INT196323
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
The majority of grade III meningiomas either show homozygous deletions of p16INK4a,p14ARF, and CDKN2B, mutations in p16INK4a and p14ARF, or lack of expression of one or more of these genes (3). | |||||||||||||||
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In the present study, we evaluated the effects in meningioma initiation and progression of p16Ink4a loss with retention of p19Arf in synergy with Nf2 loss. | |||||||||||||||
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The majority of grade III meningiomas either show homozygous deletions of p16INK4a,p14ARF, and CDKN2B, mutations in p16INK4a and p14ARF, or lack of expression of one or more of these genes (3). | |||||||||||||||
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The majority of grade III meningiomas either show homozygous deletions of p16INK4a,p14ARF, and CDKN2B, mutations in p16INK4a and p14ARF, or lack of expression of one or more of these genes (3). | |||||||||||||||
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The p16INK4a/p14ARF locus encodes two distinct cell cycle inhibitory proteins, p16INK4a and p14ARF (p19Arf in the mouse) by alternative first-exon usage and alternative reading frames (20). p16INK4a arrests cells in the G1 phase of the cell cycle by binding the cyclin-dependant kinases CDK4 and CDK6 and inhibiting their ability to phosphorylate and inactivate the retinoblastoma (RB1) family of tumor suppressor proteins (22). p14ARF acts through MDM2 to stabilize and activate the key checkpoint protein p53, which can arrest cells in both G1 and G2 or induce apoptosis (20). | |||||||||||||||
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The majority of grade III meningiomas either show homozygous deletions of p16INK4a,p14ARF, and CDKN2B, mutations in p16INK4a and p14ARF, or lack of expression of one or more of these genes (3). | |||||||||||||||
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Sequencing of p16ink4a, k-ras and Rb cDNA | |||||||||||||||
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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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