Ask about this productRelated genes to: FOXA1 antibody
- Gene:
- FOXA1 NIH gene
- Name:
- forkhead box A1
- Previous symbol:
- HNF3A
- Synonyms:
- -
- Chromosome:
- 14q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-02-11
- Date modifiied:
- 2015-02-02
Related products to: FOXA1 antibody
Related articles to: FOXA1 antibody
- The major histocompatibility complex (MHC) is a well-known gene complex that plays a fundamental role in immune recognition; however, its influence on reproductive processes in cattle is not yet fully established, particularly regarding how it modulates the female response to the embryo. Therefore, this study aimed to investigate the relationship between MHC genes and reproductive processes in cattle and to identify potential molecular targets involved in these mechanisms. - Source: PubMed
Publication date: 2026/07/30
Faverzani Louíse BZwirtes Andreia KRodrigues Dinah P AMachado Thais FOliveira Daniele ASilveira Luiza CSeixas Nathalia PSilva Evandro NSilva Danielly B SVaz Ricardo ZMelo Thaise P - - Source: PubMed
Publication date: 2026/08/26
Yang YaqinLu JunZhu YuruChen DandanTang JiayiZhang MinLu JiahuiYang YanziTian ShashaZhao Huajun - Lineage plasticity has emerged as a central mechanism through which cancer cells adapt to therapeutic pressure, evade immune surveillance, and acquire aggressive phenotypes. Although recognized across tumor types, the regulatory principles governing how cancer cells reprogram cellular identity remain incompletely understood. In this review, we propose that lineage plasticity in cancer reflects the redeployment of regulatory frameworks established during normal development. Rather than representing a stochastic byproduct of genomic instability, cancer plasticity frequently unfolds within gene regulatory architectures that also govern cell fate specification, lineage commitment, and controlled state transitions during embryogenesis and tissue homeostasis. Developmental transcription factors, including members of the SOX family, FOXA1, ASCL1, NKX2-1, and epithelial-mesenchymal transition regulators, function as lineage gatekeepers during development but are repurposed in cancer to destabilize lineage commitment and enable phenotypic switching. Similarly, epigenetic regulators that guide developmental trajectories, including chromatin remodeling complexes, Polycomb group proteins, and DNA methylation machinery, are frequently dysregulated or redistributed in tumors, altering the repression of lineage-stabilizing and alternative lineage programs and thereby weakening epigenetic barriers to lineage transitions. Together, these observations support a model in which development and cancer operate as mirror regulatory systems: one establishing and stabilizing cellular identity, the other exploiting the same regulatory architecture to permit adaptive reprogramming under selective pressure. We further discuss how emerging single-cell and spatial multi-omics technologies, integrated with artificial intelligence-based modeling, enable mapping of cell state landscapes and transitional trajectories, transforming lineage plasticity from a descriptive phenomenon into a measurable and predictable property of tumor evolution. - Source: PubMed
Publication date: 2026/08/25
Fraidenburg MelanieLi LongjunKwon RosaGhali FadyWarrick JoshuaLeapman Michael SKim Isaac YiMu Ping - Consensus molecular classes of urothelial carcinoma (UC) include basal/squamous (Ba/Sq), luminal papillary (LumP), luminal nonspecified (LumNS), luminal unstable (LumU), stroma-rich, and neuroendocrine (NE)-like. We aimed to determine the consensus molecular classifications of micropapillary (MP), plasmacytoid (PC), and sarcomatoid (SM) subtypes of bladder UC and characterize their spatial transcriptomic profiles. - Source: PubMed
Publication date: 2026/08/25
Zhao TingNawrocki ColeXiong LinjieNieman Linda TSaylor Philip JBlute Michael LMiyamoto David TTing David TDahl Douglas MWu Chin-Lee - Prostate cancer (PCa) is one of the most prevalent malignancies affecting male health globally, ranking as the fifth leading cause of cancer-related mortality in men. Post-translational modifications (PTMs), encompassing a diverse array of biochemical alterations such as methylation, acetylation, phosphorylation, ubiquitination, SUMOylation, glycosylation, and lactylation, constitute a critical category of epigenetic regulatory mechanisms that modulate numerous cellular processes in both physiological and pathological contexts. Despite their fundamental importance, the precise functional implications of PTMs in PCa pathogenesis remain incompletely elucidated. Current evidence has established that multiple oncogenic signaling pathways (including AR, PTEN/PI3K/AKT, CDK4/6-RB, Wnt/β-catenin, and JAK/STAT3), key transcription factors (such as AR, p53, ERG, NKX3.1, FOXA1, HOXB13, KLF, and MYC), and specific histone modification patterns are intimately associated with PCa progression. Furthermore, emerging studies have implicated PTMs in mediating drug resistance and immune suppression in PCa, representing two major clinical challenges in contemporary PCa management. Beyond these canonical regulatory mechanisms, metabolism-associated and emerging PTMs further connect metabolic reprogramming with AR variant splicing, lineage plasticity, immune modulation, and therapeutic resistance. We also discuss the clinical implications of PTMs in PCa, including PTM-directed clinical trials, targeted protein degradation strategies, and diagnostic or prognostic biomarker development. In light of these critical findings, this review systematically synthesizes current research elucidating the mechanistic roles of PTMs in regulating these molecular determinants of PCa progression, with the aim of providing a comprehensive understanding of PTM-mediated regulatory networks and offering translational insights for potential clinical applications. - Source: PubMed
Publication date: 2026/08/24
Ren HuanLi XuanjiJiang ZhiliangBai YunjinAi Jianzhong