Par-4 is a tumor suppressor protein first discovered and identified in 1993 by Dr. Vivek Rangnekar's laboratory in prostate cancer cells undergoing apoptosis. Par-4 (later also known as PAWR) is a naturally occurring tumor suppressor. Studies have indicated that Par-4 selectively induces apoptosis in cancer cells while leaving normal, healthy, cells unaffected. Mechanisms contributing to the cancer-selective action of Par-4 have been associated with protein kinase A activation of intracellular Par-4 in cancer cells or GRP78 expression primarily on the surface of cancer cells. Par-4 is…mehr
Par-4 is a tumor suppressor protein first discovered and identified in 1993 by Dr. Vivek Rangnekar's laboratory in prostate cancer cells undergoing apoptosis. Par-4 (later also known as PAWR) is a naturally occurring tumor suppressor. Studies have indicated that Par-4 selectively induces apoptosis in cancer cells while leaving normal, healthy, cells unaffected. Mechanisms contributing to the cancer-selective action of Par-4 have been associated with protein kinase A activation of intracellular Par-4 in cancer cells or GRP78 expression primarily on the surface of cancer cells. Par-4 is downregulated, inactivated or mutated in diverse cancers. This first of two volumes will be the first on the market on the topic of Par-4, and will provide the opportunity for researchers to discuss the future direction of studies, broaden the scope of research, and contribute a more complete understanding of the molecule's structural features, key functional domains, regulation and relevant basic and clinical/translational facets.
¿Vivek M. Rangnekar, Ph.D. is Professor and Alfred Cohen Chair in Oncology Research in the Department of Radiation Medicine and Associate Director of the Markey Cancer Center at the University of Kentucky. His laboratory studies the molecular cross-talk between oncogenes and tumor suppressor genes in an effort to tilt the balance in favor of tumor suppressor function. Dr. Rangnekar originally discovered and identified the tumor suppressor protein Par-4/PAWR in 1993.
Inhaltsangabe
IntroductionChapter 1. Discovery and Overview of Par-4Chapter 2. Significance of Par-4 Interaction with aPKCChapter 3. Structural Analysis of the C-terminal domain of Par-4Chapter 4. Crystallization and crystallographic analysis of the C-terminal domain of Par-4 (PAWR)Chapter 5. Role of ubiquitinase FBX045 in Par-4 regulationChapter 6. Regulation of Par-4 by type II phosphatidylinositol 4-kinase betaChapter 7. Role of Par-4 in regulation of cell death by circumin and ceramideChapter 8. Par-4 in dissociation induced cell death in human pluripotent stem cellsChapter 9. Role of Par-4 in EMTChapter 10. Bacillus thuringiensis Induced Par-4 and Apoptosis in Human CellsChapter 11. Role of Par-4 in ZebrafishChapter 12. Role of Par-4 in GRP78 translocationChapter 13. Interaction of THAP1 with Par-4 in PML bodiesChapter 14. Regulation of DAPK and AMIDA by Par-4Chapter 15. Regulation of Par-4 by CK2 kinase
IntroductionChapter 1. Discovery and Overview of Par-4Chapter 2. Significance of Par-4 Interaction with aPKCChapter 3. Structural Analysis of the C-terminal domain of Par-4Chapter 4. Crystallization and crystallographic analysis of the C-terminal domain of Par-4 (PAWR)Chapter 5. Role of ubiquitinase FBX045 in Par-4 regulationChapter 6. Regulation of Par-4 by type II phosphatidylinositol 4-kinase betaChapter 7. Role of Par-4 in regulation of cell death by circumin and ceramideChapter 8. Par-4 in dissociation induced cell death in human pluripotent stem cellsChapter 9. Role of Par-4 in EMTChapter 10. Bacillus thuringiensis Induced Par-4 and Apoptosis in Human CellsChapter 11. Role of Par-4 in ZebrafishChapter 12. Role of Par-4 in GRP78 translocationChapter 13. Interaction of THAP1 with Par-4 in PML bodiesChapter 14. Regulation of DAPK and AMIDA by Par-4Chapter 15. Regulation of Par-4 by CK2 kinase
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