Publications
-
A mannose-binding receptor is expressed on human keratinocytes and mediates killing of Candida albicans.
Part of Journal of Investigative Dermatology, p. 205-13, 2001.
-
A novel mechanism for anti-EGFR antibody action involves chemokine-mediated leukocyte infiltration.
Part of International Journal of Cancer, p. 2589-96, 2009.
-
Activation of toll-like receptors alters the microRNA expression profile of keratinocytes.
Part of Experimental dermatology, p. 281-3, 2014.
DOI for Activation of toll-like receptors alters the microRNA expression profile of keratinocytes.
-
Advances in microRNAs: implications for immunity and inflammatory diseases.
Part of Journal of Cellular and Molecular Medicine (Print), p. 24-38, 2009.
DOI for Advances in microRNAs: implications for immunity and inflammatory diseases.
-
Are BIC (miR-155) polymorphisms associated with eczema susceptibility?
Part of Acta Dermato-Venereologica, p. 366-7, 2013.
DOI for Are BIC (miR-155) polymorphisms associated with eczema susceptibility?
-
Budesonide, but not tacrolimus, affects the immune functions of normal human keratinocytes.
Part of International Immunopharmacology, p. 358-68, 2006.
DOI for Budesonide, but not tacrolimus, affects the immune functions of normal human keratinocytes.
-
CC chemokine ligand 18, an atopic dermatitis-associated and dendritic cell-derived chemokine, is regulated by staphylococcal products and allergen exposure.
Part of Journal of Immunology, p. 5810-7, 2004.
-
CCL1-CCR8 interactions: an axis mediating the recruitment of T cells and Langerhans-type dendritic cells to sites of atopic skin inflammation.
Part of Journal of Immunology, p. 5082-91, 2005.
-
Changes in the level of serum microRNAs in patients with psoriasis after antitumour necrosis factor-α therapy.
Part of British Journal of Dermatology, p. 563-70, 2013.
-
Characterization of EGFR and ErbB2 expression in atopic dermatitis patients.
Part of Archives of Dermatological Research, p. 773-80, 2012.
DOI for Characterization of EGFR and ErbB2 expression in atopic dermatitis patients.
-
Chemokine networks in atopic dermatitis: traffic signals of disease.
Part of Current Allergy and Asthma Reports, p. 284-90, 2005.
DOI for Chemokine networks in atopic dermatitis: traffic signals of disease.
-
Chromatin interactions in differentiating keratinocytes reveal novel atopic dermatitis- and psoriasis-associated genes
Part of Journal of Allergy and Clinical Immunology, p. 1742-1752, 2021.
DOI for Chromatin interactions in differentiating keratinocytes reveal novel atopic dermatitis- and psoriasis-associated genes Download full text (pdf) of Chromatin interactions in differentiating keratinocytes reveal novel atopic dermatitis- and psoriasis-associated genes
-
Circulating microRNAs in extracellular vesicles as potential biomarkers for psoriatic arthritis in patients with psoriasis
Part of Journal of the European Academy of Dermatology and Venereology, p. 1248-1256, 2020.
-
Constraints for monocyte-derived dendritic cell functions under inflammatory conditions.
Part of European Journal of Immunology, p. 458-69, 2012.
DOI for Constraints for monocyte-derived dendritic cell functions under inflammatory conditions.
-
Cross-talk between IFN-γ and TWEAK through miR-149 amplifies skin inflammation in psoriasis
Part of Journal of Allergy and Clinical Immunology, p. 2225-2235, 2021.
DOI for Cross-talk between IFN-γ and TWEAK through miR-149 amplifies skin inflammation in psoriasis Download full text (pdf) of Cross-talk between IFN-γ and TWEAK through miR-149 amplifies skin inflammation in psoriasis
-
Cutaneous squamous cell carcinoma-derived extracellular vesicles exert an oncogenic role by activating cancer-associated fibroblasts
Part of Cell Death Discovery, 2023.
