Ensembl 2009

Hubbard, Tim; Aken, Bronwen; Ayling, Sarah; Ballester, Benoît; Beal, Kathryn; Bragin, Eugene; Brent, Simon; Chen, Y; Clapham, Peter; Clarke, Laura; Coates, Guy; Fairley, Susan; Fitzgerald, Stephen; Fernandez-Banet, Julio; Gordon, Leo I.; Gräf, Stefan; Haider, Syed; Hammond, Martin; Holland, Richard; Howe, Kerstin; Jenkinson, Andy; Johnson, Nathan; Kähäri, Andreas; Keefe, Damian; Keenan, Stephen; Kinsella, Rhoda; Kokocinski, Felix; Kulesha, Eugene; Lawson, Daniel; Longden, Ian; Mégy, Karyn; Meidl, Patrick; Overduin, Bert; Parker, Anne; Pritchard, Bethan; Ríos, Daniel; Schuster, Michael; Slater, Guy; Smedley, Damian; Spooner, William; Spudich, Giulietta; Trevanion, Stephen J.; Vilella, Albert J.; Vogel, Jan; White, Simon; Wilder, Steven P.; Zadissa, Amonida; Birney, Ewan; Cunningham, Fiona; Curwen, V.; Durbin, Richard; Fernández‐Suárez, Xosé M.; Herrero, Javier; Kasprzyk, Arek; Proctor, G; Smith, James; Searle, Stephen M. J.; Flicek, Paul

doi:10.1093/nar/gkn828

Cited by 715 publications

(739 citation statements)

References 39 publications

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“…The gene microarray data analysis was carried out with the Anduril framework (Ovaska et al, 2010). The expression values were normalized using quantile normalization and the Illumina probe identifiers were annotated with the Ensembl mouse gene identifiers (v. 57; Hubbard et al, 2009; EMBL-EBI and Wellcome Trust Sanger Institute, Hinxton, UK). Fold changes were calculated for Jnk2À/À versus wt, and two replicates were combined by taking the mean of their fold changes.…”

Section: Immunoblot Analysismentioning

confidence: 99%

Identification of a c-Jun N-terminal kinase-2-dependent signal amplification cascade that regulates c-Myc levels in ras transformation

et al. 2011

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Ras is one of the most frequently activated oncogenes in cancer. Two mitogen-activated protein kinases (MAPKs) are important for ras transformation: extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase 2 (JNK2). Here we present a downstream signal amplification cascade that is critical for ras transformation in murine embryonic fibroblasts. This cascade is coordinated by ERK and JNK2 MAPKs, whose Rasmediated activation leads to the enhanced levels of three oncogenic transcription factors, namely, c-Myc, activating transcription factor 2 (ATF2) and ATF3, all of which are essential for ras transformation. Previous studies show that ERK-mediated serine 62 phosphorylation protects c-Myc from proteasomal degradation. ERK is, however, not alone sufficient to stabilize c-Myc but requires the cooperation of cancerous inhibitor of protein phosphatase 2A (CIP2A), an oncogene that counteracts protein phosphatase 2A-mediated dephosphorylation of c-Myc. Here we show that JNK2 regulates Cip2a transcription via ATF2. ATF2 and c-Myc cooperate to activate the transcription of ATF3. Remarkably, not only ectopic JNK2, but also ectopic ATF2, CIP2A, c-Myc and ATF3 are sufficient to rescue the defective ras transformation of JNK2-deficient cells. Thus, these data identify the key signal converging point of JNK2 and ERK pathways and underline the central role of CIP2A in ras transformation.

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Section: Immunoblot Analysismentioning

confidence: 99%

Identification of a c-Jun N-terminal kinase-2-dependent signal amplification cascade that regulates c-Myc levels in ras transformation

et al. 2011

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“…The "match" command was used to align the paired-end reads to bovine transcripts from Ensembl (release 57). 44 The resulting alignments were then merged using the "mapmerge" command and consensus sequences were generated using the "assemble" command. The "cns2snp" command was used to build a list of potential SNP sites from the consensus sequences.…”

Section: Methodsmentioning

confidence: 99%

The identification of candidate genes and SNP markers for classical bovine spongiform encephalopathy susceptibility

Thomson

Bowles

Choi

et al. 2012

Prion

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“…The frequency of genomic evolutionary rate profiling (GERP) constrained elements across 12 mammalian species was analysed to inquire intronic sequence conservation (obtained using Ensembl's EnredoPecan-Ortheus pipeline on 12 eutherian mammals 20 ). Cadherin and non-cadherin introns from each of the three length classes described were analysed separately.…”

Section: Non-coding Sequence Conservation Analysismentioning

confidence: 99%

Characterization of the intronic portion of cadherin superfamily members, common cancer orchestrators

et al. 2012

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Cadherins are cell-cell adhesion proteins essential for the maintenance of tissue architecture and integrity, and their impairment is often associated with human cancer. Knowledge regarding regulatory mechanisms associated with cadherin misexpression in cancer is scarce. Specific features of the intronic-structure and intronic-based regulatory mechanisms in the cadherin superfamily are unidentified. This study aims at systematically characterizing the intronic portion of cadherin superfamily members and the identification of intronic regions constituting putative targets/triggers of regulation, using a bioinformatic approach and biological data mining. Our study demonstrates that the cadherin superfamily genes harbour specific characteristics in comparison to all non-cadherin genes, both from the genomic and transcriptional standpoints. Cadherin superfamily genes display higher average total intron number and significantly longer introns than other genes and across the entire vertebrate lineage. Moreover, in the human genome, we observed an uncommon high frequency of MIR (mammalian-wide interspersed repeats) and MaLR (mammalian-wide interspersed repeats, a subtype of LTR) regulatory-associated repetitive elements at 5¢-located introns, concomitantly with increased de novo intronic transcription. Using this approach, we identified cadherin intronic-specific sites that may constitute novel targets/triggers of cadherin superfamily expression regulation. These findings pinpoint the need to identify mechanisms affecting particularly MIR and MaLR elements located in introns 2 and 3 of human cadherin genes, possibly important in the expression modulation of this superfamily in homeostasis and cancer.

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Ensembl 2009

Cited by 715 publications

References 39 publications

Identification of a c-Jun N-terminal kinase-2-dependent signal amplification cascade that regulates c-Myc levels in ras transformation

Identification of a c-Jun N-terminal kinase-2-dependent signal amplification cascade that regulates c-Myc levels in ras transformation

The identification of candidate genes and SNP markers for classical bovine spongiform encephalopathy susceptibility

Characterization of the intronic portion of cadherin superfamily members, common cancer orchestrators

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