AVIV I. HASSID, Ph.D., B.S.

Professor Emeritus
Physiology

Office: C315 VAN VLEET CANCER CENTER
3 NORTH DUNLAP STREET
MEMPHIS TN 381632113
Tel: (901) 448-8304
ahassid@uthsc.edu

Education

  • Brandeis University, Waltham, MA, Biochemistry
  • University of North Carolina, Chapel Hill, NC, Biochemistry
  • Robert College, Istanbul, Turkey, Physical Chemistry
  • Ph.D., University of Minnesota, Dept. of Chemistry, Chemistry
  • B.S., Robert College, Istanbul, Turkey, Chemistry
  • B.S., Robert College, Istanbul, Turkey, Chemistry

Research interest/specialty

Project 1: Nitric Oxide-PTP Interactions In Aortic Smooth Muscle

Project 2: NO-induced vascular smooth muscle cell motility

Research keywords

Vascular smooth muscle, cell growth and proliferation, atherosclerosis, vascular hypertrophy
and hyperplasia, insulin, cyclic nucleotides, eicosanoids, nitric oxide, atrial natriuretic factor,
reactive oxygen species, signal transduction, cell motility, cytoskeleton.

Research interest/specialty

Project 1: Nitric Oxide-PTP Interactions In Aortic Smooth Muscle Project 2: NO-induced vascular smooth muscle cell motility

Research keywords

Vascular smooth muscle, cell growth and proliferation, atherosclerosis, vascular hypertrophy and hyperplasia, insulin, cyclic nucleotides, eicosanoids, nitric oxide, atrial natriuretic factor, reactive oxygen species, signal transduction, cell motility, cytoskeleton.

Research description

Project 1: Nitric Oxide-PTP Interactions In Aortic Smooth Muscle This is a proposal to investigate the role of protein tyrosine phosphatase PTPIB as mediator of the inhibitory effects of nitric oxide (NO) in vascular smooth muscle and in vascular remodeling. NO plays a major inhibitory role in neointima formation after vascular injury. Mechanisms explaining this effect in cultured cells and especially in vivo are lacking. We have found that NO increases the activity of PTPIB in cultured rat aortic smooth muscle cells, without increasing its protein levels. Moreover, we have found that PDGF and FGF increase PTP1B protein levels in cultured cells and that vascular injury similarly induces increased PTP1B protein levels in injured rat carotid artery. We have also shown that NO targets the IGF1 receptor, inducing receptor tyrosine dephosphorylation and interrupting IGFl-induced signal transduction in cultured cells. Finally, we have shown that NO decreases cytoplasmic Ca and attenuates IGFl-induced hydrogen peroxide generation and that this effect is mimicked by independent lowering of intracellular Ca by a Ca chelator. These results support a possible involvement of reduced Ca in activating PTP1B. The role of IGF1 in vascular injury is currently unclear. On the one hand, vascular injury induces upregulation of IGF1 levels but on the other, IGF1 receptor mRNA levels and IGF1 receptor binding are decreased. Consistent with these findings, we have found that vascular injury decreases IGF1 receptor protein levels by about 30%, as determined by Western blot analysis; moreover, we have found that receptor activation, as measured by specific receptor tyrosine phosphorylation, is decreased by more than 80%. These novel and exciting findings describe for the first time a mechanistic link between NO and tyrosine kinase receptor dephosphorylation involving a protein tyrosine phosphatase. Taken together, our results raise the possibility of negative cross-talk between, on the one hand PDGF or FGF, and on the other IGF1 signal transduction, via the intermediacy of elevated PTP1B. Based on the above, we propose the following specific aims, to be performed in cultured rat aortic smooth muscle cells or in rats or mice: Determine whether reduction of cytoplasmic Ca is necessary and/or sufficient to induce upregulation of PTP1B activity. Determine whether upregulation of PTP1B is necessary and/or sufficient to account for NO-induced inhibition of cell proliferation and induction of apoptosis in cultured cells. Determine whether PDGF, FGF or NO induce upregulation of PTP1B protein or activity levels in vascular injury. Determine whether PTPIB plays a role in NO-induced decrease of cell proliferation, motility, apoptosis and neointima formation in models of rat or mouse vascular injury. Determine whether PTP1B plays a role in attenuating IGF receptor activation in vivo. Project 2: NO-induced vascular smooth muscle cell motility Nitric oxide (NO) is generally considered to play a protective role in blood vessels. However, others and we have obtained evidence that this may not always be the case but the mechanisms underlying diverse responses to NO are not known. The purpose of this proposal is to test an exciting new hypothesis on the capacity of chronically elevated insulin levels to switch the role of nitric oxide from protective to deleterious substance in blood vessels. We have found that the inhibitory effects of NO on both motility and proliferation are abrogated in vascular smooth muscle cells chronically treated with insulin. These findings support a new hypothesis on the role of insulin as a switcher of vascular smooth muscle cell phenotypic responses to NO. Our preliminary results indicate that the motility-stimulatory effect of NO, uncovered by chronic insulin treatment of cultured rat aortic smooth muscle cells, is associated with increased PI 3 kinase activity and requires the functional availability of angiotensin II, of the

