AFF4 antibody
- Known as:
- AFF4 (anti-)
- Catalog number:
- orb101217
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- AFF4 antibody
Related genes to: AFF4 antibody
- Gene:
- AFF4 NIH gene
- Name:
- AF4/FMR2 family member 4
- Previous symbol:
- -
- Synonyms:
- AF5Q31, MCEF
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-06-27
- Date modifiied:
- 2016-10-05
Related products to: AFF4 antibody
Related articles to: AFF4 antibody
- CHOPS syndrome is a rare, multisystem disorder caused by heterozygous pathogenic variants in the gene. The acronym CHOPS is characterized by Cognitive impairment and coarse facial features (C), Heart defects (H), Obesity (O), Pulmonary involvement (P), and Short stature/skeletal dysplasia (S). The syndrome is caused by variants in , which encodes a protein critical for RNA polymerase II elongation and transcriptional regulation. - Source: PubMed
Publication date: 2026/03/30
Gokdemir IremCetin Sirmen KizilcanKilic EsraBuyukyilmaz GonulDeligozoglu DuyguGurbuz FatihBoyraz Mehmet - BACKGROUND: Lung cancer has been the most common diagnosed cancer and the leading cause of cancer-related death. Growing evidence has demonstrated that circular RNAs (circRNAs) are closely associated with the occurrence and progression of tumors. Ferroptosis is an iron-dependent form of cell death triggered by the accumulation of lipid peroxides, and it has been considered as a potential target for cancer therapy. However, the specific mechanism by which circRNAs modulate ferroptosis in lung cancer remains largely unknown. METHODS: Through retrieval from The Cancer Genome Atlas (TCGA) database, the differential expression of AFF4 mRNA in lung cancer was identified. Further screening and validation revealed that circAFF4, a circular RNA derived from AFF4 host gene, also exhibited a similar trend in lung cancer. Subsequently, quantitative reverse transcription-PCR (qRT-PCR) and fluorescent in situ hybridization (FISH) were used to detect its expression pattern and distribution. Functional studies were conducted both in vitro and in vivo to determine the biological functions of circAFF4. Furthermore, the interaction between circAFF4 and ubiquitin-specific peptidase 10 (USP10) as well as the relationship between USP10 and Glutathione peroxidase 4 (GPX4), were investigated by biotin-labeled RNA pull-down, mass spectrometry, RNA immunoprecipitation (RIP), FISH and co-immunoprecipitation (Co-IP) assays. RESULTS: Here we demonstrated that circAFF4 was significantly downregulated in lung cancer tissues and lung cancer cells. In vitro and in vivo experiments suggested that circAFF4 inhibited the proliferation of lung cancer cells and promoted ferroptosis. Mechanistically, circAFF4 bound to the deubiquitinating enzyme USP10, which in turn suppressed USP10-mediated deubiquitination of GPX4, and enhanced the ubiquitin-dependent proteasome degradation of GPX4, thereby facilitating ferroptosis in lung cancer cells. CONCLUSIONS: Our findings reveal a novel mechanism by which circAFF4 interacts with USP10, impairing USP10-mediated stabilization of GPX4, promoting ferroptosis in lung cancer cells, and ultimately suppressing lung cancer progression. The circAFF4/USP10/GPX4 axis provides a new direction and may be a potential target for lung cancer treatment. - Source: PubMed
Publication date: 2026/04/20
Wang JianingXin SichengZhang ChuanfengXie NingKong PengYu Yuan
- Source: PubMed
- Insulin action on the skeleton is essential for bone development and whole-body energy metabolism, however a global view of signaling in this tissue is lacking. Furthermore, whether there are signaling differences that drive the gene-specific activation under insulin-resistant (IR) or ageing conditions is unknown. Here, we perform a phosphoproteomic analysis of insulin signaling in the bones of young, lean, insulin-sensitive versus old, obese, IR mice revealing a rewiring of phosphorylation. We target dysregulated phosphoproteins in a zebrafish functional genomic screen of bone development and mineralization revealing candidates important for skeletal formation. One of these is ALF Transcription Elongation Factor 4 (AFF4), the core scaffold of the Super Elongation Complex and we show that phosphorylation of S831 on AFF4 is an insulin-dependent substrate of P70S6K and attenuated in aged, IR bone. Phosphorylation of S831 is defective in IR osteoblasts and associated with reduced transcriptional elongation at discrete locations in the genome. Mechanistically, we show phosphorylation of S831 increases recruitment of chromatin remodelers, ENL/AF9 to crotonylated histone via the YEATS domain, and promotes gene-specific activation. Our analysis identifies regulators of insulin action on the skeleton, further uncovering a mechanism of IR via locus-specific changes in transcriptional elongation and gene activation. - Source: PubMed
Publication date: 2025/12/31
Dutt MrigaLiao LuopingKim Hani JieunBlazev RonnieChan AudreyKore HiteshBezawork-Geleta AyenachewDong LiRivera Isela SarahiWee Natalie K YMolendijk JeffreyWong Julian P HHaynes Vanessa RUribe VeronicaLynch Gordon SSmith Kelly AMontgomery Magdalene KWatt Matthew JYang PengyiDodd Garron TVervoort Stephin JSims Natalie AParker Benjamin L - Loss-of-function mutations in methyl-CpG binding protein 2 () cause Rett syndrome. While we know that MeCP2 binds to methylated cytosines on DNA, the full breadth of the molecular mechanisms by which MeCP2 regulates gene expression remains incompletely understood. Here, using a genetic modifier screen, we identify the super elongation complex, a P-TEFb-containing elongation factor that releases promoter-proximally paused RNA polymerase II, as a genetic interactor of . MeCP2 physically interacts with SEC subunits and directly binds AFF4, the scaffold of the SEC, via the transcriptional repression domain. Furthermore, MeCP2 facilitates the binding of AFF4 on a subset of genes in the mouse brain regulating synaptic plasticity and concordantly promotes the binding of RNA polymerase II on these genes. Last, while haploinsufficiency of does not exhibit any behavioral deficits in mice, it exacerbates the impaired contextual learning behavior of hypomorphic mice. We propose a previously unknown mechanism by which MePC2 regulates gene expression underlying synaptic plasticity. - Source: PubMed
Publication date: 2025/11/26
Sonn Jun YoungKim WonhoIwanaszko MartaAoi YukiLi YanQi GuantongParkitny LukeBrissette Janice LWeiner LorinBotas JuanAl-Ramahi IsmaelShilatifard AliZoghbi Huda Y