About: Characterization of nuclear factors modulating the apolipoprotein D promoter during growth arrest: Implication of PARP-1, APEX-1 and ERK1/2 catalytic activities

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About: Characterization of nuclear factors modulating the apolipoprotein D promoter during growth arrest: Implication of PARP-1, APEX-1 and ERK1/2 catalytic activities Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Characterization of nuclear factors modulating the apolipoprotein D promoter during growth arrest: Implication of PARP-1, APEX-1 and ERK1/2 catalytic activities
Creator	Rassart, Eric Charfi, Cyndia Levros, Louis-Charles Carmo, Sonia Legault, Philippe
Source	Elsevier; Medline; PMC
abstract	Abstract Human Apolipoprotein D (apoD) is upregulated under several stress conditions and pathological situations such as neurodegenerative diseases and cancers. We previously showed that apoD mRNA expression is induced in growth-arrested cells and demonstrated the specific binding of nuclear proteins to the region −514 to −475 of the promoter. Such region contains a pair of Serum Responsive Elements (SRE), an Ets-Binding Site (EBS) and a Glucocorticoid Responsive Element (GRE). In this study, we show that Parp-1, HnRNP-U, CBF-A, BUB-3, Kif4, APEX-1 and Ifi204 bind these regulatory elements of the apoD promoter. Specific binding of HnRNP-U and Parp-1 was confirmed by Electrophoretic Mobility Shift Assay (EMSA). In a biotin pull-down assay, Kif4 and BUB-3 bind preferentially the SRE1 and the EBS-GRE sites, respectively, while APEX-1 seems recruited indirectly to these elements. We found that the mRNA expression of some of these binding factors is upregulated in growth-arrested cells and that these proteins also transactivate the apoD promoter. In agreement with these results, mutants of APEX-1 and of Parp-1 defective for their DNA-binding and catalytic activities could not transactivate the promoter. The knockdown of Parp-1 and HnRNP-U and the use of specific inhibitors of MEK1/2 and of Parp-1 also inhibited the induction of apoD gene expression. Moreover, ERK1/2 was found activated in a biphasic manner post serum-starvation and the inhibition of Parp-1 causes a sustained activation of ERK2 but not ERK1 for up to 2h. Altogether, these findings demonstrate the importance of Parp-1, APEX-1 and ERK1/2 catalytic activities in the growth arrest-induced apoD gene expression.
has issue date	2010-09-30(xsd:dateTime)
bibo:doi	10.1016/j.bbamcr.2010.04.011
bibo:pmid	20493910
has license	els-covid
sha1sum (hex)	a1c4f431dbe459fc4023a193698d0a46020dcca6
schema:url	https://doi.org/10.1016/j.bbamcr.2010.04.011
resource representing a document's title	Characterization of nuclear factors modulating the apolipoprotein D promoter during growth arrest: Implication of PARP-1, APEX-1 and ERK1/2 catalytic activities
has PubMed Central identifier	PMC7114184
has PubMed identifier	20493910
schema:publication	Biochimica et Biophysica Acta (BBA) - Molecular Cell Research
resource representing a document's body	covid:a1c4f431dbe459fc4023a193698d0a46020dcca6#body_text
is schema:about of	named entity 'PROMOTER' named entity 'expression' named entity 'manner' named entity 'nuclear proteins' named entity 'promoter' named entity 'gene' named entity 'Element' named entity 'ERK1/2' named entity 'PARP-1' named entity 'PROMOTER' named entity 'N A' named entity 'ETS' named entity 'I E' named entity 'L H' named entity 'BUT' named entity 'ERK1' named entity 'A T' named entity 'KIF4' named entity 'APOD' named entity 'GROWTH ARREST' named entity 'ACTIVATED' named entity 'ERK1' named entity 'UPREGULATED' named entity 'POST' named entity 'PREVIOUSLY' named entity 'APEX' named entity 'ELEMENTS' named entity 'REGULATORY' named entity 'C O' named entity 'ARRESTED' named entity 'C R' named entity 'GROWTH' named entity 'CHARACTERIZATION' named entity 'NUCLEAR' named entity 'MUTANTS' named entity 'DEFECTIVE' named entity 'CANCERS' named entity 'THEIR' named entity 'APOLIPOPROTEIN D' named entity 'ACTIVITIES' named entity 'GROWTH ARREST' named entity 'INHIBITORS' named entity 'STRESS' named entity 'ELECTROPHORETIC MOBILITY SHIFT ASSAY ' named entity 'FOUND' named entity 'PATHOLOGICAL' named entity 'NUCLEAR PROTEINS' named entity 'HUMAN' named entity 'L S' named entity 'ERK2' named entity 'BIPHASIC' named entity 'RESULTS' named entity 'SUSTAINED' named entity 'DEMONSTRATED' named entity 'SERUM' named entity 'PULL' named entity 'SITES' named entity 'H O' named entity 'BINDING SITE' named entity 'RESPONSIVE' named entity 'SRE1' named entity 'EBS' named entity 'CBF-A' named entity 'BIOTIN' named entity 'BINDING' named entity 'REGION' named entity 'MODULATING' named entity 'ACTIVATION' named entity 'NEURODEGENERATIVE DISEASES' named entity 'ELEMENT' named entity 'PAIR' named entity 'GENE EXPRESSION' named entity 'USE OF' named entity 'BIND' named entity 'INHIBITION' named entity 'AGREEMENT' named entity 'INDUCTION'

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