Ask about this productRelated genes to: DEAF1 antibody
- Gene:
- DEAF1 NIH gene
- Name:
- DEAF1 transcription factor
- Previous symbol:
- -
- Synonyms:
- NUDR, SPN, ZMYND5
- Chromosome:
- 11p15.5
- Locus Type:
- gene with protein product
- Date approved:
- 2001-02-27
- Date modifiied:
- 2018-08-15
Related products to: DEAF1 antibody
Related articles to: DEAF1 antibody
- Innate immunity is a multilevel system, where each stage plays a key role in ensuring effective immune defense. At the level of chromatin, transcription factors and coactivator protein complexes play a significant role in regulating the immune response. Here, we demonstrate that the conserved transcriptional coactivator SAYP, a component of the Brahma chromatin remodeling complex, participates in the immune response of Drosophila melanogaster. Using immunoprecipitation, we detected an interaction between SAYP and the transcription factor DEAF1 and localized the domains within these proteins that mediate their association. Our data show that SAYP and DEAF1 are recruited to various regions of antimicrobial peptide (AMP) genes in a gene- and pathogen-specific manner following an immune challenge by Escherichia coli or Micrococcus luteus in S2 cell culture. SAYP knockdown significantly reduces the activation of multiple AMP genes, whereas DEAF1 knockdown has a more limited effect. In vivo analysis revealed that loss of full SAYP activity in a hypomorphic mutant significantly impairs the induction of several AMP genes in response to E. coli infection. Furthermore, we found that SAYP cooperates with Relish and DEAF1 in some regulatory regions of AMP genes. Consistently, flies harboring a hypomorphic SAYP mutation exhibited reduced survival following infection by Gram-positive and Gram-negative bacteria. Overall, these findings reveal that SAYP participates in a complex regulatory mechanism with Relish and DEAF1 that controls the innate immune response at the molecular and organismal levels. - Source: PubMed
Publication date: 2026/03/18
Ghassah MonaUlianova Yulia ABalagurov Konstantin IMusabirov Anton ALebedeva Lyubov AShidlovskii Yulii VKachaev Zaur M - DEAF1-associated neurodevelopmental disorder (DAND) is a neurodevelopmental spectrum disorder caused by two methods of inheritance: the autosomal dominant intellectual disability syndrome (Vulto-van Silfout-de Vries syndrome (VSVS), OMIM #615828), and the autosomal recessive Neurodevelopmental disorder with hypotonia and impaired expressive language with or without seizures (NEDHELS OMIM #615828) (OMIM 617171). All reported cases of VSVS have occurred de novo. In this report, we describe the case of a 2-year-old male with a history of autism spectrum disorder and behavioral concerns who was identified to be heterozygous for the c.837C>G (p.C279W) pathogenic variant in DEAF1. Functional assays demonstrate that the p.C279W variant alters DEAF1's transcriptional repression activity. This variant was also identified in his 26-year-old mother, who also has a history of autism and speech delay. To the best of our knowledge, this is the first reported case of the dominant form of DEAF1-associated neurodevelopmental disorder inherited from an affected parent. - Source: PubMed
Publication date: 2026/01/10
Katz KylieJensik PhilipVelinov Milen - Macroautophagy/autophagy protects muscle from proteotoxic stress and maintains tissue homeostasis, yet skeletal muscle relies on it more than most organs. Adult fibers endure constant mechanical strain and require continuous turnover of long-lived proteins, while muscle stem cells (MuSCs) depend on autophagy to remain quiescent, activate after injury, and regenerate effectively. How autophagy is transcriptionally regulated in muscle has been unclear. We identified DEAF1 as a transcriptional brake on autophagy. In MuSCs, DEAF1 controls activation and regeneration and becomes aberrantly elevated with age, promoting protein aggregate formation and cell death. In muscle fibers, DEAF1 is chronically induced during aging, suppressing autophagy and driving functional decline. Exercise reverses DEAF1 induction, restoring autophagy and muscle function. These findings reveal DEAF1 as a key regulator linking autophagy to regeneration and aging, highlighting a therapeutically tractable axis for preserving muscle health. - Source: PubMed
Publication date: 2025/12/31
Lee Wen XingGoh Kah YongChoy Sze MunTang Hong-Wen - Transcriptional dysregulation by aberrant transcription factors (TFs) is a key driver of drug resistance. Resistance to adriamycin (ADR) frequently develops following first-line treatment for multiple myeloma (MM). This study aims to identify novel TFs associated with ADR resistance in MM and to elucidate their underlying mechanisms. - Source: PubMed
Publication date: 2025/12/16
Deng ZhendongWei YongxinLiu ShuangChen LuWang XuhuiLiu ZihaoLiu LinglingWang YaohuiLv XinyuSun ShanliangNi HaiwenGu ChunyanYang Ye - The nuclear factor κB (NF-κB) pathway governs innate immunity, orchestrating rapid transcriptional responses to infection. While the pathway is often depicted as a linear signaling cascade, NF-κB functions within a complex network of cooperative partnerships with other transcription factors and co-regulators. Here, current data about these NF-κB-centered transcriptional partnerships are described with a focus on the model organism Drosophila melanogaster and a comparative analysis with homologous mammalian factors. We detail how Drosophila melanogaster NF-κB factors (Relish, Dif, and Dorsal) cooperate with each other and other transcription regulators, such as Charon, PARP-1, Akirin, SWI/SNF, Mediator, Stat92E, AP-1, FOXO, Nubbin, Caudal, DEAF1, and GATA family transcription factors, to precisely shape immune specificity and homeostasis. We explore the evolutionary conservation of these mechanisms in mammals, where homologous factors similarly shape NF-κB activity to control inflammatory and antiviral responses. While the core principle of NF-κB cooperativity is ancient, the network has expanded and diversified in mammals, reflecting increased genomic and regulatory complexity. This comparative perspective underscores that the functions of NF-κB are fundamentally defined by its context-dependent partnership network. - Source: PubMed
Publication date: 2025/12/03
Ulianova Yulia AGhassah MonaKachaev Zaur MLebedeva Lyubov AShidlovskii Yulii V