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      1. Author :
        Shimomura, Toshiyasu; Hasako, Shinichi; Nakatsuru, Yoko; Mita, Takashi; Ichikawa, Koji; Kodera, Tsutomu; Sakai, Takumi; Nambu, Tadahiro; Miyamoto, Mayu; Takahashi, Ikuko; Miki, Satomi; Kawanishi, Nobuhiko; Ohkubo, Mitsuru; Kotani, Hidehito; Iwasawa, Yoshikazu
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Molecular cancer therapeutics
      6. Products :
      7. Volume :
        9
      8. Issue :
        1
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Bioware; Cell Death; Cell Line, Tumor; Cell Proliferation; Cyclohexanecarboxylic Acids; HeLa-luc; Humans; Inhibitory Concentration 50; Mice; Mitosis; Protein kinase inhibitors; Protein-Serine-Threonine Kinases; Rats; Taxoids; Thiazoles; Xenograft Model Antitumor Assays
      12. Abstract :
        Aurora-A kinase is a one of the key regulators during mitosis progression. Aurora-A kinase is a potential target for anticancer therapies because overexpression of Aurora-A, which is frequently observed in some human cancers, results in aberrant mitosis leading to chromosomal instability and possibly tumorigenesis. MK-5108 is a novel small molecule with potent inhibitory activity against Aurora-A kinase. Although most of the Aurora-kinase inhibitors target both Aurora-A and Aurora-B, MK-5108 specifically inhibited Aurora-A kinase in a panel of protein kinase assays. Inhibition of Aurora-A by MK-5108 in cultured cells induced cell cycle arrest at the G(2)-M phase in flow cytometry analysis. The effect was confirmed by the accumulation of cells with expression of phosphorylated Histone H3 and inhibition of Aurora-A autophosphorylation by immunostaining assays. MK-5108 also induced phosphorylated Histone H3 in skin and xenograft tumor tissues in a nude rat xenograft model. MK-5108 inhibited growth of human tumor cell lines in culture and in different xenograft models. Furthermore, the combination of MK-5108 and docetaxel showed enhanced antitumor activities compared with control and docetaxel alone-treated animals without exacerbating the adverse effects of docetaxel. MK-5108 is currently tested in clinical trials and offers a new therapeutic approach to combat human cancers as a single agent or in combination with existing taxane therapies.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20053775
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        9006
      1. Author :
        Hickson, J; Ackler, S; Klaubert, D; Bouska, J; Ellis, P; Foster, K; Oleksijew, A; Rodriguez, L; Schlessinger, S; Wang, B; Frost, D
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Cell death and differentiation
      6. Products :
      7. Volume :
        17
      8. Issue :
        6
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Antineoplastic Agents; Apoptosis; Bioware; Caspase 3; Cell Line, Tumor; Female; Firefly Luciferin; Humans; Luminescent Agents; MDA-MB-231-D3H2LN cells; Mice; Mice, SCID; SKOV3-luc-D3 cells; Molecular Imaging; Neoplasms; Oligopeptides; Taxoids
      12. Abstract :
        Apoptosis is a highly regulated process of programmed cell death essential for normal physiology. Dysregulation of apoptosis contributes to the development and progression of various diseases, including cancer, neurodegenerative disorders, and chronic heart failure. Quantitative noninvasive imaging of apoptosis in preclinical models would allow for dynamic longitudinal screening of compounds and facilitates a more rapid determination of therapeutic efficacy. In this study, we report the in vivo characterization of Z-DEVD-aminoluciferin, a modified firefly luciferase substrate that in apoptotic cells is cleaved by caspase-3 to liberate aminoluciferin, which can be consumed by luciferase to generate a luminescent signal. In two oncology models, namely SKOV3-luc and MDA-MB-231-luc-LN, at 24, 48, and 72 h after treatment with docetaxel, animals were injected with Z-DEVD-aminoluciferin and bioluminescent images were acquired. Significantly more light was detected at 24 (P<0.05), 48 (P<0.01), and 72 h (P<0.01) in the docetaxel-treated group compared with the vehicle-treated group, with caspase-3 activation at these time points confirmed using immunohistochemistry. Importantly, whereas significant differences between groups were detected as early as 24 h after treatment by molecular imaging, caliper measurements were unable to detect a difference for 4-5 additional days. Taken together, these data show that in vivo imaging of apoptosis using Z-DEVD-aminoluciferin could provide a sensitive and rapid method for early detection of drug efficacy, which could potentially be used by numerous therapeutic programs.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20057500
