Signaling Pathways Intraepidermal Inflammation by Independent Induces Keratinocyte Apoptosis and a Activation of Cutaneous Protein Kinase C
暂无分享,去创建一个
C. Vinson | S. Yuspa | R. Wiltrout | E. Joseloff | P. Murphy | Ji-Liang Gao | R. Murillas | C. Cataisson | Gerdes | Michael | J. Subleski | Coralyn Atwell | Sara Torgerson | Alice Wang
[1] Wei Zhang,et al. IL-12 completely blocks ultraviolet-induced secretion of tumor necrosis factor alpha from cultured skin fibroblasts and keratinocytes. , 2003, The Journal of investigative dermatology.
[2] E. García-Ramallo,et al. Resident Cell Chemokine Expression Serves as the Major Mechanism for Leukocyte Recruitment During Local Inflammation , 2002, The Journal of Immunology.
[3] F. Marks,et al. Transgenic cyclooxygenase-2 overexpression sensitizes mouse skin for carcinogenesis , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[4] G. Courtois,et al. TNF-mediated inflammatory skin disease in mice with epidermis-specific deletion of IKK2 , 2002, Nature.
[5] Victor E. Marquez,et al. Diacylglycerol (DAG)-lactones, a New Class of Protein Kinase C (PKC) Agonists, Induce Apoptosis in LNCaP Prostate Cancer Cells by Selective Activation of PKCα* , 2002, The Journal of Biological Chemistry.
[6] M. Olive,et al. Adenoviral delivery of A-FOS, an AP-1 dominant negative, selectively inhibits drug resistance in two human cancer cell lines , 2002, Cancer Gene Therapy.
[7] D. Wheeler,et al. Relation of the induction of epidermal ornithine decarboxylase and hyperplasia to the different skin tumor–promotion susceptibilities of protein kinase Cα, ‐δ and ‐ϵ transgenic mice , 2001 .
[8] R. Smart,et al. Protein kinase C-alpha coordinately regulates cytosolic phospholipase A(2) activity and the expression of cyclooxygenase-2 through different mechanisms in mouse keratinocytes. , 2001, Molecular pharmacology.
[9] Joseph D. Schwartzman,et al. Mice Lacking the Chemokine Receptor CCR1 Show Increased Susceptibility to Toxoplasma gondii Infection1 , 2001, The Journal of Immunology.
[10] C. Vinson,et al. Activator protein 1 transcription factors are fundamental to v-rasHa-induced changes in gene expression in neoplastic keratinocytes. , 2000, Cancer research.
[11] Jennifer A. Clark,et al. Protein Kinase C Signaling Mediates a Program of Cell Cycle Withdrawal in the Intestinal Epithelium , 2000, The Journal of cell biology.
[12] A. Glick,et al. Conditional gene expression in the epidermis of transgenic mice using the tetracycline-regulated transactivators tTA and rTA linked to the keratin 5 promoter. , 2000, The Journal of investigative dermatology.
[13] P. Stein,et al. A PKC-eta/Fyn-dependent pathway leading to keratinocyte growth arrest and differentiation. , 2000, Molecular cell.
[14] R. Paus,et al. High‐dose proinflammatory cytokines induce apoptosis of hair bulb keratinocytes in vivo , 2000, The British journal of dermatology.
[15] H. Rosenberg,et al. The Chemokine Macrophage-Inflammatory Protein-1α and Its Receptor CCR1 Control Pulmonary Inflammation and Antiviral Host Defense in Paramyxovirus Infection , 2000, The Journal of Immunology.
[16] C. Caux,et al. Up-Regulation of Macrophage Inflammatory Protein-3α/CCL20 and CC Chemokine Receptor 6 in Psoriasis1 , 2000, The Journal of Immunology.
[17] T. Ruzicka,et al. Critical role of neutrophils for the generation of psoriasiform skin lesions in flaky skin mice. , 2000, The Journal of investigative dermatology.
[18] J. Zou,et al. Transgenic mice overexpressing protein kinase C epsilon in their epidermis exhibit reduced papilloma burden but enhanced carcinoma formation after tumor promotion. , 2000, Cancer research.
[19] R. Eckert,et al. Regulation of Human Involucrin Promoter Activity by Novel Protein Kinase C Isoforms* , 2000, The Journal of Biological Chemistry.
