INT144701
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Melan-a cells are functionally Ink4a-Arf null, expressing neither p16INK4A nor ARF proteins (Sviderskaya et al., 2002).
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Studying cells at different phases of transformation, we could show that an early event during transformation was the loss of expression of the CDKN2A locus, followed by inactivation of p53 and overexpression of c-myc. | |||||||||||||||
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Notably, hypermethylation of the CDKN2A promoter region has been shown to lead to loss of p16 expression in 19% of primary and 33% metastatic melanomas.[59] DNA methyltransferase(DNMT) inhibitors namely 5-azacytidine, 5-aza-20-deoxycytidine(decitabine), fazarabine, and dihydro-5-azacytidine have been extensively studied. | |||||||||||||||
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Sequencing of p16ink4a, k-ras and Rb cDNA | |||||||||||||||
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Two pathways are known to induce cell cycle arrest and senescence: the P16-Rb and P53-P21 pathways. | |||||||||||||||
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Lack of p16 did not rescue the angiogenic defect of irradiated rings (data not shown), consistent with the absence of induction of P16 protein in irradiated HUVEC. | |||||||||||||||
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This gene (also known as p15Ink4b) lies adjacent to the tumor suppressor gene CDKN2A and encodes a cyclin-dependent kinase. | |||||||||||||||
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Further, while expression of p19 was variably decreased in lungs from CCSPrtTA/tetO-Sox17 mice maintained on Dox for 2 days, no differences in the expression of p16 or p27 were observed after expression of Sox17 for 13 days (data not shown). | |||||||||||||||
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Silencing of p19ARF, an upstream regulator of p53, facilitates reprogramming as well [105]. | |||||||||||||||
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Genetic alterations such as the p16(INK4a) deletion, melanocortin 1 receptor (MC1R), RAS, and v-raf murine sarcoma viral oncogene homolog B1 (BRAF) may be indicative of a predisposition to melanoma development. | |||||||||||||||
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However, over-expression of Tert in the background of enhanced cancer resistance (enhanced expression of p53, p16 and p19ARF) increased lifespan in Sp53/Sp16/SArf/TgTert transgenic mice [50]. | |||||||||||||||
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However, over-expression of Tert in the background of enhanced cancer resistance (enhanced expression of p53, p16 and p19ARF) increased lifespan in Sp53/Sp16/SArf/TgTert transgenic mice [50]. | |||||||||||||||
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Melan-a cells are functionally Ink4a-Arf null, expressing neither p16INK4A nor ARF proteins (Sviderskaya et al., 2002).
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It has been shown that HDACs inhibitors can selectively induce the expression of less than 10% of genes, some of which are involved in the inhibition of tumor growth (e.g., p21WAF1, p27Kip and p16ink4a) [19, 26, 38]. | |||||||||||||||
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Other molecules that have been demonstrated to play a role in arthritis using gene transfer in various in vitro or animal models are Csk, cathepsin L, fibronectin, galectin-1, p16INK4A, p21Cip1, SOCS3, soluble CR1, superoxide dismutase and catalase, Ras, and prothymosin ? | |||||||||||||||
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General Comments
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