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8950
      1. Author :
        Zhang, H-Y; Man, J-H; Liang, B; Zhou, T; Wang, C-H; Li, T; Li, H-Y; Li, W-H; Jin, B-F; Zhang, P-J; Zhao, J; Pan, X; He, K; Gong, W-L; Zhang, X-M; Li, A-L
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Cancer gene therapy
      6. Products :
      7. Volume :
        17
      8. Issue :
        5
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Apoptosis; B16-F10-luc-G5 cells; Bioware; Blotting, Western; Cell Line, Tumor; Escherichia coli; Female; Flow Cytometry; Gene Therapy; Genetic Vectors; Humans; Immunohistochemistry; Mice; Mice, Inbred BALB C; Mice, Nude; NCI-H460-luc2; Neoplasms; Polymerase Chain Reaction; Survival Rate; TNF-Related Apoptosis-Inducing Ligand
      12. Abstract :
        The tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a potent inducer of tumor cell apoptosis, but concerns of considerable liver toxicity limit its uses in human cancer therapy. Here, we show that i.v. injected Escherichia coli DH5alpha (E. coli DH5alpha) specifically replicates in solid tumors and metastases in live animals. E. coli DH5alpha does not enter tumor cells and suits for being the vector for soluble TRAIL (sTRAIL), which induces apoptosis by activating cell-surface death receptors. With the high 'tumor-targeting' nature, we demonstrate that intratumoral (i.t.) and intravenous injection of sTRAIL-expressing E. coli DH5alpha results in the tumor-targeted release of biologically active molecules, which leads to a dramatic reduction in the tumor growth rate and the prolonged survival of tumor-bearing mice. TRAIL delivery by E. coli DH5alpha did not cause any detectable toxicity to any organs, suggesting that E. coli DH5alpha-delivered sTRAIL protein therapy may provide a feasible and effective form of treatment for solid tumors.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20075981
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8944
      1. Author :
        Dai, T.; Tegos, G. P.; Zhiyentayev, T.; Mylonakis, E.; Hamblin, M. R.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Lasers Surg Med
      6. Products :
      7. Volume :
        42
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Xen31, Xen 31, MRSA, S. aureus, IVIS, Bioluminescence, Administration, Cutaneous; Animals; Disease Models, Animal; Female; *Methicillin-Resistant Staphylococcus aureus; Mice; Mice, Inbred BALB C; Photobleaching; *Photochemotherapy; Polyethyleneimine/administration & dosage; Porphyrins/*administration & dosage; Radiation-Sensitizing Agents/*administration & dosage; Staphylococcal Skin Infections/etiology/pathology/*therapy; Wound Infection/microbiology/pathology/*therapy
      12. Abstract :
        BACKGROUND AND OBJECTIVE: Methicillin-resistant Staphylococcus aureus (MRSA) skin infections are now known to be a common and important problem in the Unites States. The objective of this study was to investigate the efficacy of photodynamic therapy (PDT) for the treatment of MRSA infection in skin abrasion wounds using a mouse model. STUDY DESIGN/MATERIALS AND METHODS: A mouse model of skin abrasion wound infected with MRSA was developed. Bioluminescent strain of MRSA, a derivative of ATCC 33591, was used to allow the real-time monitoring of the extent of infection in mouse wounds. PDT was performed with the combination of a polyethylenimine (PEI)-ce6 photosensitizer (PS) and non-coherent red light. In vivo fluorescence imaging was carried out to evaluate the effect of photobleaching of PS during PDT. RESULTS: In vivo fluorescence imaging of conjugate PEI-ce6 applied in mice indicated the photobleaching effect of the PS during PDT. PDT induced on average 2.7 log(10) of inactivation of MRSA as judged by loss of bioluminescence in mouse skin abrasion wounds and accelerated the wound healing on average by 8.6 days in comparison to the untreated infected wounds. Photobleaching of PS in the wound was overcome by adding the PS solution in aliquots. CONCLUSION: PDT may represent an alternative approach for the treatment of MRSA skin infections.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20077489
      14. Call Number :
        PKI @ kd.modi @ 3
      15. Serial :
        10553
      1. Author :
        Fogal, Valentina; Richardson, Adam D; Karmali, Priya P; Scheffler, Immo E; Smith, Jeffrey W; Ruoslahti, Erkki
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Molecular and cellular biology
      6. Products :
      7. Volume :
        30
      8. Issue :
        6
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Bioware; Carbon; Carrier Proteins; Cell Death; Cell Line, Tumor; Cell Proliferation; Cell Survival; Electron Transport Complex I; Gene Knockdown Techniques; Humans; Mass Spectrometry; MDA-MB-231-D3H2LN cells; Mice; Mitochondria; Mitochondrial Proteins; Neoplasm Metastasis; Neoplasms; Oxidative Phosphorylation; Protein Biosynthesis; Protein Stability; Rotenone
