OSMRβ mutants enhance basal keratinocyte differentiation via inactivation of the STAT5/KLF7 axis in PLCA patients

Protein Cell. 2021 Aug;12(8):653-661. doi: 10.1007/s13238-020-00818-3. Epub 2021 Jan 27.
No abstract available

Publication types

  • Letter
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amyloidosis, Familial / genetics*
  • Amyloidosis, Familial / metabolism
  • Amyloidosis, Familial / pathology
  • Animals
  • Base Sequence
  • Cell Differentiation
  • Disease Models, Animal
  • Gene Expression Profiling
  • Gene Expression Regulation
  • Gene Ontology
  • Humans
  • Keratinocytes / metabolism*
  • Keratinocytes / pathology
  • Kruppel-Like Transcription Factors / genetics*
  • Kruppel-Like Transcription Factors / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Molecular Sequence Annotation
  • Mutation
  • Oncostatin M / genetics*
  • Oncostatin M / metabolism
  • Oncostatin M Receptor beta Subunit / genetics*
  • Oncostatin M Receptor beta Subunit / metabolism
  • STAT5 Transcription Factor / genetics*
  • STAT5 Transcription Factor / metabolism
  • Signal Transduction
  • Skin / metabolism
  • Skin / pathology
  • Skin Diseases, Genetic / genetics*
  • Skin Diseases, Genetic / metabolism
  • Skin Diseases, Genetic / pathology

Substances

  • KLF7 protein, human
  • Kruppel-Like Transcription Factors
  • OSM protein, human
  • OSMR protein, human
  • Oncostatin M Receptor beta Subunit
  • STAT5 Transcription Factor
  • Oncostatin M

Supplementary concepts

  • Amyloidosis, Primary Cutaneous