Caspase-14-deficient mice are more prone to the development of parakeratosis.

[1]  S. Brady Parakeratosis. , 2020, Journal of the American Academy of Dermatology.

[2]  L. Eckhart,et al.  Mechanisms and emerging functions of DNA degradation in the epidermis. , 2012, Frontiers in bioscience.

[3]  P. Vandenabeele,et al.  Caspase-14 is required for filaggrin degradation to natural moisturizing factors in the skin. , 2011, The Journal of investigative dermatology.

[4]  C. Johansen,et al.  Regulation of caspase 14 expression in keratinocytes by inflammatory cytokines – a possible link between reduced skin barrier function and inflammation? , 2011, Experimental dermatology.

[5]  J. Rutledge,et al.  A tale of two plaques: convergent mechanisms of T‐cell‐mediated inflammation in psoriasis and atherosclerosis , 2011, Experimental dermatology.

[6]  Andrew Johnston,et al.  Genome-Wide Expression Profiling of Five Mouse Models Identifies Similarities and Differences with Human Psoriasis , 2011, PloS one.

[7]  R. Hakem,et al.  RIP3 mediates the embryonic lethality of caspase-8-deficient mice , 2011, Nature.

[8]  Mami Yamamoto,et al.  Quantification of activated and total caspase-14 with newly developed ELISA systems in normal and atopic skin. , 2011, Journal of dermatological science.

[9]  E. Wagner,et al.  Psoriasis: what we have learned from mouse models , 2010, Nature Reviews Rheumatology.

[10]  A. Bowcock,et al.  Psoriasis genetics: breaking the barrier. , 2010, Trends in genetics : TIG.

[11]  E. Fujita,et al.  Purification and characterization of active caspase‐14 from human epidermis and development of the cleavage site‐directed antibody , 2009, Journal of cellular biochemistry.

[12]  T. Kang,et al.  Caspase-8 deficiency in epidermal keratinocytes triggers an inflammatory skin disease , 2009, The Journal of experimental medicine.

[13]  J. Sundberg,et al.  Filaggrin deficiency confers a paracellular barrier abnormality that reduces inflammatory thresholds to irritants and haptens. , 2009, The Journal of allergy and clinical immunology.

[14]  L. Boon,et al.  Imiquimod-Induced Psoriasis-Like Skin Inflammation in Mice Is Mediated via the IL-23/IL-17 Axis1 , 2009, The Journal of Immunology.

[15]  Irene L. Ch’en,et al.  Dynamic expression of epidermal caspase-8 simulates a wound healing response , 2009, Nature.

[16]  J. Brandner,et al.  The skin: an indispensable barrier , 2008, Experimental dermatology.

[17]  D. Dickinson,et al.  Green tea polyphenol induces caspase 14 in epidermal keratinocytes via MAPK pathways and reduces psoriasiform lesions in the flaky skin mouse model , 2007, Experimental dermatology.

[18]  P. Vandenabeele,et al.  Caspase-14 protects against epidermal UVB photodamage and water loss , 2007, Nature Cell Biology.

[19]  R. Tazi-Ahnini,et al.  Nine procaspases are expressed in normal human epidermis, but only caspase‐14 is fully processed , 2007, The British journal of dermatology.

[20]  James G. Krueger,et al.  Pathogenesis and therapy of psoriasis , 2007, Nature.

[21]  F. Nestle,et al.  Animal models of psoriasis and psoriatic arthritis: An update , 2006, Current rheumatology reports.

[22]  A. Bowcock,et al.  Getting under the skin: the immunogenetics of psoriasis , 2005, Nature Reviews Immunology.

[23]  L. Eckhart,et al.  Stratum corneum‐derived caspase‐14 is catalytically active , 2004, FEBS letters.

[24]  P. Vandenabeele,et al.  Vitamin D3 induces caspase-14 expression in psoriatic lesions and enhances caspase-14 processing in organotypic skin cultures. , 2004, The American journal of pathology.

[25]  H. Korting,et al.  Dry skin improvement by an oleosome emulsion as a carrier for sphingolipid1 , 2004 .

[26]  U. Rassner,et al.  Basis for abnormal desquamation and permeability barrier dysfunction in RXLI. , 2004, The Journal of investigative dermatology.

[27]  P. Vandenabeele,et al.  Caspase-14 is expressed in the epidermis, the choroid plexus, the retinal pigment epithelium and thymic Hassall's bodies , 2003, Cell Death and Differentiation.

[28]  P. Vandenabeele,et al.  Epidermal differentiation does not involve the pro-apoptotic executioner caspases, but is associated with caspase-14 induction and processing , 2000, Cell Death and Differentiation.

[29]  S Lippens,et al.  Terminal differentiation of human keratinocytes and stratum corneum formation is associated with caspase-14 activation. , 2000, The Journal of investigative dermatology.

[30]  E. Choi,et al.  The changes of epidermal calcium gradient and transitional cells after prolonged occlusion following tape stripping in the murine epidermis. , 1999, The Journal of investigative dermatology.

[31]  R. Miller,et al.  Modulation of TH1 and TH2 cytokine production with the immune response modifiers, R-848 and imiquimod. , 1999, Cellular immunology.

[32]  P. Elias,et al.  Stratum corneum structure and function correlates with phenotype in psoriasis. , 1996, The Journal of investigative dermatology.

[33]  A. Steven,et al.  Differential expression and cell envelope incorporation of small proline-rich protein 1 in different cornified epithelia. , 1996, Journal of cell science.

[34]  P. Elias,et al.  The epidermal hyperplasia associated with repeated barrier disruption by acetone treatment or tape stripping cannot be attributed to increased water loss , 1996, Archives of Dermatological Research.

[35]  P. Elias,et al.  De novo sterologenesis in the skin. II. Regulation by cutaneous barrier requirements. , 1985, Journal of lipid research.

[36]  P. Vandenabeele,et al.  Acute modulations in permeability barrier function regulate epidermal cornification: role of caspase-14 and the protease-activated receptor type 2. , 2008, The American journal of pathology.

[37]  P. Vandenabeele,et al.  The caspase family , 2003 .