      12. Abstract :
        p32/gC1qR/C1QBP/HABP1 is a mitochondrial/cell surface protein overexpressed in certain cancer cells. Here we show that knocking down p32 expression in human cancer cells strongly shifts their metabolism from oxidative phosphorylation (OXPHOS) to glycolysis. The p32 knockdown cells exhibited reduced synthesis of the mitochondrial-DNA-encoded OXPHOS polypeptides and were less tumorigenic in vivo. Expression of exogenous p32 in the knockdown cells restored the wild-type cellular phenotype and tumorigenicity. Increased glucose consumption and lactate production, known as the Warburg effect, are almost universal hallmarks of solid tumors and are thought to favor tumor growth. However, here we show that a protein regularly overexpressed in some cancers is capable of promoting OXPHOS. Our results indicate that high levels of glycolysis, in the absence of adequate OXPHOS, may not be as beneficial for tumor growth as generally thought and suggest that tumor cells use p32 to regulate the balance between OXPHOS and glycolysis.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20100866
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8952
      1. Author :
        N/A
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Journal of immunology (Baltimore, Md.: 1950)
      6. Products :
      7. Volume :
        184
      8. Issue :
        5
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Amino Acid Sequence; Animals; Antimicrobial Cationic Peptides; Bacterial Infections; Bioware; Cell Line; Cells, Cultured; Chemokine CCL2; Chemokine CCL7; Chemokine CXCL1; Chemokines; Female; Humans; Interleukin-8; Leukocytes; Leukocytes, Mononuclear; Macrophages; Mice; Mice, Inbred C57BL; Molecular Sequence Data; NF-kappa B; p38 Mitogen-Activated Protein Kinases; Phosphatidylinositol 3-Kinases; Phosphorylation; Staphylococcal Infections; Staphylococcus aureus; Xen29, Xen14
      12. Abstract :
        With the rapid rise in the incidence of multidrug resistant infections, there is substantial interest in host defense peptides as templates for production of new antimicrobial therapeutics. Natural peptides are multifunctional mediators of the innate immune response, with some direct antimicrobial activity and diverse immunomodulatory properties. We have previously developed an innate defense regulator (IDR) 1, with protective activity against bacterial infection mediated entirely through its effects on the immunity of the host, as a novel approach to anti-infective therapy. In this study, an immunomodulatory peptide IDR-1002 was selected from a library of bactenecin derivatives based on its substantially more potent ability to induce chemokines in human PBMCs. The enhanced chemokine induction activity of the peptide in vitro correlated with stronger protective activity in vivo in the Staphylococcus aureus-invasive infection model, with a >5-fold reduction in the protective dose in direct comparison with IDR-1. IDR-1002 also afforded protection against the Gram-negative bacterial pathogen Escherichia coli. Chemokine induction by IDR-1002 was found to be mediated through a Gi-coupled receptor and the PI3K, NF-kappaB, and MAPK signaling pathways. The protective activity of the peptide was associated with in vivo augmentation of chemokine production and recruitment of neutrophils and monocytes to the site of infection. These results highlight the importance of the chemokine induction activity of host defense peptides and demonstrate that the optimization of the ex vivo chemokine-induction properties of peptides is a promising method for the rational development of immunomodulatory IDR peptides with enhanced anti-infective activity.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20107187
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        9033
      1. Author :
        Nijnik, A.; Madera, L.; Ma, S.; Waldbrook, M.; Elliott, M. R.; Easton, D. M.; Mayer, M. L.; Mullaly, S. C.; Kindrachuk, J.; Jenssen, H.; Hancock, R. E.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        J Immunol
      6. Products :
      7. Volume :
        184
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Xen14, Xen 14, E. coli Xen14, IVIS, Amino Acid Sequence; Animals; Antimicrobial Cationic Peptides/chemical synthesis/*pharmacology; Bacterial Infections/*metabolism/microbiology/prevention & control; Cell Line; Cells, Cultured; Chemokine CCL2/metabolism; Chemokine CCL7/metabolism; Chemokine CXCL1/metabolism; Chemokines/*metabolism; Female; Humans; Interleukin-8/metabolism; Leukocytes/cytology/*metabolism; Leukocytes, Mononuclear/cytology/drug effects/metabolism; Macrophages/cytology/drug effects/metabolism; Mice; Mice, Inbred C57BL; Molecular Sequence Data; NF-kappa B/metabolism; Phosphatidylinositol 3-Kinases/metabolism; Phosphorylation/drug effects; Staphylococcal Infections/microbiology/prevention & control; Staphylococcus aureus/drug effects; p38 Mitogen-Activated Protein Kinases/metabolism
