Sam68 regulates EMT through alternative splicing-activated nonsense-mediated mRNA decay of the SF2/ASF proto-oncogene. - Wikidata - wikimedia - TriplyDB

Sam68 regulates EMT through alternative splicing-activated nonsense-mediated mRNA decay of the SF2/ASF proto-oncogene.

Sam68 regulates EMT through alternative splicing-activated nonsense-mediated mRNA decay of the SF2/ASF proto-oncogene.

http://www.wikidata.org/entity/Q42008721

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The RNA recognition motif protein RBM11 is a novel tissue-specific splicing regulator Met receptors induce Sam68-dependent cell migration by activation of alternate extracellular signal-regulated kinase family members SAM68 regulates neuronal activity-dependent alternative splicing of neurexin-1 Splicing Regulation: A Molecular Device to Enhance Cancer Cell Adaptation SAM68: Signal Transduction and RNA Metabolism in Human Cancer Posttranscriptional Regulation of Splicing Factor SRSF1 and Its Role in Cancer Cell Biology Connecting the speckles: Splicing kinases and their role in tumorigenesis and treatment response Phosphorylation-mediated regulation of alternative splicing in cancer Molecular mechanisms of epithelial-mesenchymal transition An EMT-driven alternative splicing program occurs in human breast cancer and modulates cellular phenotype Defective control of pre-messenger RNA splicing in human disease Long non-coding RNA INXS is a critical mediator of BCL-XS induced apoptosis Versatility of RNA-Binding Proteins in Cancer High expression level and nuclear localization of Sam68 are associated with progression and poor prognosis in colorectal cancer The RNA-binding protein Sam68 regulates expression and transcription function of the androgen receptor splice variant AR-V7 Tissue-specific and SRSF1-dependent splicing of fibronectin, a matrix protein that controls host cell invasion Effects of PTCs on nonsense-mediated mRNA decay are dependent on PTC location Cell type-restricted activity of hnRNPM promotes breast cancer metastasis via regulating alternative splicing.Emerging functions of SRSF1, splicing factor and oncoprotein, in RNA metabolism and cancer.Mechanisms of HGF/Met signaling to Brk and Sam68 in breast cancer progression.The RNA binding protein SAM68 transiently localizes in the chromatoid body of male germ cells and influences expression of select microRNAs.Functional consequences of developmentally regulated alternative splicing.Intron retention in the alternatively spliced region of RON results from weak 3' splice site recognition.Ribosomal protein S6 kinase (RSK)-2 as a central effector molecule in RON receptor tyrosine kinase mediated epithelial to mesenchymal transition induced by macrophage-stimulating protein Lin28 induces epithelial-to-mesenchymal transition and stemness via downregulation of let-7a in breast cancer cells.Hsp22 (HspB8/H11) knockdown induces Sam68 expression and stimulates proliferation of glioblastoma cells.Regulation of splicing factors by alternative splicing and NMD is conserved between kingdoms yet evolutionarily flexible.Splicing programs and cancer Transforming Growth Factor-β1 Induced Epithelial Mesenchymal Transition is blocked by a chemical antagonist of translation factor eIF4E Post-transcriptional regulation in cancer progression : Microenvironmental control of alternative splicing and translation.Connecting the dots: chromatin and alternative splicing in EMT.Fluorescence-based alternative splicing reporters for the study of epithelial plasticity in vivo RBFOX2 is an important regulator of mesenchymal tissue-specific splicing in both normal and cancer tissues.Emerging roles for Sam68 in adipogenesis and neuronal development.Stay lean without dieting: Lose Sam68 Oncogenic H-ras reprograms Madin-Darby canine kidney (MDCK) cell-derived exosomal proteins following epithelial-mesenchymal transition.CONSORT: Sam68 Is Directly Regulated by MiR-204 and Promotes the Self-Renewal Potential of Breast Cancer Cells by Activating the Wnt/Beta-Catenin Signaling Pathway.Oncogenic alternative splicing switches: role in cancer progression and prospects for therapy.Posttranscriptional regulation by RNA-binding proteins during epithelial-to-mesenchymal transition.Novel signaling collaboration between TGF-β and adaptor protein Crk facilitates EMT in human lung cancer.

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P2860

Sam68 regulates EMT through alternative splicing-activated nonsense-mediated mRNA decay of the SF2/ASF proto-oncogene.

http://www.wikidata.org/entity/Q42008721

description

2010 nî lūn-bûn

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2010年の論文

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2010年学术文章

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2010年学术文章

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2010年学术文章

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2010年学术文章

@zh-my

2010年学术文章

@zh-sg

2010年學術文章

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2010年學術文章

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2010年學術文章

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name

Sam68 regulates EMT through al ...... of the SF2/ASF proto-oncogene.

@en

Sam68 regulates EMT through al ...... of the SF2/ASF proto-oncogene.

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type

label

Sam68 regulates EMT through al ...... of the SF2/ASF proto-oncogene.

@en

Sam68 regulates EMT through al ...... of the SF2/ASF proto-oncogene.

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prefLabel

Sam68 regulates EMT through al ...... of the SF2/ASF proto-oncogene.

@en

Sam68 regulates EMT through al ...... of the SF2/ASF proto-oncogene.

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Sam68 regulates EMT through al ...... of the SF2/ASF proto-oncogene

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Cristina Valacca

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Francisco Ernesto Baralle

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Serena Bonomi

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P2860

An unappreciated role for RNA surveillance

The replication factory targeting sequence/PCNA-binding site is required in G(1) to control the phosphorylation status of DNA ligase I

Regulation of CD44 alternative splicing by SRm160 and its potential role in tumor cell invasion

Contextual extracellular cues promote tumor cell EMT and metastasis by regulating miR-200 family expression

Sam68 regulates a set of alternatively spliced exons during neurogenesis

The RNA-binding protein Sam68 modulates the alternative splicing of Bcl-x

Duplexes of 21-nucleotide RNAs mediate RNA interference in cultured mammalian cells

Alternative isoform regulation in human tissue transcriptomes

Signal-dependent regulation of splicing via phosphorylation of Sam68

Sam68 haploinsufficiency delays onset of mammary tumorigenesis and metastasis

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1

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46578465

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2953442

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