DOI for Cutaneous squamous cell carcinoma-derived extracellular vesicles exert an oncogenic role by activating cancer-associated fibroblasts Download full text (pdf) of Cutaneous squamous cell carcinoma-derived extracellular vesicles exert an oncogenic role by activating cancer-associated fibroblasts
-
Differential expression of D-type cyclins in HaCaT keratinocytes and in psoriasis.
Part of Journal of Investigative Dermatology, p. 634-42, 2008.
DOI for Differential expression of D-type cyclins in HaCaT keratinocytes and in psoriasis.
-
Differentiation-regulated expression of Toll-like receptors 2 and 4 in HaCaT keratinocytes.
Part of Archives of Dermatological Research, p. 120-4, 2004.
DOI for Differentiation-regulated expression of Toll-like receptors 2 and 4 in HaCaT keratinocytes.
-
Distinct strains of Propionibacterium acnes induce selective human beta-defensin-2 and interleukin-8 expression in human keratinocytes through toll-like receptors.
Part of Journal of Investigative Dermatology, p. 931-8, 2005.
-
Dithranol upregulates IL-10 receptors on the cultured human keratinocyte cell line HaCaT.
Part of Inflammation Research, p. 44-9, 2001.
DOI for Dithranol upregulates IL-10 receptors on the cultured human keratinocyte cell line HaCaT.
-
EGFR/Ras-induced CCL20 production modulates the tumour microenvironment.
Part of British Journal of Cancer, p. 942-954, 2020.
DOI for EGFR/Ras-induced CCL20 production modulates the tumour microenvironment.
-
Expression and function of Toll-like receptors 2 and 4 in human keratinocytes.
Part of International Immunology, p. 721-30, 2003.
DOI for Expression and function of Toll-like receptors 2 and 4 in human keratinocytes.
-
Genome-Wide Screen for MicroRNAs Reveals a Role for miR-203 in Melanoma Metastasis.
Part of Journal of Investigative Dermatology, p. 882-892, 2018.
DOI for Genome-Wide Screen for MicroRNAs Reveals a Role for miR-203 in Melanoma Metastasis.
-
Hemese, a hemocyte-specific transmembrane protein, affects the cellular immune response in Drosophila.
Part of Proceedings of the National Academy of Sciences of the United States of America, p. 2622-7, 2003.
-
Histidine decarboxylase expression in human melanoma.
Part of Journal of Investigative Dermatology, p. 345-52, 2000.
DOI for Histidine decarboxylase expression in human melanoma.
-
Human adult epidermal melanocytes cultured without chemical mitogens express the EGF receptor and respond to EGF.
Part of Archives of Dermatological Research, p. 191-200, 2007.
-
Identification and characterization of a novel, psoriasis susceptibility-related noncoding RNA gene, PRINS.
Part of Journal of Biological Chemistry, p. 24159-67, 2005.
-
Identification of novel non-coding RNA-based negative feedback regulating the expression of the oncogenic transcription factor GLI1.
Part of Molecular Oncology, p. 912-26, 2014.
-
IL-31: a new link between T cells and pruritus in atopic skin inflammation.
Part of Journal of Allergy and Clinical Immunology, p. 411-7, 2006.
DOI for IL-31: a new link between T cells and pruritus in atopic skin inflammation.
-
Innate immune functions of the keratinocytes. A review.
Part of Acta microbiologica et immunologica Hungarica, p. 303-10, 2004.
DOI for Innate immune functions of the keratinocytes. A review.
-
Interleukin-8 is regulated by miR-203 at the posttranscriptional level in primary human keratinocytes.
Part of EJD. European journal of dermatology, 2013.
-
Microbial compounds induce the expression of pro-inflammatory cytokines, chemokines and human beta-defensin-2 in vaginal epithelial cells.
Part of Microbes and infection, p. 1117-27, 2005.
-
MicroRNA-125b down-regulates matrix metallopeptidase 13 and inhibits cutaneous squamous cell carcinoma cell proliferation, migration, and invasion.
