RGD Reference Report - Synthetic retinoid Am80 inhibits interaction of KLF5 with RAR alpha through inducing KLF5 dephosphorylation mediated by the PI3K/Akt signaling in vascular smooth muscle cells. - Rat Genome Database

Send us a Message



Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   

Synthetic retinoid Am80 inhibits interaction of KLF5 with RAR alpha through inducing KLF5 dephosphorylation mediated by the PI3K/Akt signaling in vascular smooth muscle cells.

Authors: Zhang, XH  Zheng, B  Han, M  Miao, SB  Wen, JK 
Citation: Zhang XH, etal., FEBS Lett. 2009 Apr 17;583(8):1231-6. Epub 2009 Mar 16.
RGD ID: 6771323
Pubmed: PMID:19292987   (View Abstract at PubMed)
DOI: DOI:10.1016/j.febslet.2009.03.016   (Journal Full-text)

Kruppel-like factor 5 (KLF5) is known to physically interact with retinoic acid receptor-alpha (RAR alpha). Here, we show that Am80 inhibited the interaction between KLF5 and RAR alpha and this inhibitory effect was accompanied by the dephosphorylation of KLF5 in VSMCs. Treating VSMCs with LY294002, the PI3K/Akt inhibitor, abrogated Am80-induced KLF5 dephosphorylation and reversed Am80-induced suppression of interaction between KLF5 and RAR alpha, whereas treating vascular smooth muscle cells (VSMCs) with SB203580, the p38 kinase inhibitor, attenuated the interaction between KLF5 and RAR alpha. Constitutively active p38 kinase MKK6b infection prevented the KLF5 dephosphorylation induced by Am80. In conclusion, Am80 induces KLF5 dephosphorylation by activating PI3K/Akt signaling, and inhibits KLF5 phosphorylation by blocking p38 signaling, subsequently leading to the suppression of interaction of KLF5 with RAR alpha.



Gene Ontology Annotations    Click to see Annotation Detail View

Molecular Function

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
RaraRattranscription factor binding  IPIKLF5 (Homo sapiens) RGD 

Objects Annotated

Genes (Rattus norvegicus)
Rara  (retinoic acid receptor, alpha)


Additional Information