Journal of Cellular Physiology

Cover image for Vol. 230 Issue 7

Edited By: Gary S. Stein, Harvey M. Florman and Constance E. Brinckerhoff

Impact Factor: 3.874

ISI Journal Citation Reports © Ranking: 2013: 14/81 (Physiology); 77/185 (Cell Biology)

Online ISSN: 1097-4652

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Top Cited Articles 2014

Franchina, T., Amodeo, V., Bronte, G., Savio, G., Ricciardi, G. R.R., Picciotto, M., Russo, A., Giordano, A. and Adamo, V.
Circulating miR-22, miR-24 and miR-34a as Novel Predictive Biomarkers to Pemetrexed-Based Chemotherapy in Advanced Non-Small Cell Lung Cancer
Journal of Cellular Physiology 2014, vol. 229, p. 97

Basile, D. P. and Yoder, M. C.
Circulating and Tissue Resident Endothelial Progenitor Cells
Journal of Cellular Physiology 2014, vol. 229, p. 10

Anderson, M., Roshanravan, H., Khine, J. and Dryer, S. E.
Angiotensin II Activation of TRPC6 Channels in Rat Podocytes Requires Generation of Reactive Oxygen Species
Journal of Cellular Physiology 2014, vol. 229, p. 434

Zhang, Y.-Y., Yue, J., Che, H., Sun, H.-Y., Tse, H.-F. and Li, G.-R
BKCa and hEag1 Channels Regulate Cell Proliferation and Differentiation in Human Bone Marrow-Derived Mesenchymal Stem Cells
Journal of Cellular Physiology 2014, vol. 229, p. 202

Basile, D. P. and Yoder, M. C.
Circulating and Tissue Resident Endothelial Progenitor Cells
Journal of Cellular Physiology 2014, vol. 229, p. 10

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JCP Spotlight Article

GRP78 / Dna K is a target for Nexavar / Stivarga / Votrient in the treatment of human malignancies, viral infections and bacterial diseases

Jane L. Roberts, Mehrad Tavallai, Aida Nourbakhsh, Abigail Fidanza, Tanya Cruz-Luna, Elizabeth Smith, Paul Siembida, Pascale Plamondon, Kelly A. Cycon, Christopher D. Doern, Laurence Booth, and Paul Dent

Abstract: Prior tumor cell studies have shown that the drugs sorafenib (Nexavar) and regorafenib (Stivarga) reduce expression of the chaperone GRP78. Sorafenib/regorafenib and the multi-kinase inhibitor pazopanib (Votrient) interacted with sildenafil (Viagra) to further rapidly reduce GRP78 levels in eukaryotes and as single agents to reduce Dna K levels in prokaryotes. Similar data were obtained in tumor cells in vitro and in drug-treated mice for: HSP70, mitochondrial HSP70, HSP60, HSP56, HSP40, HSP10 and cyclophilin A. Prolonged ‘rafenib / sildenafil treatment killed tumor cells and also rapidly decreased the expression of: the drug efflux pumps ABCB1 and ABCG2; and NPC1 and NTCP, receptors for Ebola / Hepatitis A and B viruses, respectively. Pre-treatment with the ‘Rafenib/sildenafil combination reduced expression of the Coxsackie and Adenovirus receptor in parallel with it also reducing the ability of a serotype 5 Adenovirus or Coxsackie virus B4 to infect and to reproduce. Sorafenib / pazopanib and sildenafil was much more potent than sorafenib / pazopanib as single agents at preventing Adenovirus, Mumps, Chikungunya, Dengue, Rabies, West Nile, Yellow Fever and Enterovirus 71 infection and reproduction. ‘Rafenib drugs / pazopanib as single agents killed laboratory generated antibiotic resistant E. coli which was associated with reduced Dna K and Rec A expression. Marginally toxic doses of ‘Rafenib drugs / pazopanib restored antibiotic sensitivity in pan-antibiotic resistant bacteria including multiple strains of blakpcKlebsiella pneumoniae. Thus Dna K is an antibiotic target for sorafenib, and inhibition of GRP78/Dna K has therapeutic utility for cancer and for bacterial and viral infections.

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