111. PMC 4156748. PMID 25143588.
  7. ^ a b "Cloning and Functional Expression of a Human Ca2+-Permeable Cation Channel Activated by Calcium Store Depletion: Neuron".
  8. ^ "ORCID".
  9. ^ "Analogs of nucleoside triphosphates with modified sugar residues as substrates for RNA polymerase". scholar.google.com. Retrieved 2024-03-30.
  10. ^ Krishtal, O. A.; Marchenko, S. M.; Obukhov, A. G. (December 1988). "Cationic channels activated by extracellular atp in rat sensory neurons - ScienceDirect". Neuroscience. 27 (3): 995–1000. doi:10.1016/0306-4522(88)90203-5. PMID 2855265.
  11. ^ Krishtal, Oleg A.; Marchenko, Sergey M.; Obukhov, Alexander G.; Volkova, Tatyana M. (December 14, 1988). "Receptors for ATP in rat sensory neurones: the structure-function relationship for ligands". British Journal of Pharmacology. 95 (4): 1057–1062. doi:10.1111/j.1476-5381.1988.tb11739.x. PMC 1854272. PMID 3219481.
  12. ^ "Prof. Dr. Alexander G. Obukhov".
  13. ^ "Receptor-mediated Regulation of the Nonselective Cation Channels TRPC4 and TRPC5* - Journal of Biological Chemistry".
  14. ^ "ORCID". orcid.org. Retrieved 2024-03-30.
  15. ^ a b c "Alexander G. Obukhov, PhD".
  16. ^ Li, Wennan; Chen, Xingjuan; Riley, Ashley M.; Hiett, S. Christopher; Temm, Constance J.; Beli, Eleni; Long, Xin; Chakraborty, Saikat; Alloosh, Mouhamad; White, Fletcher A.; Grant, Maria B.; Sturek, Michael; Obukhov, Alexander G. (July 29, 2017). "Long-term spironolactone treatment reduces coronary TRPC expression, vasoconstriction, and atherosclerosis in metabolic syndrome pigs". Basic Research in Cardiology. 112 (5): 54. doi:10.1007/s00395-017-0643-0. PMC 5534204. PMID 28756533 – via Springer Link.