Ask about this productRelated genes to: MAGEA4 antibody
- Gene:
- MAGEA4 NIH gene
- Name:
- MAGE family member A4
- Previous symbol:
- MAGE4
- Synonyms:
- MAGE4A, MAGE4B, MAGE-41, MAGE-X2, MGC21336, CT1.4
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 1994-04-04
- Date modifiied:
- 2015-11-13
Related products to: MAGEA4 antibody
Related articles to: MAGEA4 antibody
- Small cell lung cancer (SCLC) is an aggressive neuroendocrine (NE) carcinoma characterized by early metastasis and an immune-cold microenvironment. We show that UHRF1, a chromatin-associated effector of RB1/E2F signaling, promotes SCLC growth and metastasis across major molecular subtypes. Using human SCLC cell lines, orthotopic and intracardiac xenografts, and genetically engineered mouse models, we found that loss of UHRF1 reduces proliferation, invasion, tumor burden, and metastasis while reprogramming tumors away from NE states toward an inflamed transcriptional program. UHRF1-deficient tumors upregulate chemokines and exhibit increased infiltration of CD8 T cells and myeloid populations. Mechanistically, UHRF1 interacts with PRC2 to reinforce NE lineage programs and suppress inflammatory gene expression. UHRF1 loss derepresses DNA-methylation-silenced tumor antigens, including MAGE-A4, highlighting a potential vulnerability that could be leveraged therapeutically. Together, these findings connect RB1 loss with chromatin repression, lineage control, and immune exclusion, highlighting UHRF1-dependent repression as a therapeutic vulnerability in SCLC. - Source: PubMed
Publication date: 2026/03/24
Gu YijunDe La Torre Jamie-JeanFazeli YasaminValenzuela J MateoGuzman FrederickTinoco RobertoBenavente Claudia A - The action of immune molecular mechanisms in the intratumor microenvironment in desmoid tumors (DTs) remains unclear. The purpose of this research was to clarify the expression patterns of PD-1/PD-L1 immune checkpoint pathways and NY-ESO-1/MAGE-A4 molecular pathways in DTs. - Source: PubMed
Hashimoto KazuhikoNishimura ShunjiTan HirokiIto TomohikoGoto Koji - Correct development of the testis serves as a springboard for male fertility in adult life, yet our understanding of the timing of human Sertoli and germ cell maturation and their dynamics is incomplete. To map the developmental timeline of germ cells and Sertoli cells, we analysed an extensive set of human foetal and prepubertal testicular samples [n=48, spanning from 7 post conception weeks (PCW) to 13.5 years of age]. Octamer binding transcription factor (OCT)3/4+ gonocytes were identified as the main source of proliferative germ cells during foetal development, while melanoma associated antigen (MAGE)-A4+ (pre)spermatogonia divided at a slow rate both in utero and during childhood. In samples aged between 4 and 10 years, anti-Müllerian hormone (AMH) expression is reduced and androgen receptor (AR) expression is increased, consistent with maturation of testicular Sertoli cells. Sertoli cell proliferation peaked at 2-2.5 years and gradually declined through early childhood, becoming minimal from the age of 6, coinciding with lumen formation. These data suggest that Sertoli cell maturation precedes the initiation of spermatogenesis well before the start of puberty. Ultimately, this human testicular developmental timeline serves as a reference for the development of in vitro gametogenesis models and paves the way for fertility preservation and restoration for those at risk of infertility. - Source: PubMed
Publication date: 2026/02/06
Sanou IrisLakshmipathi MathangiSchönhage Lisette Kvan Daalen Saskia K Mde Winter-Korver Cindy MMeißner AndreasHamer Geertde Rooij Dirk GMitchell Rod TMulder Callista L - Intervertebral disc degeneration (IDD) represents a significant health concern affecting a large portion of the population and leads to chronic pain and disability. Despite the prevalence of this condition, the underlying biological mechanisms and potential biomarkers for early diagnosis remain inadequately understood. Advances in proteomics have opened new avenues for identifying blood biomarkers that can facilitate better diagnostic and therapeutic strategies. The primary aim of this study was to identify and validate specific plasma proteins associated with varying grades of IDD. This case-control study compared plasma samples from patients with grade II ( = 10) and grade V ( = 10) IDD to assess differential protein expression. Proteomic analysis was conducted via the SomaScan Assay to screen and identify candidate proteins. Six differential proteins─COL6α3, REG1β, ATF5, CAP1, MAGEA4, and LILRB3─were identified with the highest fold changes and recognized as biomarkers. Subsequent validation of these biomarkers was performed using enzyme-linked immunosorbent assay (ELISA) technology in a validation cohort of 50 patients. A final six-protein combined model achieved an optimal predictive efficacy (AUC = 0.8700). This study provides several noninvasive and rapid plasma biomarkers for the early diagnosis of IDD. - Source: PubMed
Publication date: 2026/01/23
Zhou ZiyueLi YinkunZhu LinLi HuiWang NannanZhou HaiyuanZhang JingziFang LeiLi Sen - Tumor-specific HLA/peptides (pHLA) represent attractive therapeutic targets for cancer. Two cell-based modalities can target pHLA-expressing tumors: T cell receptors (TCRs) or TCR-mimetic (TCRm) antibodies reformatted as chimeric antigen receptors (CARs). Using HLA-A2/MAGEA4 as a model pHLA, we discerned the relative potency of TCR-T and CAR-T cells, informing how to best deploy these for clinical benefit. Although TCR-T cells were more sensitive at detecting low-density pHLA, TCR-T cells exerted only transient in vivo antitumor efficacy followed by tumor relapse due to deficient TCR-T cell proliferation and persistence that was associated with a more differentiated and dysfunctional phenotype. By contrast, CAR-T cells with encoded costimulatory signaling fully regressed tumors. Insufficient TCR-T cell durability was overcome by coengaging 41BB or IL-2 signaling pathways, thereby enhancing tumor control in vivo. These data establish differential activities of human TCR-T and CAR-T cells targeting the same pHLA and inform the development of optimal targeting strategies to induce durable clinical responses. - Source: PubMed
Publication date: 2026/01/21
Decker Corinne EIdun JacquelineMohrs KatjaMeagher Thomas CraigPetriv IrynaGolas JonathonSalzler RobertHelms TimothyAjithdoss DharaniAvvaru SuhasiniWu JiaxiZhang TongSmith EricThurston GavinLin John CKirshner Jessica RDiLillo David J