1 Ocak 2020 Dergi makalesi Açık Erişim

Dincer, Tuba; Er, Asiye Busra Boz; Er, Idris; Toraman, Bayram; Yildiz, Gokhan; Kalay, Ersan

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<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Dincer, Tuba</dc:creator>
  <dc:creator>Er, Asiye Busra Boz</dc:creator>
  <dc:creator>Er, Idris</dc:creator>
  <dc:creator>Toraman, Bayram</dc:creator>
  <dc:creator>Yildiz, Gokhan</dc:creator>
  <dc:creator>Kalay, Ersan</dc:creator>
  <dc:date>2020-01-01</dc:date>
  <dc:description>Receptor-interacting serine/threonine kinase 4 (RIPK4) and transforming growth factor-beta 1 (TGF-beta 1) play critical roles in the development and maintenance of the epidermis. A negative correlation between the expression patterns of RIPK4 and TGF-beta signaling during epidermal homeostasis-related events and suppression of RIPK4 expression by TGF-beta 1 in keratinocyte cell lines suggest the presence of a negative regulatory loop between the two factors. So far, RIPK4 has been shown to regulate nuclear factor-kappa B (NF-kappa B), protein kinase C (PKC), wingless-type MMTV integration site family (Wnt), and (mitogen-activated protein kinase) MAPK signaling pathways. In this study, we examined the effect of RIPK4 on the canonical Smad-mediated TGF-beta 1 signaling pathway by using the immortalized human keratinocyte HaCaT cell line. According to our results, RIPK4 inhibits intracellular Smad-mediated TGF-beta 1 signaling events through suppression of TGF-beta 1-induced Smad2/3 phosphorylation, which is reflected in the upcoming intracellular events including Smad2/3-Smad4 interaction, nuclear localization, and TGF-beta 1-induced gene expression. Moreover, the kinase activity of RIPK4 is required for this process. The in vitro wound-scratch assay demonstrated that RIPK4 suppressed TGF-beta 1-mediated wound healing through blocking TGF-beta 1-induced cell migration. In conclusion, our results showed the antagonistic effect of RIPK4 on TGF-beta 1 signaling in keratinocytes for the first time and have the potential to contribute to the understanding and treatment of skin diseases associated with aberrant TGF-beta 1 signaling.</dc:description>
  <dc:identifier>https://aperta.ulakbim.gov.trrecord/11493</dc:identifier>
  <dc:identifier>oai:zenodo.org:11493</dc:identifier>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:rights>http://www.opendefinition.org/licenses/cc-by</dc:rights>
  <dc:source>CELL BIOLOGY INTERNATIONAL 44(3) 848-860</dc:source>
  <dc:title>RIPK4 suppresses the TGF-beta 1 signaling pathway in HaCaT cells</dc:title>
  <dc:type>info:eu-repo/semantics/article</dc:type>
  <dc:type>publication-article</dc:type>
</oai_dc:dc>