Ask about this productRelated genes to: SETD1B antibody
- Gene:
- SETD1B NIH gene
- Name:
- SET domain containing 1B, histone lysine methyltransferase
- Previous symbol:
- -
- Synonyms:
- KIAA1076, Set1B, KMT2G
- Chromosome:
- 12q24.31
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-15
- Date modifiied:
- 2018-12-21
Related products to: SETD1B antibody
Related articles to: SETD1B antibody
- Recurrent pregnancy loss (RPL) is a distressing pregnancy disorder experienced by ~2.5% of women who try to conceive. Dysregulation of decidual function is an important factor leading to RPL, but the underlying genetic factors remain unknown. We discovered that the methyltransferase SETD1B and a non-coding circular RNA (circSTK40) were significantly down-regulated in the decidual tissue of RPL patients compared to those with healthy pregnancies. SETD1B knockdown resulted in increased apoptosis, decreased autophagy, and increased glycolysis, which could disrupt decidual function among those with RPL. Circstk40 overexpression upregulated SETD1B and alleviated apoptosis, lactic acid accumulation, and autophagy inhibition. Mechanistically, circSTK40 bound to both SETD1B and histone H3, promoting interactions between the two proteins and consequently increasing H3K4 methylation levels. H3K4me2 and H3K4me3 modifications in the SETD1B promoter enhanced transcription of this gene, forming a putative positive feedback loop between SETD1B and H3K4me2/H3K4me3. SETD1B and circSTK40 coordinately promoted decidua survival and function for pregnancy maintenance. Our findings reveal a novel molecular mechanism underlying RPL, providing valuable targets for future research into functional RPL treatments. - Source: PubMed
Zhou TingtingLyu ChunziHou XianpingZhao ShaotongLiao JiaYu WenhaoZhang QianYan JunhaoLi JingNi Tianxiang - The epigenetic modification N6-methyladenosine (mA) is critical for neurodevelopment. However, its interplay with histone modifications during cerebellar development remains poorly understood. Ythdf2 is a core mA reader that promotes selective degradation of methylated transcripts to shape gene expression dynamics. However, whether Ythdf2 also coordinates epitranscriptomic regulation with chromatin remodeling during cerebellar development is unknown. Here, we generated a Ythdf2 knockout (Ythdf2) mouse model and examined cerebellar development at embryonic day 13.5 (E13.5) and postnatal day 3 (P3). Ythdf2 mice developed overt cerebellar ataxia, manifested by tremors and abnormal gait. At the molecular level, loss of Ythdf2 disrupted neural progenitor maintenance and induced premature neuronal differentiation. The expression of progenitor markers, including Sox2, Nestin and Pax6 were markedly reduced, whereas markers of neuronal differentiation such as Tuj1 and Skor2 were increased. In contrast, genes associated with neuronal maturation, including Map2 and Calb1, and astrocytic marker Gfap were downregulated. m⁶A RIP seq analysis demonstrated that Ythdf2 caused a global reduction in m⁶A levels, with the differentially expressed m⁶A modified genes enriched for histone modification and chromatin stability. Furthermore, Ythdf2 loss suppressed transcriptional activity by altering H3K4me3 deposition, thereby reducing chromatin accessibility within neuronal developmental pathways. Co-immunoprecipitation revealed a specific interaction between YTHDF2 and the H3K4 methyltransferase SETD1B, but not CXXC1 or SETD1A, and Setd1b knockdown rescued the neural self-renewal and differentiation defects caused by Ythdf2 deletion. Together, these results establish a mechanistic link in which Ythdf2 connects mA-modified transcripts to Setd1b-mediated H3K4me3 deposition, thereby sustaining chromatin accessibility and transcriptional programs required for proper cerebellar development. - Source: PubMed
Publication date: 2026/04/03
Ren XiaolongJiang JingHu XiujuanZhang MingLi JinchengLu JiafengXia WenjuanDing ChenyueMeng QingxiaHuang Boxian - Histone lysine methyltransferases such as SETD1B regulate chromatin structure and gene transcription. Ketone bodies, including butyrate, act as histone deacetylase inhibitors. We report a 4-year-old boy with SETD1B-related absence epilepsy, refractory to conventional medications, who achieved sustained > 90% seizure reduction on the Modified Atkins ketogenic diet. Single-cell RNA sequencing of 25,159 peripheral mononuclear cells across 3 samples: baseline, 3 months on-diet and age-matched control, revealed widespread dysregulation of the patient's chromatin, ribosomal, immune and mitochondrial pathways at baseline, which were reversed with ketogenic therapy. These findings suggest that the ketogenic diet can improve gene regulation in chromatin-mediated brain disorders. - Source: PubMed
Publication date: 2026/02/19
Tsang EricaGloss Brian SHayes Jessica PHolland Andrew J AMenezes Manoj PBranson Joceline AMohammad Shekeeb SYan Jingya JPatel ShrujnaHan Velda XDale Russell C - Family members of the SET domain family (SETD) of histone lysine methyltransferases (HKMTs) act as principal epigenetic regulators, modulating chromatin structure, transcription pathways, and immune responses. SETDs catalyze lysine methylation on histone and non-histone substrates, as well as non-histone proteins (e.g., p53, NF-κB). These biochemical modifications support gene activity requisite for directing immune cells, modulating cytokine cascades, and inflammatory responses. For SETD family members, systemic dysregulation has become the principal mechanistic fulcrum within the orchestration of major autoimmune and inflammatory syndromes, comprising rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), psoriasis, atherosclerosis and type 2 diabetes, and, to a lesser extent, multiple sclerosis (MS) and inflammatory bowel disease (IBD). SETD1A and SETD1B catalyze H3K4 methylation and regulate the chromatin states governing the proliferation of T-lymphocytes. SETD2 spatially regulates H3K36 trimethylation with the augmentation of DNA regulatory steps and cytokine signaling. SETD6 and SETD7, and other components, enhance the NF-κB signaling involving innate immune response and regulation of chromatin structure. Experimentally validated mutations transform transcript re-equilibration and catalysis of benign enzymes. These alterations disturb immune consistency and endorse predetermined inflammatory responses, and weaken self-tolerance. In the post-genomic era, integrated therapeutic approaches are emerging from potent SETD modulators, small inhibitors, epigenetic scissors, and multi-omics techniques. Overall, this review demonstrates the emerging domain of immuno-epigenetics, SETD enzymes, and the strategic value they could serve as therapeutic targets and biomarkers. - Source: PubMed
Publication date: 2026/01/23
Liu ChunhuiLin LeiYao GuoliangFan YonggangGuo Yongjun - T-cell large granular lymphocyte leukemia (T-LGLL) is a rare, indolent lymphoproliferative disorder of cytotoxic T cells in the peripheral blood, bone marrow, and spleen. This analysis was conducted to characterize genomic alterations and highlight potential therapeutic targets, with the goal of refining the molecular landscape of T-LGLL by emphasizing population-specific biomarkers. - Source: PubMed
Upadhyayula Bhanu SurabiSaglimbeni Grace SGobel EdieGobel AbbiMorris Tyson JSurendra AkaashHsia BeauSood AkshatTauseef Abubakar