GILZ
- Known as:
- GILZ
- Catalog number:
- 000700A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- GILZ
Related genes to: GILZ
- Gene:
- TSC22D3 NIH gene
- Name:
- TSC22 domain family member 3
- Previous symbol:
- DSIPI
- Synonyms:
- DIP, GILZ, TSC-22R, hDIP
- Chromosome:
- Xq22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-06-24
- Date modifiied:
- 2015-11-18
Related products to: GILZ
Related articles to: GILZ
- : Hematopoietic stem cell (HSC) ex vivo culture causes severe loss of repopulation and regenerative capacity without compromising multilineage differentiation, which greatly limits the efficacy of HSC transplantation. The molecular mechanisms underlying culture-triggered HSC dysfunction remain poorly understood. : Human CD34 HSCs were cultured ex vivo for 96 h to establish a culture-induced HSC dysfunction model. Single-cell RNA sequencing was applied to screen key regulatory genes. TSC22D3 function was verified via overexpression assays, and immunodeficient mice were used to assess HSC engraftment. Transcriptomic profiling were performed to explore downstream molecular mechanisms. : Ex vivo culture induced G0 quiescence exit, elevated early apoptosis and impaired in vivo repopulation in human CD34 HSCs. TSC22D3 was highly enriched in freshly isolated quiescent HSCs and gradually downregulated during culture. TSC22D3 overexpression restored HSC G0 arrest and improved hematopoietic engraftment in mice. Mechanically, TSC22D3 upregulated HSC self-renewal genes, suppressed cell cycle-related genes (CDK2/4), and activated the P53-P21-P27 pathway. : This study demonstrates that TSC22D3 preserves HSC function during ex vivo culture by maintaining stem cell quiescence and restricting excessive proliferation. These findings reveal a novel transcriptional mechanism regulating HSC homeostasis and provide a promising target for improving functional HSC ex vivo expansion for clinical transplantation. - Source: PubMed
Publication date: 2026/06/24
Hu XiaopengZhang TianPan GuangjinXue Xingkui - Glucocorticoids are major regulators of human neural development and stress adaptation, yet their transcriptional effects across experimental paradigms remain poorly integrated. This review synthesizes evidence from 13 studies employing human induced pluripotent stem cell (hiPSC)-derived neural models exposed to cortisol or dexamethasone, including neural progenitors, neurons, astrocytes, and brain organoids. When available, transcriptomic datasets from these studies were reanalyzed under standardized criteria to directly compare acute and chronic GC exposure. This comparative approach revealed that GCs modulate shared pathways related to neurogenesis, cytoskeletal organization, immune signaling, and stress response, while the duration of exposure critically shapes the underlying transcriptional architecture. Acute stimulation predominantly upregulated canonical GR targets such as FKBP5, ZBTB16, and TSC22D3 involved in early stress response and feedback control, whereas chronic exposure induced sustained remodeling of genes including MT2A, RASFAF4, and DPYSL5 linked to oxidative stress regulation and neuronal structure. A conserved downregulated core comprising NFIA, NFIB, and CCL2 was shared across paradigms, reflecting persistent suppression of glial differentiation and inflammatory signaling. Together, these findings delineate distinct yet convergent transcriptional programs governed by GC exposure, providing mechanistic insight into how temporal dynamics of glucocorticoid signaling may contribute to altered neurodevelopmental trajectories and increased vulnerability to stress-related psychiatric disorders. - Source: PubMed
Publication date: 2026/07/07
