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Tieg3/Klf11 induces apoptosis in OLI-neu cells and enhances the TGF-beta signaling pathway by transcriptional repression of Smad7.
J Cell Biochem. 2008 Jun 01; 104(3):850-61.JC

Abstract

TGF-beta signaling is indispensible for development of the nervous system since it regulates ontogenetic cell death. The recently identified TGF-beta-inducible zinc finger protein Tieg3/Klf11 belongs to the family of Sp1/Klf-like transcription factors and shares all structural and functional features with other Tieg proteins. Using the established TGF-beta-responsive oligodendroglial cell line OLI-neu, we analyzed the role of Tieg3/Klf11 in TGF-beta signaling. In this report, we show that Tieg3/Klf 11 mimics TGF-beta effects by inducing apoptotic cell death accompanied by activation of caspase-3. Moreover, we demonstrate that Tieg3/Klf11 enhances TGF-beta signaling by transcriptional repression of the inhibitory Smad7 and, thereby, disrupts the negative feedback loop of the TGF-beta signaling pathway. Loss of the N-terminal repression domains of Tieg3/Klf11 abrogates the pro-apoptotic nature of this transcription factor and abolishes the enhancement of Smad-mediated TGF-beta responses. In conclusion, we provide evidence that the recently identified transcription factor Tieg3/Klf11 is a downstream mediator of TGF-beta-induced apoptosis in the oligodendroglial cell line OLI-neu. Since other signaling molecules are able to initiate transcription of members of the Tieg family, the ability of Tieg3/Klf11 to modulate TGF-beta signaling by transcriptional inhibition of Smad7 might be an important clue for the understanding of the crosstalk between different signaling pathways.

Authors+Show Affiliations

Department of Neuroanatomy, Center of Anatomy, Georg-August-University of Göttingen, Göttingen, Germany.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18189266

Citation

Gohla, Gabriele, et al. "Tieg3/Klf11 Induces Apoptosis in OLI-neu Cells and Enhances the TGF-beta Signaling Pathway By Transcriptional Repression of Smad7." Journal of Cellular Biochemistry, vol. 104, no. 3, 2008, pp. 850-61.
Gohla G, Krieglstein K, Spittau B. Tieg3/Klf11 induces apoptosis in OLI-neu cells and enhances the TGF-beta signaling pathway by transcriptional repression of Smad7. J Cell Biochem. 2008;104(3):850-61.
Gohla, G., Krieglstein, K., & Spittau, B. (2008). Tieg3/Klf11 induces apoptosis in OLI-neu cells and enhances the TGF-beta signaling pathway by transcriptional repression of Smad7. Journal of Cellular Biochemistry, 104(3), 850-61. https://doi.org/10.1002/jcb.21669
Gohla G, Krieglstein K, Spittau B. Tieg3/Klf11 Induces Apoptosis in OLI-neu Cells and Enhances the TGF-beta Signaling Pathway By Transcriptional Repression of Smad7. J Cell Biochem. 2008 Jun 1;104(3):850-61. PubMed PMID: 18189266.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Tieg3/Klf11 induces apoptosis in OLI-neu cells and enhances the TGF-beta signaling pathway by transcriptional repression of Smad7. AU - Gohla,Gabriele, AU - Krieglstein,Kerstin, AU - Spittau,Björn, PY - 2008/1/15/pubmed PY - 2008/9/23/medline PY - 2008/1/15/entrez SP - 850 EP - 61 JF - Journal of cellular biochemistry JO - J Cell Biochem VL - 104 IS - 3 N2 - TGF-beta signaling is indispensible for development of the nervous system since it regulates ontogenetic cell death. The recently identified TGF-beta-inducible zinc finger protein Tieg3/Klf11 belongs to the family of Sp1/Klf-like transcription factors and shares all structural and functional features with other Tieg proteins. Using the established TGF-beta-responsive oligodendroglial cell line OLI-neu, we analyzed the role of Tieg3/Klf11 in TGF-beta signaling. In this report, we show that Tieg3/Klf 11 mimics TGF-beta effects by inducing apoptotic cell death accompanied by activation of caspase-3. Moreover, we demonstrate that Tieg3/Klf11 enhances TGF-beta signaling by transcriptional repression of the inhibitory Smad7 and, thereby, disrupts the negative feedback loop of the TGF-beta signaling pathway. Loss of the N-terminal repression domains of Tieg3/Klf11 abrogates the pro-apoptotic nature of this transcription factor and abolishes the enhancement of Smad-mediated TGF-beta responses. In conclusion, we provide evidence that the recently identified transcription factor Tieg3/Klf11 is a downstream mediator of TGF-beta-induced apoptosis in the oligodendroglial cell line OLI-neu. Since other signaling molecules are able to initiate transcription of members of the Tieg family, the ability of Tieg3/Klf11 to modulate TGF-beta signaling by transcriptional inhibition of Smad7 might be an important clue for the understanding of the crosstalk between different signaling pathways. SN - 1097-4644 UR - https://www.unboundmedicine.com/medline/citation/18189266/Tieg3/Klf11_induces_apoptosis_in_OLI_neu_cells_and_enhances_the_TGF_beta_signaling_pathway_by_transcriptional_repression_of_Smad7_ L2 - https://doi.org/10.1002/jcb.21669 DB - PRIME DP - Unbound Medicine ER -