Synthetic lethality between Rb, p53 and Dicer or miR-17-92 in retinal progenitors suppresses retinoblastoma formation. - Wikidata - awgldk - TriplyDB

Synthetic lethality between Rb, p53 and Dicer or miR-17-92 in retinal progenitors suppresses retinoblastoma formation.

Synthetic lethality between Rb, p53 and Dicer or miR-17-92 in retinal progenitors suppresses retinoblastoma formation.

http://www.wikidata.org/entity/Q47302451

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Orchestrating epigenetic roles targeting ocular tumors The role of miRNAs in regulating gene expression networks MicroRNAs shape circadian hepatic gene expression on a transcriptome-wide scale.Global microRNA depletion suppresses tumor angiogenesis.Inactivation of p53 is insufficient to allow B cells and B-cell lymphomas to survive without Dicer.Role of the miR-17∼92 cluster family in cerebellar and medulloblastoma development.Chromatin remodelers HELLS and UHRF1 mediate the epigenetic deregulation of genes that drive retinoblastoma tumor progression.Growth-promoting role of the miR-106a~363 cluster in Ewing sarcoma.STAT3 inhibition suppresses proliferation of retinoblastoma through down-regulation of positive feedback loop of STAT3/miR-17-92 clusters.Rescuing dicer defects via inhibition of an anti-dicing nuclease.Reversible, interrelated mRNA and miRNA expression patterns in the transcriptome of Rasless fibroblasts: functional and mechanistic implications Dicer regulates differentiation and viability during mouse pancreatic cancer initiation Novel miRNA-31 and miRNA-200a-Mediated Regulation of Retinoblastoma Proliferation A Biogenesis Step Upstream of Microprocessor Controls miR-17∼92 Expression.MicroRNA Biogenesis and Hedgehog-Patched Signaling Cooperate to Regulate an Important Developmental Transition in Granule Cell Development.MicroRNAs in Ewing Sarcoma.miR-17~92 miRNA cluster promotes kidney cyst growth in polycystic kidney disease.miR-342 overexpression results in a synthetic lethal phenotype in BRCA1-mutant HCC1937 breast cancer cells A component of the mir-17-92 polycistronic oncomir promotes oncogene-dependent apoptosis.Nucleolin-aptamer therapy in retinoblastoma: molecular changes and mass spectrometry-based imaging A dosage-dependent pleiotropic role of Dicer in prostate cancer growth and metastasis.Emerging roles of p53 and other tumour-suppressor genes in immune regulation mir-17-92: a polycistronic oncomir with pleiotropic functions.Micro RNA-19a suppresses interleukin-10 in peripheral B cells of patients with diabetic retinopathy.Systems genetics in "-omics" era: current and future development.More epigenetic hits than meets the eye: microRNAs and genes associated with the tumorigenesis of retinoblastoma.The genomic landscape of retinoblastoma: a review.Antitumor mechanisms when pRb and p53 are genetically inactivated.Dysregulation of microRNA biogenesis and gene silencing in cancer.Current views on inducing synthetic lethal RNAi responses in the treatment of cancer.DICER, DROSHA and DNA damage response RNAs are necessary for the secondary recruitment of DNA damage response factors Reduction of the tumorigenic potential of human retinoblastoma cell lines by TFF1 overexpression involves p53/caspase signaling and miR-18a regulation.Blocking the maturation of OncomiRNAs using pri-miRNA-17∼92 aptamer in retinoblastoma.MicroRNA-183 suppresses retinoblastoma cell growth, invasion and migration by targeting LRP6.Co-deleting Pten with Rb in retinal progenitor cells in mice results in fully penetrant bilateral retinoblastomas.Retinoblastoma cells activate the AKT pathway and are vulnerable to the PI3K/mTOR inhibitor NVP-BEZ235.DNA Methylomes Reveal Biological Networks Involved in Human Eye Development, Functions and Associated Disorders.Integrated Analysis of Dysregulated miRNA-gene Expression in HMGA2-silenced Retinoblastoma Cells Treating cancer when pRb and p53 cannot be reactivated.Identification of synthetic lethal pairs in biological systems through network information centrality.

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Synthetic lethality between Rb, p53 and Dicer or miR-17-92 in retinal progenitors suppresses retinoblastoma formation.

http://www.wikidata.org/entity/Q47302451

description

2012 nî lūn-bûn

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2012年の論文

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年学术文章

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2012年學術文章

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2012年學術文章

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name

Synthetic lethality between Rb ...... sses retinoblastoma formation.

@en

Synthetic lethality between Rb ...... sses retinoblastoma formation.

@nl

type

label

Synthetic lethality between Rb ...... sses retinoblastoma formation.

@en

Synthetic lethality between Rb ...... sses retinoblastoma formation.

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prefLabel

Synthetic lethality between Rb ...... sses retinoblastoma formation.

@en

Synthetic lethality between Rb ...... sses retinoblastoma formation.

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Nature Cell Biology

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Synthetic lethality between Rb ...... sses retinoblastoma formation.

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Aart Jochemsen

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Corinna Köhler

http://www.w3.org/2001/XMLSchema#string

Frederic Clermont

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Irina Lambertz

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Johannes H Schulte

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Michael A Dyer

http://www.w3.org/2001/XMLSchema#string

Pieter Mestdagh

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Søren Jensby Nielsen

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P2860

miR-17~92 cooperates with RB pathway mutations to promote retinoblastoma

Targeted deletion reveals essential and overlapping functions of the miR-17 through 92 family of miRNA clusters

MicroRNA regulation of a cancer network: consequences of the feedback loops involving miR-17-92, E2F, and Myc

Repression of the miR-17-92 cluster by p53 has an important function in hypoxia-induced apoptosis

Tumorigenicity of the miR-17-92 cluster distilled

The concept of synthetic lethality in the context of anticancer therapy

Morphogenesis in skin is governed by discrete sets of differentially expressed microRNAs

Regulating the p53 pathway: in vitro hypotheses, in vivo veritas

Impaired microRNA processing enhances cellular transformation and tumorigenesis

Compensation by tumor suppressor genes during retinal development in mice and humans.

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10.1038/NCB2556

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9

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14

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Jo Vandesompele

Alexander Schramm

Jean-Christophe Marine

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2012-08-05T00:00:00Z

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230619562

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