Cited by 162Nerve injury and regenerationEndoplasmic Reticulum Stress and DiseaseNuclear Receptors and Signaling

Activating Transcription Factor 3 and the Nervous System

Open access
Hunt, David, Raivich, Gennadij, Anderson, Patrick Norval·2012·Frontiers in Molecular Neuroscience

Abstract

Activating transcription factor 3 (ATF3) belongs to the ATF/cyclic AMP responsive element binding family of transcription factors and is often described as an adaptive response gene whose activity is usually regulated by stressful stimuli. Although expressed in a number of splice variants and generally recognized as a transcriptional repressor, ATF3 has the ability to interact with a number of other transcription factors including c-Jun to form complexes which not only repress, but can also activate various genes. ATF3 expression is modulated mainly at the transcriptional level and has markedly different effects in different types of cell. The levels of ATF3 mRNA and protein are normally very low in neurons and glia but their expression is rapidly upregulated in response to injury. ATF3 expression in neurons is closely linked to their survival and the regeneration of their axons following axotomy, and that in peripheral nerves correlates with the generation of a Schwann cell phenotype that is conducive to axonal regeneration. ATF3 is also induced by Toll-like receptor (TLR) ligands but acts as a negative regulator of TLR signaling, suppressing the innate immune response which is involved in immuno-surveillance and can enhance or reduce the survival of injured neurons and promote the regeneration of their axons.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.3389/fnmol.2012.00007

Cites

184 of 196 references verified7 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • MEK1/2 inhibition is one of a number of intracellular messengers that can activate Atf3 expression.

    “one of a number of intracellular messengers that can activate Atf3 expression [12].”

    From Tamoxifen induces cellular stress in the nervous system by inhibiting cholesterol synthesis (2015) · cites this paper as [12]

    The ATF3 Induction and Regulation section says several intracellular signaling pathways affect or induce ATF3 expression, supporting the general point. It does not say that MEK1/2 inhibition activates ATF3; its examples instead describe induction through p38 or JNK activation. No page number is available in our copy. (LLM, conf=0.84)

    Experimental — accuracy not yet measured
  • Under normal circumstances, Atf3 is expressed in very few regions of the adult nervous system.

    “Under normal circumstances, Atf3 is expressed in very few regions of the adult nervous system [12].”
  • Atf3 is one of a number of transcription factors upregulated by cellular stress, including the unfolded protein response, tyrosine kinase receptor activation, glutamate receptor hyperactivation, and cellular injury.

    “We generated a knock-in mouse expressing CreERT2 driven by the native promoter for activating transcription factor 3 (Atf3), one of a number of transcription factors upregulated by cellular stress, such as the unfolded protein response, tyrosine kinase receptor activation, glutamate receptor hyperactivation, and cellular injury [12].”

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Hunt, D., Raivich, G., & Anderson, P. N.
Affiliations
  • Newham University Hospital (GB)
  • University College London (GB)
Corresponding author
Anderson, Patrick Norval
Venue
Frontiers in Molecular Neuroscience
Published
2012
Volume
5
Pages
7-7
ISSN
1662-5099 (ISSN-L)
OpenAlex
W2124172625
Cited by
162
References
185
Citations by year
2026: 7 · 2025: 14 · 2024: 8 · 2023: 16 · 2022: 13 · 2021: 19 · 2020: 12 · 2019: 17 · 2018: 19 · 2017: 6 · 2016: 7 · 2015: 7 · 2014: 7 · 2013: 8 · 2012: 2
FWCI
3.16
Type
journal article
Language
en
Open access
Licence
cc-by-nc
Locations
  • Frontiers in Molecular Neuroscience (publishedVersion, cc-by-nc)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • UCL Discovery (University College London) (submittedVersion)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
Keywords
ATF3, ATF/CREB family, transcriptional repressor, c-Jun, neuronal injury response, axon regeneration, axotomy, Schwann cell phenotype, peripheral nerve injury, Toll-like receptor signaling, innate immune response, neuronal survival, glia

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review