[20] Luowei Li,et al. Protein Kinase Cδ Targets Mitochondria, Alters Mitochondrial Membrane Potential, and Induces Apoptosis in Normal and Neoplastic Keratinocytes When Overexpressed by an Adenoviral Vector , 1999, Molecular and Cellular Biology.
[21] I. Schieren,et al. The α isoform of protein kinase C mediates phorbol ester-induced growth inhibition and p21cip1 induction in HC11 mammary epithelial cells , 1999, Oncogene.
[22] C. Tseng,et al. Transgenic mice overexpressing protein kinase Cdelta in the epidermis are resistant to skin tumor promotion by 12-O-tetradecanoylphorbol-13-acetate. , 1999, Cancer research.
[23] R. Smart,et al. Overexpression of protein kinase C-alpha in the epidermis of transgenic mice results in striking alterations in phorbol ester-induced inflammation and COX-2, MIP-2 and TNF-alpha expression but not tumor promotion. , 1999, Journal of cell science.
[24] M. Behrens,et al. Prevention of neuronal apoptosis by phorbol ester-induced activation of protein kinase C: blockade of p38 mitogen-activated protein kinase , 1999, Neuroscience.
[25] K. Imai,et al. Protein kinase Cα promotes apoptotic cell death in gastric cancer cells depending upon loss of anchorage , 1999, Oncogene.
[26] G. Dotto. Signal transduction pathways controlling the switch between keratinocyte growth and differentiation. , 1999, Critical reviews in oral biology and medicine : an official publication of the American Association of Oral Biologists.
[27] S. Rotenberg,et al. Overexpression of protein kinase Calpha in MCF-10A human breast cells engenders dramatic alterations in morphology, proliferation, and motility. , 1999, Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.
[28] B. Nickoloff,et al. Protein Kinase Cδ Is Activated by Caspase-dependent Proteolysis during Ultraviolet Radiation-induced Apoptosis of Human Keratinocytes* , 1998, The Journal of Biological Chemistry.
[29] W. May,et al. A Functional Role for Mitochondrial Protein Kinase Cα in Bcl2 Phosphorylation and Suppression of Apoptosis* , 1998, The Journal of Biological Chemistry.
[30] N. Huh,et al. Induction of Differentiation in Normal Human Keratinocytes by Adenovirus-Mediated Introduction of the η and δ Isoforms of Protein Kinase C , 1998, Molecular and Cellular Biology.
[31] A. Saran,et al. Effect of genetic modification of acute inflammatory responsiveness on tumorigenesis in the mouse. , 1998, Carcinogenesis.
[32] B. Spiegelman,et al. Opposing activities of c-Fos and Fra-2 on AP-1 regulated transcriptional activity in mouse keratinocytes induced to differentiate by calcium and phorbol esters , 1997, Oncogene.
[33] M. Olive,et al. A Dominant Negative to Activation Protein-1 (AP1) That Abolishes DNA Binding and Inhibits Oncogenesis* , 1997, The Journal of Biological Chemistry.
[34] H. Broxmeyer,et al. Impaired Host Defense, Hematopoiesis, Granulomatous Inflammation and Type 1–Type 2 Cytokine Balance in Mice Lacking CC Chemokine Receptor 1 , 1997, The Journal of experimental medicine.
[35] Yun‐Sil Lee,et al. Definition by specific antisense oligonucleotides of a role for protein kinase Cα in expression of differentiation markers in normal and neoplastic mouse epidermal keratinocytes , 1997, Molecular carcinogenesis.
[36] E. Bröcker,et al. Differential Expression of GRO-α and IL-8 mRNA Psoriasis: A Model for Neutrophil Migration and Accumulation In Vivo , 1996 .
[37] Koichiro Nakamura,et al. Inflammatory and hyperproliferative skin disease in mice that express elevated levels of the IL-1 receptor (type I) on epidermal keratinocytes. Evidence that IL-1-inducible secondary cytokines produced by keratinocytes in vivo can cause skin disease. , 1996, The Journal of clinical investigation.
[38] B. Spiegelman,et al. Differentiation of mouse keratinocytes is accompanied by PKC-dependent changes in AP-1 proteins. , 1996, Oncogene.