      12. Abstract :
        With the rapid rise in the incidence of multidrug resistant infections, there is substantial interest in host defense peptides as templates for production of new antimicrobial therapeutics. Natural peptides are multifunctional mediators of the innate immune response, with some direct antimicrobial activity and diverse immunomodulatory properties. We have previously developed an innate defense regulator (IDR) 1, with protective activity against bacterial infection mediated entirely through its effects on the immunity of the host, as a novel approach to anti-infective therapy. In this study, an immunomodulatory peptide IDR-1002 was selected from a library of bactenecin derivatives based on its substantially more potent ability to induce chemokines in human PBMCs. The enhanced chemokine induction activity of the peptide in vitro correlated with stronger protective activity in vivo in the Staphylococcus aureus-invasive infection model, with a >5-fold reduction in the protective dose in direct comparison with IDR-1. IDR-1002 also afforded protection against the Gram-negative bacterial pathogen Escherichia coli. Chemokine induction by IDR-1002 was found to be mediated through a Gi-coupled receptor and the PI3K, NF-kappaB, and MAPK signaling pathways. The protective activity of the peptide was associated with in vivo augmentation of chemokine production and recruitment of neutrophils and monocytes to the site of infection. These results highlight the importance of the chemokine induction activity of host defense peptides and demonstrate that the optimization of the ex vivo chemokine-induction properties of peptides is a promising method for the rational development of immunomodulatory IDR peptides with enhanced anti-infective activity.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20107187
      14. Call Number :
        PKI @ kd.modi @ 6
      15. Serial :
        10393
      1. Author :
        Mitchell, Dianne; Pobre, Eileen G; Mulivor, Aaron W; Grinberg, Asya V; Castonguay, Roselyne; Monnell, Travis E; Solban, Nicolas; Ucran, Jeffrey A; Pearsall, R Scott; Underwood, Kathryn W; Seehra, Jasbir; Kumar, Ravindra
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Molecular cancer therapeutics
      6. Products :
      7. Volume :
        9
      8. Issue :
        2
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Activin Receptors, Type II; Animals; Bioware; Bone Morphogenetic Proteins; CHO Cells; Cricetinae; Cricetulus; Endothelial Cells; Endothelium, Vascular; Growth Differentiation Factor 2; Humans; MCF-7-luc-F5 cells; Mice; Neoplasms; Neovascularization, Pathologic; Surface Plasmon Resonance; Telangiectasia, Hereditary Hemorrhagic
      12. Abstract :
        Activin receptor-like kinase-1 (ALK1) is a type I, endothelial cell-specific member of the transforming growth factor-beta superfamily of receptors known to play an essential role in modulating angiogenesis and vessel maintenance. In the present study, we sought to examine the angiogenic and tumorigenic effects mediated upon the inhibition of ALK1 signaling using a soluble chimeric protein (ALK1-Fc). Of 29 transforming growth factor-beta-related ligands screened by surface plasmon resonance, only bone morphogenetic protein (BMP9) and BMP10 displayed high-affinity binding to ALK1-Fc. In cell-based assays, ALK1-Fc inhibited BMP9-mediated Id-1 expression in human umbilical vein endothelial cells and inhibited cord formation by these cells on a Matrigel substrate. In a chick chorioallantoic membrane assay, ALK1-Fc reduced vascular endothelial growth factor-, fibroblast growth factor-, and BMP10-mediated vessel formation. The growth of B16 melanoma explants was also inhibited significantly by ALK1-Fc in this assay. Finally, ALK1-Fc treatment reduced tumor burden in mice receiving orthotopic grafts of MCF7 mammary adenocarcinoma cells. These data show the efficacy of chimeric ALK1-Fc proteins in mitigating vessel formation and support the view that ALK1-Fc is a powerful antiangiogenic agent capable of blocking vascularization.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20124460
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        9010
      1. Author :
        Sharma, Praveen K; Singh, Rajesh; Novakovic, Kristian R; Eaton, John W; Grizzle, William E; Singh, Shailesh
