The epidermal G1-chalone

an endogenous tissue-specific inhibitor of epidermal cell proliferation.

K. H. Richter, Matthias Clauss, W. Höfle, R. Schnapke, F. Marks

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

An apparently macromolecular factor is isolated from aqueous skin extracts which inhibits DNA synthesis in vivo and in vitro with high efficacy (ID50 in vivo 0.2 pmol/g, in vitro 0.2 pM) and in a highly specific manner showing a point of attack in the late G1-phase of the cell cycle (epidermal G1-chalone). Preliminary characterization indicates an unusual highly amphipathic structure consisting of amino acids and carbohydrate. Despite its apparent molecular weight of approximately 10 kD the chalone is stable against denaturing agents and most enzymes, including proteases. An inverse correlation between chalone responsiveness of mouse epidermis in vivo and the development of hyperplasia due to injury indicates an important role of the factor in the regulation of tissue homeostasis. According to its physicochemical and biological properties the epidermal G1-chalone appears not to be related to other endogenous inhibitors of epidermal cell proliferation such as the pentapeptide pyroGlu-Glu-Asp-Ser-GlyOH and transforming growth factor beta (TGF beta).

Original languageEnglish (US)
Pages (from-to)204-210
Number of pages7
JournalAnnals of the New York Academy of Sciences
Volume548
StatePublished - 1988
Externally publishedYes

Fingerprint

Chalones
Cell proliferation
Tissue homeostasis
Cell Proliferation
Tissue
G1 Phase
Epidermis
Transforming Growth Factor beta
Hyperplasia
Skin
Cell Cycle
Homeostasis
Peptide Hydrolases
Molecular Weight
Molecular weight
Cells
Carbohydrates
Amino Acids
DNA
Wounds and Injuries

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

The epidermal G1-chalone : an endogenous tissue-specific inhibitor of epidermal cell proliferation. / Richter, K. H.; Clauss, Matthias; Höfle, W.; Schnapke, R.; Marks, F.

In: Annals of the New York Academy of Sciences, Vol. 548, 1988, p. 204-210.

Research output: Contribution to journalArticle

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