[39] K. Valerie,et al. Role of c-jun in human myeloid leukemia cell apoptosis induced by pharmacological inhibitors of protein kinase C. , 1996, Molecular pharmacology.
[40] J. F. Klement,et al. IkBa Deficiency Results in a Sustained NF-kB Response and Severe Widespread Dermatitis in Mice , 1996 .
[41] R. Eckert,et al. Differential expression of the fos and jun family members c-fos, fosB, Fra-1, Fra-2, c-jun, junB and junD during human epidermal keratinocyte differentiation. , 1995, Oncogene.
[42] J. Kieffer,et al. Inflammatory skin disease in transgenic mice that express high levels of interleukin 1 alpha in basal epidermis. , 1995, Proceedings of the National Academy of Sciences of the United States of America.
[43] M. Olive,et al. Extending dimerization interfaces: the bZIP basic region can form a coiled coil. , 1995, The EMBO journal.
[44] A. Ullrich,et al. Expression of a dominant negative mutant of epidermal growth factor receptor in the epidermis of transgenic mice elicits striking alterations in hair follicle development and skin structure. , 1995, The EMBO journal.
[45] P. V. D. van de Kerkhof,et al. Signal transduction pathways in epidermal proliferation and cutaneous inflammation. , 1995, Clinics in dermatology.
[46] Z. Szallasi,et al. Specific protein kinase C isozymes mediate the induction of keratinocyte differentiation markers by calcium. , 1995, Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.
[47] S. Yuspa,et al. Isolation and utilization of epidermal keratinocytes for oncogene research. , 1995, Methods in enzymology.
[48] S. Yuspa,et al. Alterations in murine keratinocyte differentiation induced by activated rasHa genes are mediated by protein kinase C-alpha. , 1994, Cancer research.
[49] D. Carrasco,et al. Expression of the chemokine N51/KC in the thymus and epidermis of transgenic mice results in marked infiltration of a single class of inflammatory cells , 1994, The Journal of experimental medicine.
[50] M. Vidal,et al. Sequences 5' of the bovine keratin 5 gene direct tissue- and cell-type-specific expression of a lacZ gene in the adult and during development. , 1994, Differentiation; research in biological diversity.
[51] R. Flavell,et al. AP‐1 transcriptional activity requires both T‐cell receptor‐mediated and co‐stimulatory signals in primary T lymphocytes. , 1994, The EMBO journal.
[52] J. Jorcano,et al. Analysis of the control of expression and tissue specificity of the keratin 5 gene, characteristic of basal keratinocytes. Fundamental role of an AP-1 element. , 1994, The Journal of biological chemistry.
[53] T. Kuroki,et al. Differentiation-associated localization of nPKC eta, a Ca(++)-independent protein kinase C, in normal human skin and skin diseases. , 1993, The Journal of investigative dermatology.
[54] J. Celis,et al. Evidence for an altered protein kinase C (PKC) signaling pathway in psoriasis. , 1993, The Journal of investigative dermatology.
[55] James T. Elder,et al. Differential Expression of Protein Kinase C Isoenzymes in Normal and Psoriatic Adult Human Skin: Reduced Expression of Protein Kinase C-βII in Psoriasis , 1993 .
[56] S. Yuspa,et al. Coordinate changes in gene expression which mark the spinous to granular cell transition in epidermis are regulated by protein kinase C , 1993, The Journal of cell biology.
[57] K. Punnonen,et al. Analysis of phospholipid metabolism in murine keratinocytes transformed by the v-ras oncogene: relationship of phosphatidylinositol turnover and cytokine stimulation to the transformed phenotype. , 1992, Carcinogenesis.
[58] K. Turksen,et al. Cachexia and graft-vs.-host-disease-type skin changes in keratin promoter-driven TNF alpha transgenic mice. , 1992, Genes & development.
[59] J. Voorhees,et al. Increased phospholipase C-catalyzed hydrolysis of phosphatidylinositol-4,5-bisphosphate and 1,2-sn-diacylglycerol content in psoriatic involved compared to uninvolved and normal epidermis. , 1990, The Journal of investigative dermatology.
[60] T. Slaga,et al. Cutaneous changes during prolonged application of 12-O-tetradecanoylphorbol-13-acetate on mouse skin and residual effects after cessation of treatment. , 1985, Cancer research.