Cited by 1,068Estrogen and related hormone effectsGenomics and Chromatin DynamicsAdrenal Hormones and Disorders

The DOI matches its Crossref record; 55 of the 55 references it cites were found in a registry or an index.

DNA Binding of the Glucocorticoid Receptor Is Not Essential for Survival

Open access

Abstract

Transcriptional regulation by the glucocorticoid receptor (GR) is essential for survival. Since the GR can influence transcription both through DNA-binding-dependent and -independent mechanisms, we attempted to assess their relative importance in vivo. In order to separate these modes of action, we introduced the point mutation A458T into the GR by gene targeting using the Cre/loxP system. This mutation impairs dimerization and therefore GRE-dependent transactivation while functions that require cross-talk with other transcription factors, such as transrepression of AP-1-driven genes, remain intact. In contrast to GR-/- mice, these mutants termed GRdim are viable, revealing the in vivo relevance of DNA-binding-independent activities of the GR.

Overview

Integrity signals

Registry

Crossref · 10.1016/s0092-8674(00)81183-6

Cites

55 of 55 references verified0 citation errors · 0 not checkable

Statistics

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Verification

Claims the paper makes

We couldn’t retrieve this paper’s full text, so its claims and self-check weren’t run. The registry and citation checks still apply.

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?

  • In GRdim mice, NF-kappaB and AP-1 target genes can still be silenced by GCs.

    “Contrastingly, other findings indicate that in GRdim mice NF-κB and AP-1 target genes can still be silenced by GCs (107, 108), that the GC-inducible gene MKP-1 is normally expressed in macrophages (82) and that irritant dermatitis can successfully be treated with GCs (22).”
  • Initial evidence suggested that classic transactivation by GRs was defective in GRdim mice and that this mechanism was required for the full range of GC immunosuppressive actions.

    “Initial evidence suggested that classic transactivation by GRs was defective in these mice and that this mechanism was required for the full range of GC immunosuppressive actions (107, 108).”

Citations

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Research works printed but not linked: 3

  1. Caldenhoven, 1995, Negative cross-talk between RelA and the glucocorticoid receptor, Mol. Endocrinol., 9, 401
  2. Chang, 1993, Inhibition of mouse GATA-1 function by the glucocorticoid receptor, Mol. Endocrinol., 7, 528
  3. Miner, 1991, Joints in the regulatory lattice, Cell Growth Differ., 2, 525

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Metadata

Authors
Reichardt, H. M., Kaestner, K. H., Tuckermann, J., Kretz, O., Wessely, O., Bock, R., Gass, P., Schmid, W., Herrlich, P., Angel, P., & Schütz, G.
Affiliations
  • German Cancer Research Center (DE)
  • Saarland University (DE)
Corresponding author
Schütz, Günther
Venue
Cell
Publisher
Elsevier BV
Published
1998-05
Volume
93
Issue
4
Pages
531-541
ISSN
0092-8674 (ISSN-L)
OpenAlex
W1997510672
Cited by
1,068
References
54
Citations by year
2026: 2 · 2025: 11 · 2024: 7 · 2023: 16 · 2022: 21 · 2021: 22 · 2020: 21 · 2019: 28 · 2018: 24 · 2017: 26 · 2016: 18 · 2015: 24 · 2014: 40 · 2013: 36 · 2012: 34
FWCI
38.04
Type
journal article
Language
en
Open access
Locations
  • Cell (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
Keywords
glucocorticoid receptor, DNA binding, receptor dimerization, gene targeting, Cre-loxP system, transcriptional regulation, survival
MeSH terms
Amino Acid Sequence, Animals, Cells, Cultured, Dexamethasone, DNA, Feedback, Gene Expression Regulation, Glucocorticoids, Hypothalamo-Hypophyseal System, Molecular Sequence Data, Pituitary-Adrenal System, Protein Binding, Receptors, Glucocorticoid, T-Lymphocytes, Transcription, Genetic, Erythroid Precursor Cells, Apoptosis, Point Mutation, Mice, Knockout, Mice

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