TSC22D3 predesign siRNA
- Known as:
- TSC22D3 predesign small interfearing RNA
- Catalog number:
- RI15491
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- TSC22D3 predesign siRNA
Related genes to: TSC22D3 predesign siRNA
- 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: TSC22D3 predesign siRNA
Related articles to: TSC22D3 predesign siRNA
- 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 - In livestock, understanding the genetic basis of adaptation to the environment is essential for enhancing resilience to climate change and sustaining productivity in diverse environments. Indigenous Ethiopian cattle represent an ideal model for such studies, as they have evolved across a wide range of environments from the cool, oxygen-limited highlands to the hot, pathogen-rich lowlands. These environmental gradients imposed intense selective pressures, shaping their genomic landscape. In this study, we performed the first comprehensive analysis of X-linked adaptive signatures in Ethiopian indigenous cattle using whole-genome sequencing data. - Source: PubMed
Publication date: 2026/04/10
Ayalew WondossenTarekegn Getinet MXiaoyun WuChu MinNaboulsi RakanTessema Tesfaye SBongcam-Rudloff ErikNegussie EnyewPing YanZhang Zhe - Effector CD8 T cells are key cellular drivers of type 1 diabetes (T1D) pathogenesis, yet questions remain regarding the molecular defects leading to altered cytotoxicity, their signature in peripheral tissues, and their receptor specificity. Thus, we analyzed human pancreatic lymph nodes (pLN) using mass cytometry and single cell RNA sequencing (scRNAseq) with combined proteomic and T cell receptor (TCR) profiling. Cytometric analysis revealed an enriched population of T stem-cell memory (TSCM)-like cells (CD8CD45RACD27CD28CCR7CXCR3 T cells) in T1D pLNs. scRNAseq profiling indicated an elevated inflammatory cytokine gene signature (, ) along with regulators of terminal differentiation (, ), coupled with reduced expression of exhaustion-associated genes (, , ) in CD8 T cells in T1D pLN. Additionally, effector CD8 T cells expressed features of progenitor exhausted cells () in T1D pLN. Immune Response Enrichment Analysis (IREA) indicated IL-15 signaling as a significant driver of these phenotypes. Integrated TCR and transcriptomic analysis revealed a cluster of diverse naïve-like CD8 T cell clones in T1D pLN. When comparing pLN and pancreatic slice cellular isolates, we observed sharing of effector CD8 T cells, with upregulation of terminal effector signatures detected within the pancreas relative to paired pLN samples. Multiplex imaging revealed differential localization of TCF1 and TOX expressing T cells in the pancreas, with TCF1TOX cells located in closer proximity to the islets and displaying a mixture of activation and exhaustion-associated phenotypes. Thus, we provide multimodal cellular profiles enriched in T1D tissues for consideration in therapeutic targeting. - Source: PubMed
Publication date: 2026/04/01
Peters Leeana DSeay Howard RSmith JustinPosgai Amanda LBerkowitz ReedWasserfall Clive HAtkinson Mark ABacher RhondaBrusko Maigan ABrusko Todd M