Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of human MCL1 over-expressing B-NHL cells


ABSTRACT: To get insight into the mechanisms of MCL1-induced survival and transformation, we screened 41,000 human genes in a genome-wide gene expression profile analysis of MCL1 over-expressing B-NHL cells. Experiment Overall Design: Two-color (Cy5-CTP/ Cy3-CTP) microarray-based gene expression formats presenting high-density oligonucleotide probes printed on a single glass slide were used (Agilent technologies, Cat No# G4112A whole human genome 41K). Total RNAs from MCL1 over-expressing RAMOS RA-1 and Z-138 B-cells were labeled with Cy5-CTP, whereas RNAs from references (empty vector/ RAMOS RA-1 and empty vector/ Z-138 B-cells) were labeled with Cy3-CTP. After competitive hybridization [RNA-Cy5 from MCL1 over-expressing RAMOS RA-1 or MCL1 over-expressing Z-138 versus RNA-Cy3 from either empty vector/ RAMOS RA-1 or empty vector/ Z-138 respectively] gene expression data were pre-processed using Feature Extraction software and GEPAS tools (http://gepas.bioinfo.cipf.es/).

ORGANISM(S): Homo sapiens

SUBMITTER: Antonio Ruiz-Vela 

PROVIDER: E-GEOD-8834 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Lentiviral (HIV)-based RNA interference screen in human B-cell receptor regulatory networks reveals MCL1-induced oncogenic pathways.

Ruiz-Vela Antonio A   Aggarwal Mohit M   de la Cueva Paloma P   Treda Cezary C   Herreros Beatriz B   Martín-Pérez Daniel D   Dominguez Orlando O   Piris Miguel A MA  

Blood 20071121 3


Aberrant inhibition of B-cell receptor (BCR)-induced programmed cell death pathways is frequently associated with the development of human auto-reactive B-cell lymphomas. Here, we integrated loss-of-function, genomic, and bioinformatics approaches for the identification of oncogenic mechanisms linked to the inhibition of BCR-induced clonal deletion pathways in human B-cell lymphomas. Lentiviral (HIV)-based RNA interference screen identified MCL1 as a key survival molecule linked to BCR signaling  ...[more]

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