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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  <identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/11493</identifier>
  <creators>
    <creator>
      <creatorName>Dincer, Tuba</creatorName>
      <givenName>Tuba</givenName>
      <familyName>Dincer</familyName>
      <affiliation>Karadeniz Tech Univ, Fac Med, Dept Med Biol, TR-61080 Trabzon, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Er, Asiye Busra Boz</creatorName>
      <givenName>Asiye Busra Boz</givenName>
      <familyName>Er</familyName>
      <affiliation>Karadeniz Tech Univ, Inst Hlth Sci, Dept Med Biol, TR-61080 Trabzon, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Er, Idris</creatorName>
      <givenName>Idris</givenName>
      <familyName>Er</familyName>
      <affiliation>Karadeniz Tech Univ, Inst Hlth Sci, Dept Med Biol, TR-61080 Trabzon, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Toraman, Bayram</creatorName>
      <givenName>Bayram</givenName>
      <familyName>Toraman</familyName>
      <affiliation>Karadeniz Tech Univ, Fac Med, Dept Med Biol, TR-61080 Trabzon, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Yildiz, Gokhan</creatorName>
      <givenName>Gokhan</givenName>
      <familyName>Yildiz</familyName>
      <affiliation>Karadeniz Tech Univ, Fac Med, Dept Med Biol, TR-61080 Trabzon, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Kalay, Ersan</creatorName>
      <givenName>Ersan</givenName>
      <familyName>Kalay</familyName>
      <affiliation>Karadeniz Tech Univ, Fac Med, Dept Med Biol, TR-61080 Trabzon, Turkey</affiliation>
    </creator>
  </creators>
  <titles>
    <title>Ripk4 Suppresses The Tgf-Beta 1 Signaling Pathway In Hacat Cells</title>
  </titles>
  <publisher>Aperta</publisher>
  <publicationYear>2020</publicationYear>
  <dates>
    <date dateType="Issued">2020-01-01</date>
  </dates>
  <resourceType resourceTypeGeneral="Text">Journal article</resourceType>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/11493</alternateIdentifier>
  </alternateIdentifiers>
  <relatedIdentifiers>
    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1002/cbin.11282</relatedIdentifier>
  </relatedIdentifiers>
  <rightsList>
    <rights rightsURI="http://www.opendefinition.org/licenses/cc-by">Creative Commons Attribution</rights>
    <rights rightsURI="info:eu-repo/semantics/openAccess">Open Access</rights>
  </rightsList>
  <descriptions>
    <description descriptionType="Abstract">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.</description>
  </descriptions>
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