Publications

  1. Xi, Q, Adebiyi, A, Zhao, G, Chapman, KE, Waters, CM, Hassid, A, Jaggar, JH. IP3 Constricts Cerebral Arteries via IP3 Receptor-Mediated TRPC3 Channel Activation and Independently of Sarcoplasmic Reticulum Ca2+ Release. Circ Res, 2008.
  2. Desai, LP, Sinclair, SE, Chapman, KE, Hassid, A, Waters, CM. High tidal volume mechanical ventilation with hyperoxia alters alveolar type II cell adhesion. Am J Physiol Lung Cell Mol Physiol, 293 (3), L769-78, 2007.
  3. Liu, X, Sun, SQ, Hassid, A, Ostrom, RS. cAMP inhibits transforming growth factor-beta-stimulated collagen synthesis via inhibition of extracellular signal-regulated kinase 1/2 and Smad signaling in cardiac fibroblasts. Mol Pharmacol, 70 (6), 1992-2003, 2006.
  4. Rafiq, K, Kolpakov, MA, Abdelfettah, M, Streblow, DN, Hassid, A, Dell'Italia, LJ, Sabri, A. Role of protein-tyrosine phosphatase SHP2 in focal adhesion kinase down-regulation during neutrophil cathepsin G-induced cardiomyocytes anoikis. J Biol Chem, 281 (28), 19781-92, 2006.
  5. Ceacareanu, AC, Ceacareanu, B, Zhuang, D, Chang, Y, Ray, RM, Desai, L, Chapman, KE, Waters, CM, Hassid, A. Nitric oxide attenuates IGF-I-induced aortic smooth muscle cell motility by decreasing Rac1 activity: essential role of PTP-PEST and p130cas. Am J Physiol Cell Physiol, 290 (4), C1263-70, 2006.
  6. Chang, Y, Ceacareanu, B, Zhuang, D, Zhang, C, Pu, Q, Ceacareanu, AC, Hassid, A. Counter-regulatory function of protein tyrosine phosphatase 1B in platelet-derived growth factor- or fibroblast growth factor-induced motility and proliferation of cultured smooth muscle cells and in neointima formation. Arterioscler Thromb Vasc Biol, 26 (3), 501-7, 2006.
  7. Dixit, M, Loot, AE, Mohamed, A, Fisslthaler, B, Boulanger, CM, Ceacareanu, B, Hassid, A, Busse, R, Fleming, I. Gab1, SHP2, and protein kinase A are crucial for the activation of the endothelial NO synthase by fluid shear stress. Circ Res, 97 (12), 1236-44, 2005.
  8. Chapman, KE, Sinclair, SE, Zhuang, D, Hassid, A, Desai, LP, Waters, CM. Cyclic mechanical strain increases reactive oxygen species production in pulmonary epithelial cells. Am J Physiol Lung Cell Mol Physiol, 289 (5), L834-41, 2005.
  9. Gidron, Y, Hassid, A, Yisrael, H, Biderman, A. Do psychological factors predict occurrence of influenza-like symptoms in vaccinated elderly residents of a sheltered home. Br J Health Psychol, 10 (Pt 3), 411-20, 2005.
  10. Zhuang, D, Ceacareanu, AC, Ceacareanu, B, Hassid, A. Essential role of protein kinase G and decreased cytoplasmic Ca2+ levels in NO-induced inhibition of rat aortic smooth muscle cell motility. Am J Physiol Heart Circ Physiol, 288 (4), H1859-66, 2005.
  11. Desai, LP, Aryal, AM, Ceacareanu, B, Hassid, A, Waters, CM. RhoA and Rac1 are both required for efficient wound closure of airway epithelial cells. Am J Physiol Lung Cell Mol Physiol, 287 (6), L1134-44, 2004.
  12. Tomar, A, Wang, Y, Kumar, N, George, S, Ceacareanu, B, Hassid, A, Chapman, KE, Aryal, AM, Waters, CM, Khurana, S. Regulation of cell motility by tyrosine phosphorylated villin. Mol Biol Cell, 15 (11), 4807-17, 2004.
  13. Chang, Y, Zhuang, D, Zhang, C, Hassid, A. Increase of PTP levels in vascular injury and in cultured aortic smooth muscle cells treated with specific growth factors. Am J Physiol Heart Circ Physiol, 287 (5), H2201-8, 2004.