Dal Molin Eloiza AdrianeKaster Manuella PintoNascimento Juliana Minardi - Systemic administration of glucocorticoids (GCs) has immunosuppressive effects that involve the upregulation of the transcription factor TSC22D3 in dendritic cells (DCs), thereby reducing their capacity for antigen presentation to T lymphocytes. Recently, we found that this effect is not mediated by direct action on the GC receptor in DCs but rather involves an indirect signaling circuitry. Indeed, GCs act on the GC receptor expressed by many cell types to cause the upregulation and release of the tissue hormone DBI/ACBP (diazepam binding inhibitor, acyl-CoA binding protein). DBI/ACBP, which is an inhibitor of macroautophagy/autophagy, then acts on the benzodiazepine-binding site of the gamma-aminobutyric acid type A receptor (GABAR) to elicit the upregulation of TSC22D3. The indirect, DBI/ACBP-dependent upregulation of TSC22D3 by GCs is observed both in vivo (mice) and in vitro, in murine splenocytes and bone marrow-derived DCs, as well as in human peripheral blood mononuclear cells and monocyte-derived DCs. Inhibition of human mixed lymphocyte reactions (confronting DCs and lymphocytes from distinct donors) by DCs is reduced by DBI/ACBP neutralizing antibodies. Similarly, the suppression of antitumor immune responses (elicited by vaccination with dying cancer cells, immunogenic chemotherapy or PDCD1/PD-1 blockade) by GCs is reversed by DBI/ACBP neutralization. Epistatic experiments indicate that knockout of in DCs and inhibition of DBI/ACBP act on the pathway to reverse GC-mediated inhibition of cancer immunosurveillance. Of note, the benzodiazepine diazepam restores GC-induced immunosuppression when DBI/ACBP is inhibited. Altogether, these findings support a role for the DBI/ACBP-GABAR system in immunosuppression by GCs. - Source: PubMed
Publication date: 2026/05/03
Shen ZhePan HuiZhao LiweiLiu PengKepp OliverMaiuri Maria ChiaraMa YutingMartins IsabelleKroemer Guido - Atherosclerosis (AS), myocarditis and vasculitis constitute a spectrum of prevalent cardiovascular diseases (CVDs) where immune dysregulation acts as a central pathogenic driver. Consequently, targeting the immune-cardiovascular axis represents a promising therapeutic frontier. This review systematically elucidates the shared immunological mechanisms underpinning these distinct yet interconnected conditions. The specific pathogenic landscapes are dissected, ranging from lipid-driven endothelial dysfunction and plaque instability in AS, to pathogen- or autoimmune-mediated myocardial injury in myocarditis, and necrotizing vessel wall inflammation in vasculitis. The fundamental roles of innate and adaptive immunity in driving cardiovascular pathology are delineated, highlighting the significant cross-talk and convergent immunological signatures among AS, myocarditis and vasculitis. Central to this convergence, CXCR4, PYCARD, TSC22D3 (GILZ), and HSPA1A are identified as critical hubs orchestrating leukocyte trafficking, inflammasome activation, immune tolerance, and proteostatic stress, respectively. Furthermore, precision strategies targeting these hubs are evaluated, utilizing agents such as Plerixafor, Lycorine, Dexamethasone, and Tanespimycin. Finally, emerging frontiers, including natural products and biomaterials, are assessed, providing a perspective on current clinical trials and future directions for resolving cardiovascular inflammation. - Source: PubMed
Publication date: 2026/04/07
Liao Yuan-PengWei Yu-XinZhang Feng-MeiZhang Zhao-ShanXu Sen-PingYou Yong-HaoGuo Jia-Wei - A major technical challenge in single-cell transcriptomics is the absence of an integrative analytic pipeline that can simultaneously leverage gene regulatory network (GRN) architecture, AI-assisted gene panel discovery, and functional relevance analyses to generate coherent biological insights. Existing approaches often treat these components independently, focusing on clusters, marker genes, or predictive features without integrating them into a mechanistically grounded framework. Consequently, comprehensive screening that links regulatory association, gene signature screening, and functional interpretation within single-cell datasets remains limited, underscoring the need for an integrated strategy. - Source: PubMed
Publication date: 2026/04/06
Borra SantoshiYan DaWelner Robert SYue Zongliang