Involvement of P38 MAP kinase in the augmentation of UVB-mediated apoptosis via the epidermal platelet-activating factor receptor.

Involvement of P38 MAP kinase in the augmentation of UVB-mediated apoptosis via the epidermal platelet-activating factor receptor. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Involvement of P38 MAP kinase in the augmentation of UVB-mediated apoptosis via the epidermal platelet-activating factor receptor. Abstract Text:

Megan Landis,Qiaofang Yi,Ann-Marie Hyatt,Angela R Travers,Davina A Lewis,Jeffrey B Travers,

Platelet-activating factor (PAF) is a group of phosphocholines with various biological effects, which are mediated by the PAF receptor (PAF-R). Our previous studies have demonstrated that ultraviolet B radiation (UVB) is a potent stimulus for PAF production, and that the presence of the PAF-R on epithelial cells results in an augmentation of UVB-induced apoptosis. Inasmuch as PAF-R activation results in numerous signal transduction pathways, the present study was designed to characterize the signal transduction pathway responsible for PAF-R-mediated enhanced UVB-induced cytotoxicity. Using a model system of PAF-R-negative and -positive epithelioid KB cells, we demonstrate that inhibitors of p38 MAP kinase block the augmentation of UVB-mediated apoptosis seen in PAF-R-positive KB cells. In contrast, pharmacological and/or molecular inhibition of other pathways linked to PAF-R activation including ERK MAP kinase and NFkappaB do not affect PAF-R-mediated cytotoxicity. This study demonstrates the important role that p38 MAP kinase plays in PAF-R-mediated augmentation of UVB cytotoxicity.

Involvement of P38 MAP kinase in the augmentation of UVB-mediated apoptosis via the epidermal platelet-activating factor receptor. Publishing Authors By Initials

M Landis,Q Yi,AM Hyatt,AR Travers,DA Lewis,JB Travers,

For similar enzymes and coenzymes: enzymes: transferases: phosphotransferases: phosphotransferases (alcohol group acceptor): protein kinases: protein-serine-threonine kinases: mitogen-activated protein kinases: p38 mitogen-activated protein kinases research abstracts see: enzymes and coenzymes: enzymes: transferases: phosphotransferases: phosphotransferases (alcohol group acceptor): protein kinases: protein-serine-threonine kinases: mitogen-activated protein kinases: p38 mitogen-activated protein kinases research

PUBMED ID PMID:

MEDLINE DATE:

Involvement of P38 MAP kinase in the augmentation of UVB-mediated apoptosis via the epidermal platelet-activating factor receptor. Journal Published:

PUBLICATION TYPE: Research Support, U.S. Gov't,

Journal: Archives of dermatological research

VOLUME: 299

Page Numbers: 263-6

Journal Abbreviation: Arch. Dermatol. Res.

ISSN: 0340-3696

DAY: 17

MONTH: 04

YEAR: 2007

Involvement of P38 MAP kinase in the augmentation of UVB-mediated apoptosis via the epidermal platelet-activating factor receptor. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8000462

Involvement of P38 MAP kinase in the augmentation of UVB-mediated apoptosis via the epidermal platelet-activating factor receptor. Keywords Mesh Terms:

KEYWORDS: p38 Mitogen-Activated Protein Kinases

MESH TERMS: metabolism

Chemical & Substance for Abstract: Involvement of P38 MAP kinase in the augmentation of UVB-mediated apoptosis via the epidermal platelet-activating factor receptor. Information

Substance Name: p38 Mitogen-Activated Protein Kinases

Registry Number: EC 2.7.1.37

Grant and Affiliation Information for Involvement of P38 MAP kinase in the augmentation of UVB-mediated apoptosis via the epidermal platelet-activating factor receptor.

AFFILIATION: Department of Dermatology, H. B. Wells Center for Pediatric Research, James Whitcomb Riley Hospital for Children, Indiana University School of Medicine, Indianapolis, IN 46202, USA.

Country: Germany

AGENCY: United States NIAID

GRANT: U19 AI070448

ACRONYM: AI

MEDLINETA: Arch Dermatol Res

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Involvement of P38 MAP kinase in the augmentation of UVB-mediated apoptosis via the epidermal platelet-activating factor receptor Related Publications

• A Drosophila Smyd4 homologue is a muscle-specific transcriptional modulator involved in development.
• A variable topology for the 30-nm chromatin fibre.
• Activation of platelet-activating factor receptor in SZ95 sebocytes results in inflammatory cytokine and prostaglandin E2 production.
• An assessment of toxicity in profundal lake sediment due to deposition of heavy metals and persistent organic pollutants from the atmosphere.
• Case report: thyroid hormone resistance and its therapeutic challenges.
• Contrast-medium-induced electrocardiographic abnormalities: comparison of bolus and infusion of methylglucamine iodamide and methylglucamine/sodium diatrizoate.
• Current incidence of N-nitrosodimethylamine in beers worldwide.
• Differential effects of aging on processes underlying task switching.
• Does this patient meet the criteria for emergency severity index level 2?
• Double-blind clinical trial of topical steroids in anterior uveitis.
• High-affinity DNA binding sites for H-NS provide a molecular basis for selective silencing within proteobacterial genomes.
• Identification of the HLA-DM/HLA-DR interface.
• Involvement of P38 MAP kinase in the augmentation of UVB-mediated apoptosis via the epidermal platelet-activating factor receptor.
• Licking and gaping elicited by microstimulation of the nucleus of the solitary tract.
• Moxifloxacin-associated drug hypersensitivity syndrome with toxic epidermal necrolysis and fulminant hepatic failure.
• Perforation of intestine by fishbone.
• Reflex topography in the nucleus of the solitary tract.
• SUPPRESSION OF VISION IN SQUINT AND ITS ASSOCIATION WITH RETINAL CORRESPONDENCE AND AMBLYOPIA.
• Single neurons in the nucleus of the solitary tract respond selectively to bitter taste stimuli.
• Supercontinuum generation in a water-core photonic crystal fiber.
• THE ORIGIN OF ABNORMAL RETINAL CORRESPONDENCE.
• Taste-evoked Fos expression in nitrergic neurons in the nucleus of the solitary tract and reticular formation of the rat.
• The chromatin remodelling factor dATRX is involved in heterochromatin formation.
• Tracking the temporal dynamics of updating cognitive control: an examination of error processing.
• Tramtrack69 interacts with the dMi-2 subunit of the Drosophila NuRD chromatin remodelling complex.
• Two modes of degradation of the tramtrack transcription factors by siah homologues.
• UVB radiation-mediated inhibition of contact hypersensitivity reactions is dependent on the platelet-activating factor system.