Part of Journal of Biological Chemistry, p. 29899-908, 2012.
-
MicroRNA-132 enhances transition from inflammation to proliferation during wound healing.
Part of Journal of Clinical Investigation, p. 3008-26, 2015.
DOI for MicroRNA-132 enhances transition from inflammation to proliferation during wound healing.
-
MicroRNA-132 with Therapeutic Potential in Chronic Wounds.
Part of Journal of Investigative Dermatology, p. 2630-2638, 2017.
DOI for MicroRNA-132 with Therapeutic Potential in Chronic Wounds.
-
MicroRNA-146a suppresses IL-17-mediated skin inflammation and is genetically associated with psoriasis.
Part of Journal of Allergy and Clinical Immunology, p. 550-561, 2017.
-
MicroRNA-203 Inversely Correlates with Differentiation Grade, Targets c-MYC, and Functions as a Tumor Suppressor in cSCC.
Part of Journal of Investigative Dermatology, p. 2485-2494, 2016.
-
MicroRNA-31 is overexpressed in psoriasis and modulates inflammatory cytokine and chemokine production in keratinocytes via targeting serine/threonine kinase 40.
Part of Journal of Immunology, p. 678-88, 2013.
-
MicroRNA-31 Promotes Skin Wound Healing by Enhancing Keratinocyte Proliferation and Migration.
Part of Journal of Investigative Dermatology, p. 1676-1685, 2015.
-
MicroRNAs and immunity: novel players in the regulation of normal immune function and inflammation.
Part of Seminars in Cancer Biology, p. 131-40, 2008.
-
microRNAs in inflammation.
Part of International Reviews of Immunology, p. 535-61, 2009.
-
MicroRNAs: novel regulators in skin inflammation.
Part of Clincal and Experimental Dermatology, p. 312-5, 2008.
-
miR ‐378a regulates keratinocyte responsiveness to interleukin‐17A in psoriasis
Part of British Journal of Dermatology, p. 211-222, 2022.
DOI for miR ‐378a regulates keratinocyte responsiveness to interleukin‐17A in psoriasis Download full text (pdf) of miR ‐378a regulates keratinocyte responsiveness to interleukin‐17A in psoriasis
-
MiR-125b, a microRNA downregulated in psoriasis, modulates keratinocyte proliferation by targeting FGFR2.
Part of Journal of Investigative Dermatology, p. 1521-9, 2011.
-
MiR-130a Acts as a Tumor Suppressor MicroRNA in Cutaneous Squamous Cell Carcinoma and Regulates the Activity of the BMP/SMAD Pathway by Suppressing ACVR1
Part of Journal of Investigative Dermatology, p. 1922-1931, 2021.
DOI for MiR-130a Acts as a Tumor Suppressor MicroRNA in Cutaneous Squamous Cell Carcinoma and Regulates the Activity of the BMP/SMAD Pathway by Suppressing ACVR1 Download full text (pdf) of MiR-130a Acts as a Tumor Suppressor MicroRNA in Cutaneous Squamous Cell Carcinoma and Regulates the Activity of the BMP/SMAD Pathway by Suppressing ACVR1
-
MiR-146a negatively regulates TLR2-induced inflammatory responses in keratinocytes.
Part of Journal of Investigative Dermatology, p. 1931-1940, 2014.
DOI for MiR-146a negatively regulates TLR2-induced inflammatory responses in keratinocytes.
-
MiR-155 is overexpressed in patients with atopic dermatitis and modulates T-cell proliferative responses by targeting cytotoxic T lymphocyte-associated antigen 4.
Part of Journal of Allergy and Clinical Immunology, p. 581-9.e1, 2010.
-
miR-193b/365a cluster controls progression of epidermal squamous cell carcinoma.
Part of Carcinogenesis, p. 1110-20, 2014.
DOI for miR-193b/365a cluster controls progression of epidermal squamous cell carcinoma.
