Evidence map›Paper›PMID 8756618›Full record

ArticleMolecular and cellular biology1996

Activation of codependent transcription factors is required for transcriptional induction of the vgf gene by nerve growth factor and Ras.

G D'Arcangelo, R Habas, S Wang, S Halegoua, S R Salton

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.0field-weighted citation impact, top 26% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Neuroendocrine Role for VGF.Frontiers in endocrinology · 2015
    Review
  5. Trk retrograde signaling requires persistent, Pincher-directed endosomes.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  6. Neuropeptides in depression: role of VGF.Behavioural brain research · 2009
    Review
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  12. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

G D'ArcangeloDepartment of Neurobiology and Behavior and Institute for Cell and Developmental Biology, State University of New York at Stony Brook, 11794-5230, USA.
R Habas
S Wang
S Halegoua
S R Salton
State University of New York · USIcahn School of Medicine at Mount Sinai · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nerve growth factor (NGF) treatment of PC12 cells leads to the elaboration of a neuronal phenotype, including the induction of neuronally expressed genes such as vgf. To study vgf transcription, we have created chimeric vgf/beta-globin genes in which vgf promoter sequences drive the expression of the beta-globin reporter gene or of a chimeric beta-globin gene fused to 3' untranslated vgf gene sequences. We have found that the level of inducibility of the latter construct by NGF resembles that of the endogenous vgf gene. Using transient transfection of the chimeric reporter genes into PC12 cells, into PC12 subclones expressing activated or dominantly interfering mutant Ras proteins, and into PC12 variants expressing specific NGF receptor/Trk mutants, we show that transcriptional regulation of the vgf promoter by NGF is mediated through a Ras-dependent signaling pathway. By mutational analysis of the vgf promoter, we have identified three promoter elements involved in mediating transcriptional induction by NGF and Ras. In addition to the cyclic AMP-responsive element (CRE), which binds to ATF-1, ATF-2, and CRE-binding protein in PC12 nuclear extracts, a novel CCAAT element and its binding proteins were identified, which, like the CRE, is necessary but not sufficient for the Ras-dependent induction of the vgf gene by NGF. We also identify a G(S)G element unusually located between the TATA box and transcriptional start site, which binds the NGF- and Ras-induced transcription factor, NGFI-A, and amplifies the transcriptional response. Integrating data from studies of vgf promoter regulation and NGF signal transduction, we present a model for vgf gene induction in which transcriptional activation is achieved through the persistent, direct activation of multiple interacting transcription factors binding to CRE and CCAAT elements, coordinated with the delayed transcription factor action at a G(S)G element resulting from the induced expression of NGFI-A.

Indexed as

Gene Expression RegulationTranscription, GeneticAnimalsBase SequenceCyclic AMPEndothelial Growth FactorsGenesGenes, ReporterGlobinsLymphokinesMolecular Sequence DataNeoplasm ProteinsNerve Growth FactorsNeuronsPC12 CellsPromoter Regions, GeneticCyclic AMPEndothelial Growth FactorsGlobinsLymphokinesNeoplasm ProteinsNerve Growth FactorsProto-Oncogene Proteins p21(ras)Receptors, Nerve Growth FactorRecombinant Fusion ProteinsTranscription FactorsVascular Endothelial Growth Factor AVascular Endothelial Growth Factors

Identifiers

PMID8756618
PMCPMC231461
OpenAlexW2158692390

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.