FOXN1 antibody - N-terminal region (ARP30053_T100)
- Known as:
- FOXN1 (anti-) - N-terminal region (ARP30053_T100)
- Catalog number:
- arp30053_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- FOXN1 antibody - N-terminal region (ARP30053_T100)
Related genes to: FOXN1 antibody - N-terminal region (ARP30053_T100)
- Gene:
- FOXN1 NIH gene
- Name:
- forkhead box N1
- Previous symbol:
- WHN, RONU
- Synonyms:
- FKHL20
- Chromosome:
- 17q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-07
- Date modifiied:
- 2019-04-23
Related products to: FOXN1 antibody - N-terminal region (ARP30053_T100)
Related articles to: FOXN1 antibody - N-terminal region (ARP30053_T100)
- T cells play a vital role in antigen presentation, immune tolerance imbalance, and secretion of pathogenic cytokines in the progression of Myasthenia Gravis (MG). Previous studies have founded that patients with thymic hyperplasia accompanied by MG exhibit autoreactive T cells in thymus that can recognize self-antigens at the neuromuscular junction (NMJ), leading to the destruction of acetylcholine receptors (AChR) and the appearance of muscle weakness. Furthermore, Thymic hyperplasia is associated with T-cell-related autoimmune diseases, and increased expression of WNT4 and FOXN1 are beneficial to the growth of thymic cells and the maintenance of the thymic microenvironment. - Source: PubMed
Publication date: 2026/03/23
Wang XueminChen PeiYang WenjingChen JiaxinLi ShiyinLuo ChuanmingHuang Xin - Natural killer (NK) cells, key effectors of innate immunity, are classically categorized into CD56 and CD56 subsets in humans. While murine NK cell heterogeneity has become increasingly recognized, the classification of mature NK cell subsets remains incompletely defined. Here, we comprehensively characterized CD127 NK cells in mice and identified them as a distinct, mature subset, developing independently of the thymus and interleukin (IL)-15 signaling. Flow cytometric analyses revealed that CD127 NK cells are broadly distributed across lymphoid and non-lymphoid tissues-including in C57BL/6 wild-type and athymic Foxn1 mice-and exhibit a surface phenotype distinct from CD127 NK and thymus-derived CD127 NK cells. Functional assays demonstrated that CD127 NK cells produce interferon-γ and exert cytotoxic activity, despite expressing markers typically associated with immature NK cells. CD127 NK cells were absent in IL-7Rα mice but present in IL-15 and IL-15Rα mice, indicating a selective dependence on IL-7 signaling. IL-7 promoted their proliferation and activation both in vitro and in vivo. These findings revise current models of NK cell development by identifying a novel, IL-7-responsive, IL-15-independent, thymus-independent, and functionally competent CD127 NK cell subset that is phenotypically distinct from helper-like innate lymphoid cells (ILCs). This study provides a framework for future investigations on NK cell heterogeneity, tissue specialization, and cytokine-mediated regulation. - Source: PubMed
Publication date: 2026/03/14
Kim YunaHwang Seon-YeongKwon Young-JinKim Ji-EunRajbongshi LataLee Su-RinJoo SeongwonPark SeongheumOh Sae-OckKim Byoung-SooLee DongjunYoon Sik - The thymus plays a critical role in sustaining T-cell immunity, although its function is highly vulnerable to acute injury and physiologically declines with age, resulting in compromised immune responses. Impaired thymic function represents a major clinical challenge, particularly in settings of immunosuppression associated with cancer therapy and aging. Yet, effective strategies to rejuvenate the thymus remain limited. To explore novel regenerative approaches, we focused on FOXN1, a master regulator of thymic epithelial cell (TEC) development and function. By developing a custom screening platform, we tested a library of FDA-approved compounds for their ability to induce FOXN1 in TECs. Proteasome inhibition emerged as a potent and previously unrecognized mechanism for upregulating FOXN1 in both murine and human primary TECs. Among the hits identified in the screening, the antiparasitic drug nitazoxanide (NTZ) stood out for its proteasome inhibitory activity and for inducing Foxn1 expression while preserving cell viability, unlike other proteasome inhibitors. Mechanistically, NTZ-induced proteasome inhibition triggered endoplasmic reticulum stress (ER) and the adaptive unfolded protein response (UPR), ultimately engaging autophagy in TECs. In this context, the induction of autophagy acted as a compensatory mechanism to support cell survival in response to proteasome inhibition. Notably, when administered in mice, NTZ significantly accelerated functional thymic recovery after radiation-induced damage, promoting restoration of thymic architecture and cellularity of both stromal and hematopoietic compartments without disrupting physiological T-cell selection or tolerance mechanisms. Consistent with our in vitro findings, NTZ treatment induced Foxn1 and its downstream targets in TECs in vivo and conferred protection to TECs following irradiation. These findings uncover proteasome inhibition and, more broadly, modulation of ER stress and UPR pathways as a previously unrecognized mechanism regulating Foxn1 expression and position NTZ as a promising pharmacological strategy to enhance immunity in patients experiencing T-cell deficiencies due to cancer-related immunosuppression, infections, and age-related thymic atrophy. - Source: PubMed
Publication date: 2026/03/26
Genah ShirleyPellegrino MarshaGiansanti ManuelaMancusi AngelicaTaviani AlessioCardinale AntonellaRosichini MarcoFlamini SaraCatanoso Maria LuigiaGiorda EzioVolpe GabrielePiccione MichelaNazio FrancescaDudakov Jarrod Avan den Brink Marcel R Mde Billy EmmanuelLocatelli FrancoVelardi Enrico - To develop an immunodeficient retinal degenerate (RD) rat model with fluorescent label for studying retinal degeneration and transplant-host connectivity. - Source: PubMed
Publication date: 2026/03/06
Seiler Magdalene JNguyen HeliosEndejan DevanLin BinZhao GuojunKlaskala Lauren - The thymus is a primary lymphoid organ in which diverse and self-tolerant T cells are produced from bone marrow-derived hematopoietic progenitors. Progressive, age-associated thymic involution reduces T-cell output and impairs adaptive immunity; however, the molecular mechanisms underlying this process remain elusive. Here, we report that the conditional deletion of the RNA-binding proteins Zfp36l1 and Zfp36l2 in thymic epithelial cells (TECs) leads to a pronounced reduction in the number of TECs during the embryonic stage and early neonatal stage, despite a largely preserved thymus size. Postnatally, these mice exhibit excessive medullary TEC (mTEC) expansion, elevated intrathymic proinflammatory cytokine production, FOXN1 downregulation, and premature thymic involution. These findings reveal a protective role for Zfp36 Tristetraprolin (TTP) family proteins in regulating cytokine levels within the thymic microenvironment and preventing premature thymic involution. Moreover, our results suggest a previously unappreciated connection between central tolerance induction and the onset of age-associated thymic involution. - Source: PubMed
Publication date: 2026/03/16
Han JianxunGolzari-Sorkheh MahdiehRajan VinothkumarZúñiga-Pflücker Juan Carlos