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Apoptosis

Yıl 2023, Cilt: 49 Sayı: 1, 1 - 10, 10.04.2023
https://doi.org/10.35238/sufefd.1210651

Öz

Apoptosis is an energy-requiring physiological process known as programmed cell death, and apoptosis plays a critical role in embryological development and maintenance of adult tissues. Apoptosis, known as programmed cell death, is a mechanism that controls and destroys cells that the organism does not need, that have completed their biological task or that are damaged at the genetic level. Various diseases occur when the rate of apoptosis is impaired, slowed down or increased. The apoptosis process can be triggered by intracellular signals, such as genotoxic stress, or by extrinsic signals, such as ligands binding to cell surface death receptors. The mechanism of apoptosis involves various proteins and molecules. Deregulation in the mechanism of apoptotic cell death is the hallmark of cancer. Apoptosis alteration is responsible not only for tumor development and progression, but also for tumor resistance to treatments. Most anticancer drugs currently used in clinical oncology exploit intact apoptotic signaling pathways to induce cancer cell death. In this review, the effects of apoptosis on tumor-inducing and tumor suppressor genes and its functional properties in cancer are outlined.

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Apoptozis

Yıl 2023, Cilt: 49 Sayı: 1, 1 - 10, 10.04.2023
https://doi.org/10.35238/sufefd.1210651

Öz

Apoptoz, programlı hücre ölümü olarak bilinen enerji gerektiren fizyolojik bir süreçtir ayrıca apoptoz embriyolojik gelişim ve erişkin dokuların devamlılığında kritik rol oynar. Programlı hücre ölümü olarak bilinen apoptoz, organizmanın ihtiyaç duymadığı, biyolojik görevini tamamlamış ya da hasarlı hücreleri genetik düzeyde de kontrol ederek yok eden bir mekanizmadır. Apoptoz hızının bozulduğu, yavaşladığı veya arttığı durumlarda çeşitli hastalıklar ortaya çıkmaktadır. Apoptosis süreci genotoksik stres gibi hücre içinden gelen sinyaller veya ligandların hücre yüzeyi ölüm reseptörlerine bağlanması gibi dışsal sinyaller tarafından tetiklenebilir. Apoptosis mekanizması, çeşitli proteinleri ve molekülleri içerir. Apoptotik hücre ölümü mekanizmasındaki kuralsızlaştırma, kanserin ayırt edici özelliğidir. Apoptoz değişikliği sadece tümör gelişimi ve ilerlemesinden değil, aynı zamanda tedavilere karşı tümör direncinden de sorumludur. Şu anda klinik onkolojide kullanılan çoğu antikanser ilacı, kanser hücresi ölümünü tetiklemek için bozulmamış apoptotik sinyal yollarından yararlanır. Bu derlemede, apoptosisin tümör indükleyici ve ayrıca tümör baskılayıcı genlerdeki etkileri ve kanserdeki fonksiyonel özellikleri genel hatlarıyla ifade edilmiştir.

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  • Thornborrow, E. C., Patel, S., Mastropietro, A. E., Schwartzfarb, E. M., Manfredi, J. J. (2002). A conserved intronic response element mediates direct p53‐dependent transcriptional activation of both the human and murine bax gene. Oncogene, 21, 990‐ 999.
  • Tinel, A., Tschopp, J. (2004). The PIDDosome, a protein complex implicated in activation of caspase-2 in response to genotoxic stress. Science, 304, 843–46 [PubMed: 15073321]
  • Tomita, Y., Marchenko, N., Erster, S., Nemajerova, A., Dehner, A., Klein, C., Pan, H., Kessler, H., Pancoska, P., Moll, U. M. (2006). WT p53, but not tumor‐derived mutants, bind to Bcl2 via the DNA binding domain and induce mitochondrial permeabilization. JBC, 281, 8600–8606.
  • Tourneur, L., Buzyn, A., Chiocchia, G. (2005). FADD adaptor in cancer. Med Immunol., 4, 1.
  • Tourneur, L., Delluc, S., Levy, V., Valesi, F., Radford‐Weiss, I., Legrand, O., Vargftig, J., Boix, C., Macintyre, E. A., Varet, B., Chiocchia, G., Buzyn, A. (2004). Absence or low expression of fas‐associated protein with death domain in acute myeloid leukemia cells predicts resistance to chemotherapy and poor outcome. Cancer Res., 64, 8101‐8108.
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  • Van Opdenbosch, N., Van Gorp, H., Verdonckt, M., Saavedra, P. H. V., Vasconcelos, N. M. (2017). Caspase-1 engagement and TLR-induced c-FLIP expression suppress ASC/caspase-8-dependent apoptosis by inflammasome sensors NLRP1b and NLRC4. Cell Rep., 21, 3427–44 [PubMed:29262324]
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  • Wang, J., Chun, H. J., Wong, W. (2001). Caspase-10 is an initiator caspase in death receptor signaling. Proceedings of the National Academy of Sciences of the United States of America, 98, 13884–13888. https://doi.org/10.1073/pnas.241358198.
  • Wang, C., ve Youle, R. J. (2009). The role of mitochondria in apoptosis. Annual Review of Genetics, 43, 95–118.
  • Wang, X. J., Cao, Q., Zhang, Y., Su, X. D. (2015). Activation and regulation of caspase-6 and its role in neurodegenerative diseases. Annu. Rev. Pharmacol. Toxicol, 55:553–72 [PubMed: 25340928]
  • Watanabe, A., Yasuhira, S., Inoue, T., Kasai, S., Shibazaki, M., Takahashi, K., Akasaka, T., Masuda, T., Maesawa, C. (2013). BCL2 and BCLxL are key determinants of resistance to antitubulin chemotherapeutics in melanoma cells. Exp Dermatol., 22, 518‐523.
  • Williams, J., Lucas, P. C., Griffith, K. A., Choi, M., Fogoros, S., Hu, Y. Y., Liu, J. R. (2005). Expression of Bcl‐xL in ovarian carcinoma is associated with chemoresistance and recurrent disease. Gynecol Oncol., 96, 287‐295.
  • Wong, R. S. Y. (2011). Apoptosis in cancer: from pathogenesis to treatment. JECCR, 30:87.
  • Wu, G. S., Burns, T. F., McDonald III, E. R., Jiang, W., Meng, R., Krantz, I. D., Kao, G., Gan, D. D., Zhou, J. Y., Muschel, R., Hamilton, S. R., Spinner, N. B., Matkowitz, S. (1997). KILLER/DR5 is a DNA damage‐induced p53‐regulated death receptor gene. Nat Genet., 17, 141‐143.
  • Yu, J., Wang, Z., Kinzler, K. W., Vogelstein, B., Zhang, L. (2003). PUMA mediates the apoptotic response to p53 in colorectal cancer cells. Proc Natl Acad Sci USA., 100, 1931‐1936.
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Toplam 131 adet kaynakça vardır.