  14. Zhuang, D, Ceacareanu, AC, Lin, Y, Ceacareanu, B, Dixit, M, Chapman, KE, Waters, CM, Rao, GN, Hassid, A. Nitric oxide attenuates insulin- or IGF-I-stimulated aortic smooth muscle cell motility by decreasing H2O2 levels: essential role of cGMP. Am J Physiol Heart Circ Physiol, 286 (6), H2103-12, 2004.
  15. Dixit, M, Zhuang, D, Ceacareanu, B, Hassid, A. Treatment with insulin uncovers the motogenic capacity of nitric oxide in aortic smooth muscle cells: dependence on Gab1 and Gab1-SHP2 association. Circ Res, 93 (10), e113-23, 2003.
  16. Lin, Y, Ceacareanu, AC, Hassid, A. Nitric oxide-induced inhibition of aortic smooth muscle cell motility: role of PTP-PEST and adaptor proteins p130cas and Crk. Am J Physiol Heart Circ Physiol, 285 (2), H710-21, 2003.
  17. Yigzaw, Y, Poppleton, HM, Sreejayan, N, Hassid, A, Patel, TB. Protein-tyrosine phosphatase-1B (PTP1B) mediates the anti-migratory actions of Sprouty. J Biol Chem, 278 (1), 284-8, 2003.
  18. Bhanoori, M, Yellaturu, CR, Ghosh, SK, Hassid, A, Jennings, LK, Rao, GN. Thiol alkylation inhibits the mitogenic effects of platelet-derived growth factor and renders it proapoptotic via activation of STATs and p53 and induction of expression of caspase1 and p21(waf1/cip1). Oncogene, 22 (1), 117-30, 2003.
  19. Yellaturu, CR, Ghosh, SK, Rao, RK, Jennings, LK, Hassid, A, Rao, GN. A potential role for nuclear factor of activated T-cells in receptor tyrosine kinase and G-protein-coupled receptor agonist-induced cell proliferation. Biochem J, 368 (Pt 1), 183-90, 2002.
  20. Chang, Y, Ceacareanu, B, Dixit, M, Sreejayan, N, Hassid, A. Nitric oxide-induced motility in aortic smooth muscle cells: role of protein tyrosine phosphatase SHP-2 and GTP-binding protein Rho. Circ Res, 91 (5), 390-7, 2002.
  21. Sreejayan, N, Lin, Y, Hassid, A. NO attenuates insulin signaling and motility in aortic smooth muscle cells via protein tyrosine phosphatase 1B-mediated mechanism. Arterioscler Thromb Vasc Biol, 22 (7), 1086-92, 2002.
  22. Brown, C, Lin, Y, Hassid, A. Requirement of protein tyrosine phosphatase SHP2 for NO-stimulated vascular smooth muscle cell motility. Am J Physiol Heart Circ Physiol, 281 (4), H1598-605, 2001.
  23. Hassid, A, Yao, J, Huang, S. NO alters cell shape and motility in aortic smooth muscle cells via protein tyrosine phosphatase 1B activation. Am J Physiol, 277 (3 Pt 2), H1014-26, 1999.
  24. Hassid, A, Huang, S, Yao, J. Role of PTP-1B in aortic smooth muscle cell motility and tyrosine phosphorylation of focal adhesion proteins. Am J Physiol, 277 (1 Pt 2), H192-8, 1999.
  25. Brown, C, Pan, X, Hassid, A. Nitric oxide and C-type atrial natriuretic peptide stimulate primary aortic smooth muscle cell migration via a cGMP-dependent mechanism: relationship to microfilament dissociation and altered cell morphology. Circ Res, 84 (6), 655-67, 1999.
  26. Kaur, K, Yao, J, Pan, X, Matthews, C, Hassid, A. NO decreases phosphorylation of focal adhesion proteins via reduction of Ca in rat aortic smooth muscle cells. Am J Physiol, 274 (5 Pt 2), H1613-9, 1998.
  27. Dhaunsi, GS, Matthews, C, Kaur, K, Hassid, A. NO increases protein tyrosine phosphatase activity in smooth muscle cells: relationship to antimitogenesis. Am J Physiol, 272 (3 Pt 2), H1342-9, 1997.
