TSC22D3 Antibody, FITC conjugated

1. The mRNA expression of GILZ was significantly correlated with Systemic Lupus Erythematosus Disease Activity Index score. PMID: 28601944
2. We propose a novel role of GILZ in contributing to corticoid-induced leptin and leptin receptor expression in osteoarthritis synovial fibroblasts PMID: 27716396
3. TSC22D3 gene expression is significantly associated with long-term changes in Blood Pressure, providing a link between gene expression and Blood Pressure. PMID: 28784648
4. Overall, these results suggest that GILZ antagonizes the pro-inflammatory effects of TNFa in human adipocytes, and its downregulation in obesity may contribute to adipose inflammation and dysregulated adipokine production, and thereby systemic metabolism. PMID: 27178044
5. Under endoplasmic reticulum stress conditions, overexpression of GILZ significantly reduced activation of mitochondrial pathway of apoptosis by maintaining Bcl-xl level. GILZ protein affects the unfolded protein response signaling shifting the balance towards pro-survival signals as judged by down-regulation of CHOP, ATF4, XBP1s mRNA and increase in GRP78 protein level. PMID: 27416758
6. results reveal GILZ to be a new actor in apoptosis regulation in neutrophil-like cells involving JNK and Mcl-1. PMID: 26384220
7. GILZ is a non-redundant regulator of B cell activity, with important potential clinical implications in systemic lupus erythematosus. PMID: 26612340
8. our data suggest that GILZ is a key regulator of macrophage functions. PMID: 25964494
9. L-GILZ stabilizes p53 proteins by decreasing p53 ubiquitination and increasing MDM2 ubiquitination. PMID: 25168242
10. The N-terminal part of L-GILZ protein is responsible for Ras/L-GILZ protein-to-protein interaction, important for the control of proliferation rate of spermatogonia. PMID: 24993177
11. PUVA directly stimulates GILZ expression. PMID: 24215840
12. Data show a diminished expression of the anti-inflammatory mediator GILZ in the inflamed vasculature and indicate that GILZ downregulation requires the mRNA binding protein ZFP36. PMID: 24747114
13. Inhibition of epithelial injury repair by dexamethasone is mediated in part by activation of GILZ. PMID: 23573276
14. study suggests that GILZ variants are not common causes of SCO and NOA in Australian or American men PMID: 23494955
15. Exogenous GILZ exerts inhibitory effects on endothelial cell adhesive function via a novel pathway involving modulation of NF-kappaB p65 DNA binding and MAPK activity. PMID: 23729444
16. Delta-sleep inducing peptide entrapment and release from polymer hydrogels based on modified polyvinyl alcohol in vitro PMID: 23650723
17. DC-SCRIPT serves an important role in regulating GR function in DCs, corepressing GR-dependent upregulation of the tolerance-inducing transcription factor GILZ. PMID: 23440419
18. Glucocorticoid-inducible genes GILZ and SGK-1 might be promising candidate markers for hippocampal volume changes relevant for diseases like MDD. PMID: 22832853
19. 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. PMID: 22539300
20. High GILZ mRNA expression was independently associated with increased risk for a high level of posttraumatic stress disorder symptoms. PMID: 22137507
21. these results demonstrate that GILZ is a key inhibitor of the mTORC2 pathway. PMID: 21804606
22. Data show that together with GILZ, chemokine CX3CL1 emerges as a regulator of cell proliferation, which may be of potential clinical relevance for the selection of the most appropriate treatment for EOC patients. PMID: 21750716
23. UL14 of herpes simplex virus type 1 interacts with cellular factor TSC22D3 during replication. PMID: 21512757
24. The glucocorticoid-induced leucine zipper protein GILZ is a glucocorticoid-responsive molecule with signal transduction interactions, many of which are operative in inflammatory diseases; it could be a key endogenous regulator of the immune response. PMID: 21556028
25. Taking into account the unique role of DCs within the allo-HSCT context, novel preventive and curative therapeutics for GVHD might be based on the selective induction of GILZ expression in vivo PMID: 20970683
26. GILZ1 inhibits SGK1 ubiquitinylation and subsequent proteasome-mediated degradation, thereby prolonging its half-life and increasing its steady-state expression. PMID: 20947508
27. GILZ expression provokes a Crm-1-dependent nuclear exclusion of FOXO3 leading to its relocalization to the cytoplasm. PMID: 20018851
28. Implication of the transcription factor GILZ in the pathophysiology of glucocorticoid-induced osteoporosis by regulating osteoblast maturation and bone turnover. PMID: 19875485
29. GILZ activates AKT, a crucial signaling molecule in tumorigenesis appearing as a potential key molecule in epithelial ovarian cancer. PMID: 19814803
30. Glucocorticoids and IL-10 stimulated macrophage production of GILZ, which displayed activities related to anti-inflammatory and immunosuppressive effects. PMID: 12393603
31. GILZ is a transiently expressed protein induced upon IL-2 withdrawal that protects T cells from the onset of apoptosis. PMID: 15031210
32. Overexpression of the Forkhead transcription factor FoxO3 enhances GC-induced gilz mRNA expression. PMID: 15705665
33. analysis of a novel link between GILZ and regulation of epithelial sodium transport through modulation of ERK signaling PMID: 16216878
34. GILZ is critical for commitment of DCs to differentiate into regulatory DCs and to the generation of antigen-specific Tregs. PMID: 17356131
35. multiple GILZ isoforms are expressed in most cells and tissues and that these play distinct roles in regulating proliferation and ion transport. PMID: 17956870
36. Lower basal plasma cortisol levels and a lower expression of corticosteroid receptors and GILZ in fibromyalgia patients when compared to healthy controls. PMID: 18468809
37. GILZ is a mediator of glucocorticoid killing, and is regulated by PI3-kinase/AKT. PMID: 18499442
38. Down-regulated expression of GILZ may contribute to the pathogenesis of CRSsNP and CRSwNP and associate with response to surgery. GILZ expression in the upper airways can be regulated differentially by different cytokines. PMID: 19260870
39. GILZ1 and SGK1 provide a physical and functional link between the PI3K- and Raf-1-dependent signaling modules PMID: 19380724

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HGNC: 3051

OMIM: 300506

KEGG: hsa:1831

STRING: 9606.ENSP00000314655

UniGene: Hs.522074