-
miR-19a/b and miR-20a promote wound healing by regulating the inflammatory response of keratinocytes
Part of Journal of Investigative Dermatology, p. 659-671, 2021.
DOI for miR-19a/b and miR-20a promote wound healing by regulating the inflammatory response of keratinocytes Download full text (pdf) of miR-19a/b and miR-20a promote wound healing by regulating the inflammatory response of keratinocytes
-
MiR-21 is up-regulated in psoriasis and suppresses T cell apoptosis.
Part of Experimental dermatology, p. 312-4, 2012.
DOI for MiR-21 is up-regulated in psoriasis and suppresses T cell apoptosis.
-
MYCN-regulated microRNAs repress estrogen receptor-alpha (ESR1) expression and neuronal differentiation in human neuroblastoma.
Part of Proceedings of the National Academy of Sciences of the United States of America, p. 1553-8, 2010.
-
Negative regulatory effect of histamine in DNFB-induced contact hypersensitivity.
Part of International Immunology, p. 1781-8, 2004.
DOI for Negative regulatory effect of histamine in DNFB-induced contact hypersensitivity.
-
Next-Generation Sequencing Identifies the Keratinocyte-Specific miRNA Signature of Psoriasis.
Part of Journal of Investigative Dermatology, p. 2547-2550.e12, 2019.
-
Proliferating keratinocytes are putative sources of the psoriasis susceptibility-related EDA+ (extra domain A of fibronectin) oncofetal fibronectin.
Part of Journal of Investigative Dermatology, p. 537-46, 2004.
-
Propionibacterium acnes and lipopolysaccharide induce the expression of antimicrobial peptides and proinflammatory cytokines/chemokines in human sebocytes.
Part of Microbes and infection, p. 2195-205, 2006.
-
Protein kinase C-dependent upregulation of miR-203 induces the differentiation of human keratinocytes
Part of Journal of Investigative Dermatology, p. 124-134, 2010.
-
Serum factors regulate the expression of the proliferation-related genes alpha5 integrin and keratin 1, but not keratin 10, in HaCaT keratinocytes.
Part of Archives of Dermatological Research, p. 206-13, 2001.
-
The expression of keratinocyte growth factor receptor (FGFR2-IIIb) correlates with the high proliferative rate of HaCaT keratinocytes.
Part of Experimental dermatology, p. 596-605, 2006.
-
The expression of microRNA-203 during human skin morphogenesis.
Part of Experimental dermatology, p. 854-6, 2010.
DOI for The expression of microRNA-203 during human skin morphogenesis.
-
The human antimicrobial peptide LL-37 suppresses apoptosis in keratinocytes.
Part of Journal of Investigative Dermatology, p. 937-44, 2009.
DOI for The human antimicrobial peptide LL-37 suppresses apoptosis in keratinocytes.
-
The Long Noncoding RNA LINC00958 Is Induced in Psoriasis Epidermis and Modulates Epidermal Proliferation
Part of Journal of Investigative Dermatology, p. 999-1010, 2023.
-
The role of innate immunity in the pathogenesis of acne.
Part of Dermatology, p. 96-105, 2003.
DOI for The role of innate immunity in the pathogenesis of acne.
-
Tofacitinib Represses the Janus Kinase-Signal Transducer and Activators of Transcription Signalling Pathway in Keratinocytes.
Part of Acta Dermato-Venereologica, p. 772-775, 2018.
-
Toll-like receptor 9-independent suppression of skin inflammation by oligonucleotides.
Part of Journal of Investigative Dermatology, p. 746-8, 2007.
DOI for Toll-like receptor 9-independent suppression of skin inflammation by oligonucleotides.
-
Tumor immune escape by the loss of homeostatic chemokine expression.
Part of Proceedings of the National Academy of Sciences of the United States of America, p. 19055-60, 2007.
DOI for Tumor immune escape by the loss of homeostatic chemokine expression.