  28. Dhaunsi, GS, Hassid, A. Atrial and C-type natriuretic peptides amplify growth factor activity in primary aortic smooth muscle cells. Cardiovasc Res, 31 (1), 37-47, 1996.
  29. Bourcier, T, Dockter, M, Hassid, A. Synergistic interaction of interleukin-1 beta and growth factors in primary cultures of rat aortic smooth muscle cells. J Cell Physiol, 164 (3), 644-57, 1995.
  30. Hassid, A, Arabshahi, H, Bourcier, T, Dhaunsi, GS, Matthews, C. Nitric oxide selectively amplifies FGF-2-induced mitogenesis in primary rat aortic smooth muscle cells. Am J Physiol, 267 (3 Pt 2), H1040-8, 1994.
  31. Cahill, PA, Hassid, A. ANF-C-receptor-mediated inhibition of aortic smooth muscle cell proliferation and thymidine kinase activity. Am J Physiol, 266 (1 Pt 2), R194-203, 1994.
  32. Garg, UC, Hassid, A. Mechanisms of nitrosothiol-induced antimitogenesis in aortic smooth muscle cells. Eur J Pharmacol, 237 (2-3), 243-9, 1993.
  33. Cahill, PA, Hassid, A. Differential antimitogenic effectiveness of atrial natriuretic peptides in primary versus subcultured rat aortic smooth muscle cells: relationship to expression of ANF-C receptors. J Cell Physiol, 154 (1), 28-38, 1993.
  34. Cahill, PA, Hassid, A. Clearance receptor-binding atrial natriuretic peptides inhibit mitogenesis and proliferation of rat aortic smooth muscle cells. Biochem Biophys Res Commun, 179 (3), 1606-13, 1991.
  35. Lermioglu, F, Goyal, J, Hassid, A. Cell density modulates the decrease of cytosolic free Ca2+ induced by atrial natriuretic hormone, S-nitroso-N-acetylpenicillamine and 8-bromo cyclic GMP in cultured rat mesangial cells. Biochem J, 274 ( Pt 2), 323-8, 1991.
  36. Garg, UC, Hassid, A. Nitric oxide decreases cytosolic free calcium in Balb/c 3T3 fibroblasts by a cyclic GMP-independent mechanism. J Biol Chem, 266 (1), 9-12, 1991.
  37. Garg, UC, Hassid, A. Nitric oxide-generating vasodilators inhibit mitogenesis and proliferation of BALB/C 3T3 fibroblasts by a cyclic GMP-independent mechanism. Biochem Biophys Res Commun, 171 (1), 474-9, 1990.
  38. Songu-Mize, E, Bealer, SL, Hassid, AI. Centrally administered ANF promotes appearance of a circulating sodium pump inhibitor. Am J Physiol, 258 (6 Pt 2), H1655-9, 1990.
  39. Yu, YM, Lermioglu, F, Hassid, A. Modulation of Ca by agents affecting voltage-sensitive Ca channels in mesangial cells. Am J Physiol, 257 (6 Pt 2), F1094-9, 1989.
  40. Garg, UC, Hassid, A. Inhibition of rat mesangial cell mitogenesis by nitric oxide-generating vasodilators. Am J Physiol, 257 (1 Pt 2), F60-6, 1989.
  41. Garg, UC, Hassid, A. Nitric oxide-generating vasodilators and 8-bromo-cyclic guanosine monophosphate inhibit mitogenesis and proliferation of cultured rat vascular smooth muscle cells. J Clin Invest, 83 (5), 1774-7, 1989.
  42. Schlondorff, D, Singhal, P, Hassid, A, Satriano, JA, DeCandido, S. Relationship of GTP-binding proteins, phospholipase C, and PGE2 synthesis in rat glomerular mesangial cells. Am J Physiol, 256 (1 Pt 2), F171-8, 1989.
  43. Hassid, A, Yu, YM. Mechanism of atriopeptin-induced decrease of cytosolic free Ca in rat vascular smooth muscle cells: evidence for an intracellular locus of action. J Cardiovasc Pharmacol, 14 Suppl 6, S34-8, 1989.
  44. Johnson, A, Lermioglu, F, Garg, UC, Morgan-Boyd, R, Hassid, A. A novel biological effect of atrial natriuretic hormone: inhibition of mesangial cell mitogenesis. Biochem Biophys Res Commun, 152 (2), 893-7, 1988.