Ayrıntılar

Birincil Dil Türkçe
Konular Yapısal Biyoloji
Bölüm Derleme Makaleleri
Yazarlar

Derya Babacan 0000-0001-6758-8556

Yayımlanma Tarihi 10 Nisan 2023
Gönderilme Tarihi 27 Kasım 2022
Yayımlandığı Sayı Yıl 2023 Cilt: 49 Sayı: 1

Kaynak Göster

APA Babacan, D. (2023). Apoptozis. Selçuk Üniversitesi Fen Fakültesi Fen Dergisi, 49(1), 1-10. https://doi.org/10.35238/sufefd.1210651
AMA Babacan D. Apoptozis. sufefd. Nisan 2023;49(1):1-10. doi:10.35238/sufefd.1210651
Chicago Babacan, Derya. “Apoptozis”. Selçuk Üniversitesi Fen Fakültesi Fen Dergisi 49, sy. 1 (Nisan 2023): 1-10. https://doi.org/10.35238/sufefd.1210651.
EndNote Babacan D (01 Nisan 2023) Apoptozis. Selçuk Üniversitesi Fen Fakültesi Fen Dergisi 49 1 1–10.
IEEE D. Babacan, “Apoptozis”, sufefd, c. 49, sy. 1, ss. 1–10, 2023, doi: 10.35238/sufefd.1210651.
ISNAD Babacan, Derya. “Apoptozis”. Selçuk Üniversitesi Fen Fakültesi Fen Dergisi 49/1 (Nisan 2023), 1-10. https://doi.org/10.35238/sufefd.1210651.
JAMA Babacan D. Apoptozis. sufefd. 2023;49:1–10.
MLA Babacan, Derya. “Apoptozis”. Selçuk Üniversitesi Fen Fakültesi Fen Dergisi, c. 49, sy. 1, 2023, ss. 1-10, doi:10.35238/sufefd.1210651.
Vancouver Babacan D. Apoptozis. sufefd. 2023;49(1):1-10.

Dergi Sahibi: Selçuk Üniversitesi Fen Fakültesi Adına Rektör Prof. Dr. Hüseyin YILMAZ
Selçuk Üniversitesi Fen Fakültesi Fen Dergisi temel bilimlerde ve diğer uygulamalı bilimlerde özgün sonuçları olan Türkçe ve İngilizce makaleleri kabul eder. Dergide ayrıca güncel yenilikleri içeren derlemelere de yer verilebilir.
Selçuk Üniversitesi Fen Fakültesi Fen Dergisi;
İlk olarak 1981 yılında S.Ü. Fen-Edebiyat Fakültesi Dergisi olarak yayın hayatına başlamış; 1984 yılına kadar (Sayı 1-4) bu adla yayınlanmıştır.
1984 yılında S.Ü. Fen-Edeb. Fak. Fen Dergisi olarak adı değiştirilmiş 5. sayıdan itibaren bu isimle yayınlanmıştır.
3 Aralık 2008 tarih ve 27073 sayılı Resmi Gazetede yayımlanan 2008/4344 sayılı Bakanlar Kurulu Kararı ile Fen-Edebiyat Fakültesi; Fen Fakültesi ve Edebiyat Fakültesi olarak ayrılınca 2009 yılından itibaren dergi Fen Fakültesi Fen Dergisi olarak çıkmıştır.
2016 yılından itibaren DergiPark’ta taranmaktadır.


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