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  • Küçük Resim
    Yayın
    Molecular mechanisms of heat shock proteins in distinct diseases
    (Scientific Scholar, 2023) Yürekli, Nazlıcan; Tutar, Merve; Niyazov, Laziz; Sağır, Fatma; Açıkalın Coşkun, Kübra; Al, Mervenur; Uçar Çifçi, Kezban; Abay, Cansu; Gök Yurttaş, Asiye; Okat, Zehra; Tutar, Yusuf; Asea, Alexzander A. A.; Kaur, Punit
    Heat shock proteins (HSPs) modulate the molecular mechanics of cells and cellular systems. Properly folded proteins are required for cellular processes and organisms use molecular mechanics to keep substrate proteins in their native state. Therefore, cellular compartments employ redundant isoforms of HSP to maintain substrate protein homeostasis and keep them functional. Hence, HSP folder function is critical for cell, HSPs are universally conserved. HSPs play essential roles in cellular signalling and in immune system besides their folder function. To this purpose, the roles of distinct HSP are described in this review to describe their molecular mechanisms in diseases.
  • Küçük Resim
    Yayın
    Role of p53 in human cancers
    (IntechOpen, 2022) Açıkalın Çoşkun, Kübra; Tutar, Merve; Al, Mervenur; Gök Yurttaş, Asiye; Abay, Elif Cansu; Yürekli, Nazlıcan; Yeman Kıyak, Bercem; Uçar, Kezban; Tutar, Yusuf; Anwar, Mumtaz
    TP53 codes tumor protein 53-p53 that controls the cell cycle through binding DNA directly and induces reversible cell-cycle arrest. The protein activates DNA repair genes if mutated DNA will be repaired or activates apoptotosis if the damaged DNA cannot be fixed. Therefore, p53, so-called the “guardian of the genome,” promote cell survival by allowing for DNA repair. However, the tumor-suppressor function of p53 is either lost or gained through mutations in half of the human cancers. In this work, functional perturbation of the p53 mechanism is elaborated at the breast, bladder, liver, brain, lung cancers, and osteosarcoma. Mutation of wild-type p53 not only diminishes tumor suppressor activity but transforms it into an oncogenic structure. Further, malfunction of the TP53 leads accumulation of additional oncogenic mutations in the cell genome. Thus, disruption of TP53 dependent survival pathways promotes cancer progression. This oncogenic TP53 promotes cell survival, prevents cell death through apoptosis, and contributes to the proliferation and metastasis of tumor cells. The purpose of this chapter is to discuss the contribution of mutant p53 to distinct cancer types.