The effects of calcium on NF-KB pathway in hacat cells containing connexin26 kid syndrome mutations
tarafından
Yaşarbaş, Sümeyye Şüheda, author.
Başlık
:
The effects of calcium on NF-KB pathway in hacat cells containing connexin26 kid syndrome mutations
Yazar
:
Yaşarbaş, Sümeyye Şüheda, author.
Yazar Ek Girişi
:
Yaşarbaş, Sümeyye Şüheda, author.
Fiziksel Tanımlama
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xiii, 64 leaves: illustrarions, charts; 29 cm + 1 computer laser optical disc.
Özet
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Keratitis-ichthyosis-deafness (KID) syndrome is a rare genetic disorder characterized by deafness, corneal defects, and thickened, scaly skin and associated with mutations in Connexin26 (Cx26), resulting in the formation of hyperactive hemichannels that disrupt calcium (Ca2+) transfer. Ca2+ is crucial for normal epidermal cell function and may contribute to characteristics of KID syndrome. While unregulated Ca2+transfer through aberrant Cx26 hemichannels is known to impact keratinocyte proliferation and differentiation, the specific mechanisms remained unclear. An increase in the molecules associated with the nuclear factor-κB (NF-κB) signaling pathway was observed in the D50Y mutation of KID syndrome. This suggests that Cx26 mutant channels may disrupt keratinocyte physiology through NF-κB signaling. Our study hypothesizes that Ca2+ signals altered due to Cx26 mutations affect the NF-κB pathway, potentially contributing to KID syndrome by modifying keratinocyte cell physiology. Our study showed that NF-κB activation significantly increased in D50Y cells, linked to hyperproliferation and activation was dependent on intracellular Ca2+. This was associated with increased p65 activation and nuclear localization due to hyperactive Cx26 channels in D50Y cells. These findings reveal a direct link between aberrant Ca2+transport through Cx26 channels due to the D50Y mutation and NF-κB activation, shedding light on the hyperproliferative characteristics of Cx26 D50Y KID syndrome. Our goal was to understand how Ca2+ mechanisms impact the NF-κB pathway, potentially altering the physiology of keratinocytes expressing D50Y and G45E mutations. This research offers insights into the potential targeting of the NF-κB pathway for treating KID syndrome caused by Cx26 mutations.
Konu Başlığı
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Gap junctions (Cell biology)
Connexins
Yazar Ek Girişi
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Meşe Özçivici, Gülistan,
Tüzel Kişi Ek Girişi
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İzmir Institute of Technology. Molekular Biology and Genetics.
Tek Biçim Eser Adı
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Thesis (Masterl)-- İzmir Institute of Technology: Molekular Biology and Genetics.
İzmir Institute of Technology: Molekular Biology and Genetics. (Master)
Elektronik Erişim
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Library | Materyal Türü | Demirbaş Numarası | Yer Numarası | Durumu/İade Tarihi |
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IYTE Library | Tez | T002898 | QH603.C4 Y29 2023 | Tez Koleksiyonu |