Abstract
The human ELL gene on chromosome 19 undergoes frequent translocations with the trithorax-like MLL gene on chromosome 11 in acute myeloid leukemias. Here, ELL was shown to encode a previously uncharacterized elongation factor that can increase the catalytic rate of RNA polymerase II transcription by suppressing transient pausing by polymerase at multiple sites along the DNA. Functionally, ELL resembles Elongin (SIII), a transcription elongation factor regulated by the product of the von Hippel-Lindau (VHL) tumor suppressor gene. The discovery of a second elongation factor implicated in oncogenesis provides further support for a close connection between the regulation of transcription elongation and cell growth.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Amino Acid Sequence
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Animals
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Cloning, Molecular
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DNA-Binding Proteins / chemistry
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DNA-Binding Proteins / genetics*
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DNA-Binding Proteins / metabolism
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Elongin
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Genes, Tumor Suppressor
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Histone-Lysine N-Methyltransferase
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Humans
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Leukemia / genetics
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Molecular Sequence Data
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Myeloid-Lymphoid Leukemia Protein
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Neoplasm Proteins*
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Peptide Elongation Factors*
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Proto-Oncogenes*
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RNA Polymerase II / metabolism*
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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Rats
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Recombinant Proteins / metabolism
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Transcription Factors / chemistry
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Transcription Factors / genetics*
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Transcription Factors / metabolism
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Transcription, Genetic
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Transcriptional Elongation Factors
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Translocation, Genetic
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von Hippel-Lindau Disease / genetics
Substances
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DNA-Binding Proteins
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ELL protein, human
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Elongin
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KMT2A protein, human
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Neoplasm Proteins
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Peptide Elongation Factors
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RNA, Messenger
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Recombinant Proteins
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Transcription Factors
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Transcriptional Elongation Factors
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Myeloid-Lymphoid Leukemia Protein
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Histone-Lysine N-Methyltransferase
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RNA Polymerase II