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Type of publication: Journal Article
Type of document: Review

Year: 2008

Authors: Kornfeld, JW; Grebien, F; Kerenyi, MA; Friedbichler, K; Kovacic, B; Zankl, B; Hoelbl, A; Nivarti, H; Beug, H; Sexl, V; Muller, M; Kenner, L; Mullner, EW; Gouilleux, F; Moriggl, R

Title: The different functions of Stat5 and chromatin alteration through Stat5 proteins.

Source: Front Biosci. 2008; 13:6237-6254



Authors Vetmeduni Vienna:

Grebien Florian
Hölbl-Kovacic Andrea
Kenner Lukas
Kovacic Boris
Müller Mathias
Sexl Veronika

Vetmed Research Units
Institute of Animal Breeding and Genetics


Abstract:
Stat5 proteins modulate gene transcription upon cytokine- and growth factor action. Stat5a and Stat5b proteins alone are weak activators of transcription. They can modify chromatin organization through oligomerization and they act predominantly in co-operation and interaction with other proteins. The conservative view of exclusively nuclear functions of Stat5 was challenged by the observation of additional Stat5 effects in the cytoplasm, resulting in activation of the PI3K-Akt pathway. We summarize biological consequences of mutations in conserved domains of Stat5 or of deletions in the N- or C-terminal domains with impact on target gene transcription. Formation of higher-order oligomers is dramatically changed upon amino- or carboxyterminal deletions in Stat5 proteins. Mutations in or deletion of the Stat5 N-terminus leads to diminished leukemogenic potential of oncogenic Stat5, probably due to the inability to form Stat5 tetramers. The Stat5 N-terminal domain prevents persistent activation and can act as a DNA-docking platform for the glucocorticoid receptor (GR). The corresponding protocols should facilitate follow-up studies on Stat5 proteins and their contribution to normal physiological versus pathological processes through differential chromatin binding.

Keywords Pubmed: Animals
Autoimmune Diseases/physiopathology
Chromatin/physiology*
DNA/genetics
DNA/metabolism
Humans
Inflammation/physiopathology
Mice
Mice, Knockout
Models, Animal
Myeloproliferative Disorders/physiopathology
Neoplasms/physiopathology
Protein Isoforms/physiology
STAT5 Transcription Factor/deficiency
STAT5 Transcription Factor/genetics
STAT5 Transcription Factor/physiology*


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