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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

TSC22 domain family, member 3

GILZ, Glucocorticoid-Induced Leucine Zipper, TSC22D3
The protein encoded by this gene shares significant sequence identity with the murine TSC-22 and Drosophila shs, both of which are leucine zipper proteins, that function as transcriptional regulators. The expression of this gene is stimulated by glucocorticoids and interleukin 10, and it appears to play a key role in the anti-inflammatory and immunosuppressive effects of this steroid and chemokine. Transcript variants encoding different isoforms have been identified for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: V1a, GCS, CAN, FKBP51, Interleukin-6
Papers on GILZ
Genetic regulation analysis reveals involvement of tumor necrosis factor and alpha-induced protein 3 in stress response in mice.
Cao et al., Nantong, China. In Gene, Feb 2016
We confirmed a significant influence of Tnfaip3 depletion on the expression of Tsc22d3, Pex7, Rap2a, Slc2a3, and Gap43.
TSC-22 Promotes Interleukin-2-Deprivation Induced Apoptosis in T-Lymphocytes.
Biola-Vidamment et al., Châtenay-Malabry, France. In J Cell Biochem, Feb 2016
Along with GILZ (Glucocorticoid-Induced Leucine Zipper), TSC-22 belongs to the evolutionary conserved TSC-22 Domain family.
Endocrine-Disrupting Effects of Pesticides through Interference with Human Glucocorticoid Receptor.
Liu et al., Riverside, United States. In Environ Sci Technol, Feb 2016
In J774A.1 cells, λ-cyhalothrin, resmethrin, 3-PBA, o,p'-DDT, p,p'-DDT, p,p'-DDE, methoxychlor- and tolylfluanid-reduced cortisol-stimulated GILZ expression.
Combined oral contraceptive synergistically activates mineralocorticoid receptor through histone code modifications.
Kim et al., Taegu, South Korea. In Eur J Pharmacol, Jan 2016
Treatment with COC increased renal cortical expression of MR target genes such as serum and glucocorticoid-regulated kinase 1 (Sgk-1), glucocorticoid-induced leucine zipper (Gilz), epithelial Na(+)channel (Enac) and Na(+)-K(+)-ATPase subunit α1 (Atp1a1).
Obesity is associated with a downregulation of the glucocorticoid receptor-GILZ pathway in Kupffer cells which promotes liver inflammation in mice.
Cassard et al., Clamart, France. In J Hepatol, Dec 2015
The glucocorticoid receptor (GR) induces glucocorticoid-induced leucine zipper (GILZ) expression in monocytes/macrophages and is involved in several inflammatory processes.
Glucocorticoid-induced leucine zipper (GILZ) inhibits B cell activation in systemic lupus erythematosus.
Morand et al., Melbourne, Australia. In Ann Rheum Dis, Dec 2015
We studied whether B cells in SLE are regulated by the glucocorticoid-induced leucine zipper (GILZ) protein, an endogenous mediator of anti-inflammatory effects of glucocorticoids.
Glucocorticoid-induced leucine zipper (GILZ) in immuno suppression: master regulator or bystander?
Kiemer et al., Saarbrücken, Germany. In Oncotarget, Dec 2015
Induction of glucocorticoid-induced leucine zipper (GILZ) by glucocorticoids has been reported to be essential for their anti-inflammatory actions.
Glucocorticoid-Induced Leucine Zipper Is Expressed in Human Neutrophils and Promotes Apoptosis through Mcl-1 Down-Regulation.
Biola-Vidamment et al., Châtenay-Malabry, France. In J Innate Immun, Oct 2015
UNASSIGNED: Glucocorticoid-induced leucine zipper (GILZ) is a potent anti-inflammatory protein, the expression of which is mainly induced by glucocorticoids (GCs) in haematopoietic cells.
[TSC-22D proteins: new regulators of cell homeostasis?].
Pallardy et al., Châtenay-Malabry, France. In Med Sci (paris), 2015
The GILZ (glucocorticoid-induced leucine zipper) protein has first been identified as a glucocorticoid-responsive gene and is now presented as a major regulator of inflammation.
