Ask about this productRelated genes to: SATB1 antibody
- Gene:
- SATB1 NIH gene
- Name:
- SATB homeobox 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 3p24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-05-03
- Date modifiied:
- 2015-10-08
Related products to: SATB1 antibody
Related articles to: SATB1 antibody
- The chromatin organizer SATB1 is indispensable for thymic regulatory T cell (Treg cell) development and T helper cell induction. Several gene loci have been described to be SATB1-controlled, including the transcription factor GATA3 and the cytokine loci IL-4 and IL-17. However, the global effects of SATB1 on fully differentiated human CD4 conventional T cells (Tconv cells) and Treg cells, and thus SATB1's potential as a target for T cell engineering, are poorly understood. We describe SATB1-regulated gene signatures as largely subset-specific, with broader effects on Treg cells. Despite of the distinct gene-regulatory patterns, we observe overarching dysregulated cytokine and JAK-STAT signaling after ablation. Functionally, KO reduces human Treg cell suppressive capacities but boosts tumor clearance via CD4 CAR T cells in a preclinical, humanized mouse model. Together, Treg destabilization and simultaneous increased activation of CD4 CAR T cells by SATB1 modulation may be an interesting strategy to boost the efficiency of CAR T cell therapies. - Source: PubMed
Publication date: 2026/02/16
Kolb SaskiaDiekmann LeonieLochert Elizabeth DWarmuth LindaRitter JuliaWeber MichaelHoffmann MarkusList MarkusKotlarz DanielSerr IsabelleDaniel CarolinBusch Dirk HSchmidl ChristianSchumann Kathrin - Cutaneous T-cell lymphoma (CTCL) comprises a heterogeneous group of extranodal non-Hodgkin lymphomas. With the publication of the fifth edition of the World Health Organization Classification of Hematolymphoid Tumors, the diagnostic framework for CTCL has shifted from primarily morphologic phenotypes toward an emphasis on molecular drivers. Current research suggests that malignant clones may arise from somatic mutations at the hematopoietic stem cell stage and may follow a continuous hematogenous dissemination model with bidirectional trafficking between the skin and systemic circulation. At the molecular level, genomic instability, often associated with somatic copy-number variations, may promote activation of the janus kinase-signal transducer and activator of transcription (JAK/STAT) signaling pathway through gene-dosage effects. In parallel, chromatin remodeling linked to EZH2 overexpression and reduced special SATB1 expression may support a Th2-polarized program. This phenotype may contribute to epidermal barrier impairment via cytokines such as Interleukins-4 (IL-4) and IL-13, potentially creating conditions permissive for colonization. Microbial superantigens and exotoxins may further contribute to tumor progression and therapeutic resistance by reinforcing JAK/STAT signaling, particularly STAT3, and reducing CD8+ T-cell-mediated immune surveillance. In the dermis, reprogramming of cancer-associated fibroblasts and polarization of macrophages toward an M2 phenotype may collectively contribute to an immunosuppressive niche. Emerging biomarkers, including CD74, and acquired resistance mechanisms after anti-C-C chemokine receptor 4 therapy further extend the translational relevance of recent pathologic findings. Overall, CTCL evolution appears to be a systemic process shaped by interactions between tumor-intrinsic genetic alterations and the skin microenvironment. - Source: PubMed
Publication date: 2026/04/04
Zhang TingHu YiWang KexinZhang ZhaohuaiWang YingZhang YuZhao Zuotao - Obesity-associated inflammation in white adipose tissue (WAT) worsens outcomes of influenza A virus (IAV) infection. A recently identified thoracic cavity WAT (tcWAT) supports IAV replication. However, tcWAT's immune cell composition, functional properties and role in IAV disease severity remains unclear. - Source: PubMed
Publication date: 2026/04/07
Ulanowicz Cassidy JAlarcon Pablo CDamen Michelle S M AWayland Jennifer LSawada KeisukeEom JohnStankiewicz Traci EChung HakLampe KristinSzabo SaraMoreno-Fernandez Maria ESalomonis NathanDivanovic Senad - Eggshell strength is a critical economic trait that declines with hen age, yet the molecular mechanisms distinguishing stable genetic determinants from age-responsive pathways remain unclear. This study implemented a multi-stage comparative framework using uterine transcriptomes from Rhode Island Red hens at peak lay (60 weeks) and late lay (90 weeks) to address this question. At each age, hens were stratified into Weak and Strong shell strength groups based on longitudinal records (5 time points for the 90-week cohort), with 5 individuals per group selected for RNA-seq analysis. Uterine transcriptomic analysis revealed a conserved core of 86 differentially expressed genes associated with shell strength at both ages, with 96.5% exhibiting concordant regulation direction and highly correlated fold-changes (r = 0.84). Weighted gene co-expression network analysis identified two pivotal modules: a stable intrinsic module (MElightcyan) at 60 weeks correlated with peak-lay strength, and an aging-amplified module (MEyellow) at 90 weeks whose correlation with strength progressively increased from mid- to late lay (r = 0.57 at 40 weeks to 0.72 at 90 weeks). Functionally, enriched pathways shifted from cellular structure (MElightcyan) to calcium signaling and hormone regulation (MEyellow) with age. Transcriptional network analysis identified 8 conserved transcription factors (including SATB1 and RXRG) orchestrating this core program. Integrative analysis prioritizing differential expression, longitudinal phenotypic correlation, and QTL mapping highlighted high-confidence candidate genes, including CNTNAP5 (peak-lay) and SLCO1C1 (late-lay). We propose a two-tiered regulatory model wherein a stable core genetic program interacts with dynamic, age-adapted effector networks to determine shell strength. This model provides a dual-strategy framework, distinguishing targets for genetic selection (core program) from pathways for precision management (age-adapted networks) to mitigate age-related decline in shell quality. - Source: PubMed
Publication date: 2026/03/18
Wang LiyuanLiu LeiBai YingWang YanhengZheng ChuanweiWang JinweiChang ShiminMao ZhiqiongLiu XiaohuiGao Yahui - - Source: PubMed
Publication date: 2026/03/12