  45. Spagnuolo, PJ, Ellner, JJ, Hassid, A, Dunn, MJ. Mediation of augmented monocyte adhesiveness by thromboxane. Inflammation, 12 (1), 1-9, 1988.
  46. Hassid, A. Atriopeptins decrease resting and hormone-elevated cytosolic Ca in cultured mesangial cells. Am J Physiol, 253 (6 Pt 2), F1077-82, 1987.
  47. Morgan-Boyd, R, Stewart, JM, Vavrek, RJ, Hassid, A. Effects of bradykinin and angiotensin II on intracellular Ca2+ dynamics in endothelial cells. Am J Physiol, 253 (4 Pt 1), C588-98, 1987.
  48. Crowley, WR, Hassid, A, Kalra, SP. Neuropeptide Y enhances the release of luteinizing hormone (LH) induced by LH-releasing hormone. Endocrinology, 120 (3), 941-5, 1987.
  49. Hassid, A, Pidikiti, N, Gamero, D. Effects of vasoactive peptides on cytosolic calcium in cultured mesangial cells. Am J Physiol, 251 (6 Pt 2), F1018-28, 1986.
  50. Hassid, A. Increase of cyclic AMP concentrations in cultured vascular smooth muscle cells by vasoactive peptide hormones. Role of endogenous prostaglandins. J Pharmacol Exp Ther, 239 (2), 334-9, 1986.
  51. Hassid, A. Atriopeptin II decreases cytosolic free Ca in cultured vascular smooth muscle cells. Am J Physiol, 251 (5 Pt 1), C681-6, 1986.
  52. Erman, A, Hassid, A, Baer, PG, Nasjletti, A. Treatment with dexamethasone increases glomerular prostaglandin synthesis in rats. J Pharmacol Exp Ther, 239 (1), 296-301, 1986.
  53. Hassid, A, Oudinet, JP. Relationship between cellular calcium and prostaglandin synthesis in cultured vascular smooth muscle cells. Prostaglandins, 32 (3), 457-78, 1986.
  54. Kreisberg, JI, Hassid, A. Functional properties of glomerular cells in culture. Miner Electrolyte Metab, 12 (1), 25-31, 1986.
  55. Pidikiti, N, Gamero, D, Gamero, J, Hassid, A. Bradykinin-evoked modulation of cytosolic Ca2+ concentrations in cultured renal epithelial (MDCK) cells. Biochem Biophys Res Commun, 130 (2), 807-13, 1985.
  56. Hassid, A. Stimulation of prostacyclin synthesis by thromboxane A2-like prostaglandin endoperoxide analogues in cultured vascular smooth muscle cells. Biochem Biophys Res Commun, 123 (1), 21-6, 1984.
  57. Hassid, A, Williams, C. Vasoconstrictor-evoked prostaglandin synthesis in cultured vascular smooth muscle. Am J Physiol, 245 (3), C278-82, 1983.
  58. Hassid, A. Modulation of cyclic 3'5'-adenosine monophosphate in cultured renal (MDCK) cells by endogenous prostaglandins. J Cell Physiol, 116 (3), 297-302, 1983.
  59. Lederman, MM, Liebman, ML, Hassid, AI, Berk, GI. Pre-incubation of human monocytes results in loss of effector activity and diminished stimulation of the autologous mixed lymphocyte reaction. Clin Exp Immunol, 53 (2), 482-90, 1983.
  60. Rosner, IA, Malemud, CJ, Hassid, AI, Goldberg, VM, Boja, BA, Moskowitz, RW. Estradiol and tamoxifen stimulation of lapine articular chondrocyte prostaglandin synthesis. Prostaglandins, 26 (1), 123-38, 1983.
  61. Konieczkowski, M, Dunn, MJ, Stork, JE, Hassid, A. Glomerular synthesis of prostaglandins and thromboxane in spontaneously hypertensive rats. Hypertension, 5 (4), 446-52, 1983.
  62. Hassid, A. Inhibition of prostaglandin biosynthesis in renal (MDCK) cells by cAMP. Am J Physiol, 244 (5), C369-76, 1983.