A focused Real Time PCR strategy to determine GILZ expression in mouse tissues.
Riccardi et al., Perugia, Italy. In Journal 2093-4947, 2014
Glucocorticoid-Induced Leucine Zipper (GILZ) is a glucocorticoid-inducible gene that mediates glucocorticoid anti-inflammatory effects.
Targeting glucocorticoid side effects: selective glucocorticoid receptor modulator or glucocorticoid-induced leucine zipper? A perspective.
Riccardi et al., Perugia, Italy. In Faseb J, 2014
We highlight GC-induced leucine zipper (GILZ), a gene cloned in our laboratory, as a mediator of GC anti-inflammatory and immunosuppressive effects, to outline our perspective on the future of GC therapy.
GILZ as a Mediator of the Anti-Inflammatory Effects of Glucocorticoids.
Riccardi et al., Perugia, Italy. In Front Endocrinol (lausanne), 2014
Glucocorticoid-induced leucine zipper (GILZ) is a dexamethasone-inducible gene that mediates glucocorticoid (GC) actions in a variety of cell types, including many cells of immune system.
GILZ: a new link between the hypothalamic pituitary adrenal axis and rheumatoid arthritis?
Leech et al., Australia. In Immunol Cell Biol, 2014
Glucocorticoid-induced leucine zipper (GILZ) is an anti-inflammatory protein, the expression of which is upregulated by GC.
Development of novel treatment strategies for inflammatory diseases-similarities and divergence between glucocorticoids and GILZ.
Yang et al., Australia. In Front Pharmacol, 2013
One of these is glucocorticoid-induced leucine zipper (GILZ), which inhibits inflammatory responses in a number of important immune cell lineages in vitro, as well as in animal models of inflammatory diseases in vivo.
The glucocorticoid-induced leucine zipper (gilz/Tsc22d3-2) gene locus plays a crucial role in male fertility.
Hummler et al., Lausanne, Switzerland. In Mol Endocrinol, 2012
Tsc22d3-2-deficient mice demonstrated a previously uncharacterized function of glucocorticoid-induced leucine zipper protein in testis development.
Glucocorticoid-induced leucine zipper is downregulated in human alveolar macrophages upon Toll-like receptor activation.
Kiemer et al., Saarbrücken, Germany. In Eur J Immunol, 2012
The data showed a MyD88- and TTP-dependent GILZ downregulation in human macrophages upon Toll-like receptor activation. Suppression of GILZ is mediated by mRNA destabilization, which might represent a regulatory mechanism in macrophage activation.
Glucocorticoid receptor pathway components predict posttraumatic stress disorder symptom development: a prospective study.
Heijnen et al., Utrecht, Netherlands. In Biol Psychiatry, 2012
High GILZ mRNA expression was independently associated with increased risk for a high level of posttraumatic stress disorder symptoms.
Glucocorticoid-induced leucine zipper (GILZ) antagonizes TNF-α inhibition of mesenchymal stem cell osteogenic differentiation.
Shi et al., Augusta, United States. In Plos One, 2011
Glucocorticoid-induced leucine zipper (GILZ) antagonizes TNF-alpha inhibition of mesenchymal stem cell osteogenic differentiation
The Glucocorticoid-induced leucine zipper (GILZ) Is essential for spermatogonial survival and spermatogenesis.
Nef et al., Genève, Switzerland. In Sex Dev, 2011
The data emphasize the essential role played by GILZ in mediating spermatogonial survival and spermatogenesis.
A new dexamethasone-induced gene of the leucine zipper family protects T lymphocytes from TCR/CD3-activated cell death.
Riccardi et al., Perugia, Italy. In Immunity, 1997
By comparing mRNA species expressed in dexamethasone (DEX)-treated and untreated murine thymocytes, we have identified a gene, glucocorticoid-induced leucine zipper (GILZ), encoding a new member of the leucine zipper family.
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