mTORC2-dependent regulationof Gilz expression
Başlık çevirisi mevcut değil.
- Tez No: 706882
- Danışmanlar: PROF. KWON HYOCKMAN
- Tez Türü: Yüksek Lisans
- Konular: Biyoteknoloji, Biotechnology
- Anahtar Kelimeler: Belirtilmemiş.
- Yıl: 2018
- Dil: İngilizce
- Üniversite: Hankuk University of Foreign Studies
- Enstitü: Yurtdışı Enstitü
- Ana Bilim Dalı: Belirtilmemiş.
- Bilim Dalı: Belirtilmemiş.
- Sayfa Sayısı: 37
Özet
Özet yok.
Özet (Çeviri)
Rheumatoid arthritis (RA) is a systemic autoimmune inflammatory disorder affecting nearly 1% of the population and characterized by progressive joint destruction and bone erosion. Glucocorticoids (GCs), as the major medication to suppress the inflammation, are highly effective but come with severe side effects including but not limited to bone loss, diabetes mellitus, hypertension and infection. In search of alternative therapeutic strategies to avoid these detrimental side effects, GILZ, as the antiinflammatory effect mediator of GCs, and the mediator of bone anabolic actions, emerged as a potential target. These key functions of GILZ directed researchers to find a non-steroid drug inducing GILZ expression. In this study, a novel non-steroid compound called Mini2001 (Mini) was used to induce expression of GILZ independently from GC-induced pathway. Next-generation sequencing (NGS) results of adipose-derived stem cells (ADSCs) treated with glycosylated form of this compound, Hub3115 (Hub), showed increased expression of GILZ. Here, I tried to shed light to the mechanism behind Hub-induced GILZ expression. According to the data, GILZ expression is not only induced by Mini, but also induced synergistically by GC and Mini. Although Mini induces FoxO3 nuclear localization and its binding to FHRE, the interaction between FoxO3a and FHRE at GILZ promoter is not the primary reason for enhanced GILZ expression. Mini increases c-Myc phosphorylation at Ser62, but c-Myc protein level decreases progressively in a long-term Mini treatment. Phosphorylation of Ser62 of c-Myc activates c-Myc, and the GILZ promoter contains 2 three c-Myc binding sites. By considering the results, activation of c-Myc by phosphorylation and its-binding to c-Myc binding element on GILZ promoter may be the main reason for the enhanced GILZ expression and this effect of Mini is likely to be mediated by mTORC2 inhibition.
Benzer Tezler
- Temsirolimusun NCI-H1975 akciğer kanser hücrelerinde mTOR protein aktivitesi üzerine etkileri
Effects of temsirolimus on mTOR protein activity in NCI-H1975 lung cancer cells
BİRCAN ÖNEL
Yüksek Lisans
Türkçe
2015
BiyolojiAkdeniz ÜniversitesiBiyoloji Ana Bilim Dalı
YRD. DOÇ. DR. ESRA AYDEMİR
- CDK inhibitörlerinin mTOR susturması gerçekleştirilen LNCaP, DU145 ve PC3 prostat kanseri hücrelerinde terapotik etkisinin incelenmesi
Investigation of therapeutic effects of the CDK inhibitors on mTOR-silenced LNCaP, DU145 and PC3 prostate cancer cells
ÇAĞRI GÜMÜŞKAPTAN
Yüksek Lisans
Türkçe
2015
Biyokimyaİstanbul Kültür ÜniversitesiMoleküler Biyoloji ve Genetik Ana Bilim Dalı
DOÇ. DR. ELİF DAMLA ARISAN
- Sıçanlarda kronik rezistans egzersizinin indüklediği hipertrofide mTOR yolağına bağlı otofajinin rolü
The role of mTOR dependent autophagy pathway on chronic resistance exerciseinduced muscular hypertrophy in rats
TÜLİN ALTINOLUK
- Age-dependent changes in mtor/s6k1/srebp-1c signal pathway activation in rat liver tissues
Sıçan karaciğer dokularında mtor/s6k1/srebp-1c sinyal yolu aktivasyonunda yaşa bağımlı değişiklikler
MELTEM YALÇIN
Yüksek Lisans
İngilizce
2019
FizyolojiYeditepe ÜniversitesiFizyoloji Ana Bilim Dalı
DOÇ. DR. MEHTAP KAÇAR
- Detection of C-ABL tyrosine kinase and the mammalian target of rapamycin (MTOR) regulation in mouse oocyte maturation
Fare oosit maturasyonunda C-ABL tirozin kinaz ve memeli rapamisin hedefi (MTOR) düzenlenmesinin belirlenmesi
MELEK OBAIDEEN
Yüksek Lisans
İngilizce
2022
Histoloji ve EmbriyolojiYeditepe ÜniversitesiHistoloji ve Embriyoloji Ana Bilim Dalı
DOÇ. DR. AYLİN YABA UÇAR