  63. Pugliese, F, Sato, M, Williams, S, Aikawa, M, Hassid, A, Dunn, M. Rabbit and rat renal papillary collecting tubule cells in culture: the interactions of arginine vasopressin, prostaglandins, and cyclic AMP. Adv Prostaglandin Thromboxane Leukot Res, 11, 517-23, 1983.
  64. Hassid, A, Sebrosky, A, Dunn, MJ. Metabolism of prostaglandins by human renal enzymes: presence of 9-hydroxyprostaglandin dehydrogenase activity in human kidney. Adv Prostaglandin Thromboxane Leukot Res, 11, 499-504, 1983.
  65. Smith, MC, Danviriyasup, K, Crow, JW, Cato, AE, Park, GD, Hassid, A, Dunn, MJ. Prostacyclin substitution for heparin in long-term hemodialysis. Am J Med, 73 (5), 669-78, 1982.
  66. Hassid, A. Regulation of prostaglandin biosynthesis in cultured cells. Am J Physiol, 243 (5), C205-11, 1982.
  67. Jim, K, Hassid, A, Sun, F, Dunn, MJ. Lipoxygenase activity in rat kidney glomeruli, glomerular epithelial cells, and cortical tubules. J Biol Chem, 257 (17), 10294-9, 1982.
  68. Beck, TR, Hassid, A, Dunn, MJ. Desamino-D-Arginine vasopressin induces fatty acid cyclooxygenase activity in the renal medulla of diabetes insipidus rats. J Pharmacol Exp Ther, 221 (2), 269-74, 1982.
  69. Hassid, A. Transport-active renal tubular epithelial cells (MDCK and LLC-PK1) in culture. Prostaglandin biosynthesis and its regulation by peptide hormones and ionophore. Prostaglandins, 21 (6), 985-1001, 1981.
  70. Malemud, CJ, Moskowitz, RW, Hassid, A. Prostaglandin biosynthesis by lapine articular chondrocytes in culture. Biochim Biophys Acta, 663 (2), 480-90, 1981.
  71. Kinter, LB, Dunn, MJ, Beck, TR, Beeuwkes, R, Hassid, A. The interactions of prostaglandins and vasopressin in the kidney. Ann N Y Acad Sci, 372, 163-79, 1981.
  72. Beck, TR, Hassid, A, Dunn, MJ. The effect of arginine vasopressin and its analogs on the synthesis of prostaglandin E2 by rat renal medullary interstitial cells in culture. J Pharmacol Exp Ther, 215 (1), 15-9, 1980.
  73. Spagnuolo, PJ, Ellner, JJ, Hassid, A, Dunn, MJ. Thromboxane A2 mediates augmented polymorphonuclear leukocyte adhesiveness. J Clin Invest, 66 (3), 406-14, 1980.
  74. Hassid, A, Dunn, MJ. Microsomal prostaglandin biosynthesis of human kidney. J Biol Chem, 255 (6), 2472-5, 1980.
  75. Hassid, A, Konieczkowski, M, Dunn, MJ. Prostaglandin synthesis in isolated rat kidney glomeruli. Proc Natl Acad Sci U S A, 76 (3), 1155-9, 1979.
  76. Levine, L, Hassid, A. Effects of phorbol-12,13-diesters on prostaglandin production and phospholipase activity in canine kidney (MDCK) cells. Biochem Biophys Res Commun, 79 (2), 477-84, 1977.
  77. Hassid, A, Levine, L. Stimulation of phospholipase activity and prostaglandin biosynthesis by melittin in cell culture and in vivo. Res Commun Chem Pathol Pharmacol, 18 (3), 507-17, 1977.
  78. Hassid, A, Levine, L. Induction of fatty acid cyclooxygenase activity in canine kidney cells (MDCK) by benzo(a)pyrene. J Biol Chem, 252 (19), 6591-3, 1977.
  79. Levine, L, Hassid, A. Epidermal growth factor stimulates prostaglandin biosynthesis by canine kidney (MDCK) cells. Biochem Biophys Res Commun, 76 (4), 1181-7, 1977.
  80. Zeeberg, B, Hassid, A, Caplow, M. Microtubular protein catalytic interactions with nucleotides. J Biol Chem, 252 (6), 2101-5, 1977.
  81. Hassid, A, Levine, L. Multiple molecular forms of prostaglandin 15-hydroxydehydrogenase and 9-ketoreductase in chicken kidney. Prostaglandins, 13 (3), 503-16, 1977.