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        International journal of cancer. Journal international du cancer
      6. Products :
      7. Volume :
        127
      8. Issue :
        9
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Antineoplastic Agents; Apoptosis; Bioware; Caspase 3; Cell Line, Tumor; Chemokines, CC; Disease Progression; Enzyme Activation; Etoposide; Humans; Male; Mice; Mice, Nude; PC-3M-luc; Phosphatidylinositol 3-Kinases; Prostatic Neoplasms; Proto-Oncogene Proteins c-akt; Receptors, CCR; Signal Transduction
      12. Abstract :
        Despite recent advances in treatment and management of prostate cancer (PCa), it remains the second leading cause of cancer-related deaths among men in the US. Chemotherapy is one of the treatment alternatives for hormone refractory metastatic PCa. However, current chemotherapeutic regimens provide palliative benefit but relatively modest survival advantage primarily due to chemo-resistance and upregulated antiapoptotic machineries in PCa cells. Therefore, blocking the mechanisms responsible for suppression of apoptosis might improve current chemotherapeutic regimens. In this study, we show that CC chemokine receptor-9 (CCR9) and its natural ligand CCL25 interaction upregulates antiapoptotic proteins (i.e., PI3K, AKT, ERK1/2 and GSK-3beta) and downregulate activation of caspase-3 in PCa cells. Significant downregulation of these CCR9-mediated antiapoptotic proteins in the presence of a PI3K inhibitor (wortmannin), further suggests that the antiapoptotic action of CCR9 is primarily regulated through PI3K. Furthermore, the cytotoxic effect of etoposide was significantly inhibited in the presence of CCL25, and this inhibitory effect of CCL25 was abrogated when CCR9-CCL25 interaction was blocked using anti-CCR9 monoclonal antibodies. In conformation to these in vitro studies, significant reduction in tumor burden was found in mice receiving CCL25 neutralizing antibodies and etoposide together as compared to both as a single agent. These results suggest that the CCR9-CCL25 axis mediates PI3K/AKT-dependent antiapoptotic signals in PCa cells and could be a possible reason for low apoptosis and modest chemotherapeutic response. Therefore, targeting CCR9-CCL25 axis with cytotoxic agents may provide better therapeutic outcomes than using cytotoxic agents alone.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20127861
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8945
      1. Author :
        Quintela-Fandino, Miguel; Arpaia, Enrico; Brenner, Dirk; Goh, Theo; Yeung, Faith Au; Blaser, Heiko; Alexandrova, Roumiana; Lind, Evan F; Tusche, Mike W; Wakeham, Andrew; Ohashi, Pamela S; Mak, Tak W
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Proceedings of the National Academy of Sciences of the United States of America
      6. Products :
      7. Volume :
        107
      8. Issue :
        6
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Actins; Animals; B16-F10-luc-G5; Bioware; Breast Neoplasms; Cell Line, Tumor; Cell Movement; Cofilin 1; Cytoskeleton; Female; Humans; Immunoblotting; Immunoprecipitation; Male; Mammary Neoplasms, Experimental; MDA-MB-231-D3H2LN cells; Melanoma, Experimental; Mice; Mice, Inbred C57BL; Neoplasm Invasiveness; Neoplasm Metastasis; Phosphorylation; Protein Binding; Protein Kinases; Protein Phosphatase 2; Protein-Serine-Threonine Kinases; RNA Interference; Transplantation, Heterologous
      12. Abstract :
        Metastasis leads to the death of most cancer patients, and basal breast cancer is the most aggressive breast tumor type. Metastasis involves a complex cell migration process dependent on cytoskeletal remodeling such that targeting such remodeling in tumor cells could be clinically beneficial. Here we show that Hormonally Up-regulated Neu-associated Kinase (HUNK) is dramatically down-regulated in tumor samples and cell lines derived from basal breast cancers. Reconstitution of HUNK expression in basal breast cancer cell lines blocked actin polymerization and reduced cell motility, resulting in decreased metastases in two in vivo murine cancer models. Mechanistically, HUNK overexpression sustained the constitutive phosphorylation and inactivation of cofilin-1 (CFL-1), thereby blocking the incorporation of new actin monomers into actin filaments. HUNK reconstitution in basal breast cancer cell lines prevented protein phosphatase 2-A (PP2A), a phosphatase putatively acting on CFL-1, from binding to CFL-1. Our investigation of HUNK suggests that the interaction between PP2A and CFL-1 may be a target for antimetastasis therapy, particularly for basal breast cancers.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20133759
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8951
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