Retinoids induce apoptosis in cultured keratinocytes

Background Apoptosis is a genetically controlled process linked to growth and differentiation, involving specific molecular and cellular events activated as a result of a variety of internal and external stimuli.

[1]  W. Fujimoto,et al.  Expression of the bcl-2 family of genes in the course of keratinocyte differentiation. , 1999, European journal of dermatology : EJD.

[2]  M. Raff,et al.  Caspase activation in the terminal differentiation of human epidermal keratinocytes , 1999, Current Biology.

[3]  L. Goldsmith,et al.  Evidence that apoptosis and terminal differentiation of epidermal keratinocytes are distinct processes , 1999, Experimental dermatology.

[4]  A. Vahlquist.  What Are Natural Retinoids? , 1998, Dermatology.

[5]  H. Wulf,et al.  Two pathways for induction of apoptosis by ultraviolet radiation in cultured human keratinocytes. , 1997, The Journal of investigative dermatology.

[6]  T. McDonnell,et al.  Altered sensitivity to retinoid-induced apoptosis associated with changes in the subcellular distribution of Bcl-2. , 1997, Experimental cell research.

[7]  A. Levin,et al.  Didehydroretinoic acid: retinoid receptor-mediated transcriptional activation and binding properties. , 1997, Biochemical pharmacology.

[8]  A. Haake,et al.  Incomplete differentiation of fetal keratinocytes in the skin equivalent leads to the default pathway of apoptosis. , 1997, Experimental cell research.

[9]  R. Lotan.  Retinoids in cancer chemoprevention , 1996, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[10]  P. Chambon.  A decade of molecular biology of retinoic acid receptors , 1996, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[11]  J. Voorhees,et al.  Molecular mechanisms of retinoid actions in skin , 1996, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[12]  D. Bikle,et al.  Squamous carcinoma cell lines fail to respond to 1,25-Dihydroxyvitamin D despite normal levels of the vitamin D receptor. , 1996, The Journal of investigative dermatology.

[13]  S. Korsmeyer.  BCL-2 gene family and the regulation of programmed cell death. , 1995, Cancer research.

[14]  John Calvin Reed,et al.  Immunohistochemical determination of in vivo distribution of Bax, a dominant inhibitor of Bcl-2. , 1994, The American journal of pathology.

[15]  Z. Oltvai,et al.  Checkpoints of dueling dimers foil death wishes , 1994, Cell.

[16]  G. Melino,et al.  Tissue transglutaminase and apoptosis: sense and antisense transfection studies with human neuroblastoma cells , 1994, Molecular and cellular biology.

[17]  E. Maytin,et al.  Heat shock modulates UVB-induced cell death in human epidermal keratinocytes: evidence for a hyperthermia-inducible protective response. , 1994, The Journal of investigative dermatology.

[18]  T. McDonnell,et al.  Bcl-2 oncogene blocks differentiation and extends viability but does not immortalize normal human keratinocytes. , 1994, International journal of oncology.

[19]  John Calvin Reed,et al.  Tumor suppressor p53 is a regulator of bcl-2 and bax gene expression in vitro and in vivo. , 1994, Oncogene.

[20]  R. Ashman,et al.  Decreased membrane phospholipid packing and decreased cell size precede DNA cleavage in mature mouse B cell apoptosis. , 1994, Journal of immunology.

[21]  M. Piacentini,et al.  Apoptosis in human skin development: Morphogenesis, periderm, and stem cells , 1994, Developmental dynamics : an official publication of the American Association of Anatomists.

[22]  D. Mangelsdorf,et al.  Synthesis of high specific activity [3H]-9-cis-retinoic acid and its application for identifying retinoids with unusual binding properties. , 1994, Journal of medicinal chemistry.

[23]  S. Bohm,et al.  Inducible and cell type-specific expression of VL30 U3 subgroups correlate with their enhancer design , 1994, Journal of virology.

[24]  T. Bugge,et al.  The long terminal repeat of VL30 retrotransposons contains sequences that determine retinoic acid-induced transcription in cultured keratinocytes. , 1993, The Journal of biological chemistry.

[25]  H. Jiang,et al.  Induction of tissue transglutaminase and apoptosis by retinoic acid in the limb bud. , 1992, Teratology.

[26]  J. Voorhees,et al.  Acute or chronic topical retinoic acid treatment of human skin in vivo alters the expression of epidermal transglutaminase, loricrin, involucrin, filaggrin, and keratins 6 and 13 but not keratins 1, 10, and 14. , 1992, The Journal of investigative dermatology.

[27]  L. Fésüs,et al.  Apoptosis: molecular mechanisms in programmed cell death. , 1991, European journal of cell biology.

[28]  J. Cohen,et al.  Programmed cell death in terminally differentiating keratinocytes: role of endogenous endonuclease. , 1991, The Journal of investigative dermatology.

[29]  A. Jetten,et al.  Regulation of type I (epidermal) transglutaminase mRNA levels during squamous differentiation: down regulation by retinoids , 1989, Molecular and cellular biology.

[30]  R. Sasaki,et al.  Amino acid sequence of guinea pig liver transglutaminase from its cDNA sequence. , 1988, Biochemistry.

[31]  M. Negrini,et al.  Molecular analysis of mbcl-2: Structure and expression of the murine gene homologous to the human gene involved in follicular lymphoma , 1987, Cell.

[32]  K. Danno,et al.  SUNBURN CELL: FACTORS INVOLVED IN ITS FORMATION. , 1987, Photochemistry and photobiology.

[33]  P. Chomczyński,et al.  Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction. , 1987, Analytical biochemistry.

[34]  B. Weissman,et al.  Members of the src and ras oncogene families supplant the epidermal growth factor requirement of BALB/MK-2 keratinocytes and induce distinct alterations in their terminal differentiation program , 1985, Molecular and cellular biology.

[35]  C. Dani,et al.  Various rat adult tissues express only one major mRNA species from the glyceraldehyde-3-phosphate-dehydrogenase multigenic family. , 1985, Nucleic acids research.

[36]  S. Yuspa,et al.  Retinoic acid-induced transglutaminase in mouse epidermal cells is distinct from epidermal transglutaminase. , 1985, The Journal of biological chemistry.

[37]  P. Steinert,et al.  Retinoic acid induces transglutaminase activity but inhibits cornification of cultured epidermal cells. , 1982, The Journal of biological chemistry.

[38]  Z. Darżynkiewicz,et al.  Measurement of apoptosis. , 1998, Advances in biochemical engineering/biotechnology.

[39]  G. Núñez,et al.  Apoptosis in keratinocytes is not dependent on induction of differentiation. , 1997, Laboratory investigation; a journal of technical methods and pathology.

[40]  G. Majno,et al.  Apoptosis, oncosis, and necrosis. An overview of cell death. , 1995, The American journal of pathology.

[41]  P. Chambon,et al.  Biologic activities of retinoic acid and 3,4-didehydroretinoic acid in human keratinocytes are similar and correlate with receptor affinities and transactivation properties. , 1994, The Journal of investigative dermatology.

[42]  Z. Darżynkiewicz,et al.  Assays of cell viability: discrimination of cells dying by apoptosis. , 1994, Methods in cell biology.

[43]  S. Pemrick,et al.  The retinoid receptors. , 1994, Leukemia.

[44]  P Chambon,et al.  Retinoic acid receptors and retinoid X receptors: interactions with endogenous retinoic acids. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[45]  D. Hohl,et al.  Cornified cell envelope. , 1990, Dermatologica.