نتایج جستجو برای: ژن p73

تعداد نتایج: 17030  

2015
Flaviana Marzano Annamaria Ventura Mariano Francesco Caratozzolo Italia Aiello Francesca Mastropasqua Giacomina Brunetti Luciano Cavallo Elisabetta Sbisà Maria Felicia Faienza Apollonia Tullo Kunxin Luo

The regulation of insulin-like growth factor-binding protein 3 (IGFBP3) gene expression is complex, because it can be induced by agents that both stimulate and inhibit the proliferation. The principal aim of this study was to investigate whether p73, a member of the p53 gene family, has a role in the regulation of the IGFBP3 expression and whether this regulation occurs in a context of cell sur...

2016
Olivier Billant Alice Léon Solenn Le Guellec Gaëlle Friocourt Marc Blondel Cécile Voisset

The tumor suppression activity of p53 is frequently impaired in cancers even when a wild-type copy of the gene is still present, suggesting that a dominant-negative effect is exerted by some of p53 mutants and isoforms. p63 and p73, which are related to p53, have also been reported to be subjected to a similar loss of function, suggesting that a dominant-negative interplay might happen between ...

2016
Nevin M Al Azhary Mahmoud M Kamel Yahia M Ismail Amal A Mahmoud Enas M Radwan

Background: Breast cancer is the commonest cancer in Egyptian females. Nrf2 is involved in oxidative stress while P73 functions in response to DNA damage. This study aimed to assess the role of Nrf2 promoter and P73 G4C14 to A4T14 SNPs in breast cancer in Egypt. Patients: Eighty-five female patients with breast tumours (41 malignant, 44 benign) were included. Nrf2 (rs6721961) and p73 (G4A) SNPs...

Journal: :The Journal of biological chemistry 2007
Ramakrishna Kommagani Vandana Payal Madhavi P Kadakia

p63 and p73, members of the p53 family, have been shown to be functionally distinct from p53. Vitamin D receptor (VDR) is a ligand (vitamin D(3))-dependent transcription factor, which is shown to play a major role in calcium homeostasis and keratinocyte differentiation. Vitamin D and its analogues in combination with DNA-damaging agents are extensively used for cancer chemotherapy. In this repo...

2015
Junwei Cao Qiliang Lai Jun Yuan Zongze Shao

Celeribacter indicus P73(T), isolated from deep-sea sediment from the Indian Ocean, is capable of degrading a wide range of polycyclic aromatic hydrocarbons (PAHs) and is the first fluoranthene-degrading bacterium within the family Rhodobacteraceae. Here, the complete genome sequence of strain P73(T) is presented and analyzed. Besides a 4.5-Mb circular chromosome, strain P73(T) carries five pla...

2012
Yuan Yao Marcia Bellon Shary N. Shelton Christophe Nicot

Background: Inactivation of p53 and reactivation of telomerase expression are two of the most common events in human cancer. Results: Here we report the mechanisms used by p53, p63, and p73 to suppress telomerase expression. Conclusion: p53, p63, and p73 suppress telomerase expression through distinct pathways that involve E2F, E-box, c-Myc, and NF-YB. Significance: This study provides new insi...

2003
Ute M. Moll

The Role of p63 and p73 in Tumor Formation and Progression: Coming of Age Toward Clinical Usefulness Commentary re: F. Koga et al., Impaired p63 Expression Associates with Poor Prognosis and Uroplakin III Expression in Invasive Urothelial Carcinoma of the Bladder. Clin. Cancer Res., 9: 5501–5507, 2003, and P. Puig et al., p73 Expression in Human Normal and Tumor Tissues: Loss of p73 Expression ...

Journal: :Journal of the National Cancer Institute 1999
W G Kaelin

Perturbation of p53 protein function is a common, if not universal, finding in human cancer. Tumor suppression by p53 is due, at least in part, to its ability to activate transcription of certain genes involved in cell cycle control and apoptosis (programmed cell death). Two additional members of the mammalian p53 family, p73 and p51, which is also known as p40, p63, KET, or p73L, were recently...

Journal: :Blood 2008
Masahiro Kawahara Toshiyuki Hori Kazuhisa Chonabayashi Tsutomu Oka Marius Sudol Takashi Uchiyama

Down-regulation of the Kpm/Lats2 tumor suppressor is observed in various malignancies and associated with poor prognosis in acute lymphoblastic leukemia. We documented that Kpm/Lats2 was markedly decreased in several leukemias that were highly resistant to conventional chemotherapy. Silencing of Kpm/Lats2 expression in leukemic cells did not change the rate of cell growth but rendered the cells...

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