Ask about this productRelated genes to: SFRS17A antibody
- Gene:
- AKAP17A NIH gene
- Name:
- A-kinase anchoring protein 17A
- Previous symbol:
- CXYorf3, SFRS17A
- Synonyms:
- XE7, XE7Y, DXYS155E, MGC39904, 721P, CCDC133
- Chromosome:
- Xp22.33 and Yp11.32
- Locus Type:
- gene with protein product
- Date approved:
- 2006-09-22
- Date modifiied:
- 2015-11-17
Related products to: SFRS17A antibody
Related articles to: SFRS17A antibody
- Transposable elements (TEs) threaten genomic integrity, yet their pervasive presence indicates the limitations of existing silencing mechanisms. A recent paper in (Zhao . 2025) discovered the SOS splicing system, which provides an RNA-level defense that excises DNA transposons from mRNAs, thereby restoring gene sequence. This spliceosome-independent pathway, mediated by AKAP17A, CAAP1, and RTCB, recognizes dsRNA hairpins formed by inverted terminal repeats (ITRs) and religates the resulting RNA fragments. From an evolutionary perspective, SOS splicing exemplifies a post-transcriptional error-correction mechanism that mitigates the deleterious consequence of TE insertions, paralleling the Constructive Neutral Evolution (CNE) framework. In contrast, ADAR-mediated A-to-I RNA editing suppresses the MDA5-triggered innate immune responses to TE-derived dsRNAs, effectively tolerating rather than eliminating TEs. There may be partial overlap between ADAR and SOS substrates. ADAR editing may delay but not prevent SOS splicing, while SOS excision removes ADAR substrates. The lethality of ADAR loss underscores its role as the mechanism mitigating purifying selection on TEs and thus may contribute to their genomic tolerance and proliferation. Collectively, while ADAR masks the harm of TEs, SOS splicing actively repairs the resulting damage, together illustrating a delicate evolutionary balance between TE tolerance and transcriptomic rescue. - Source: PubMed
Publication date: 2026/02/26
Cao QiDuan Yuange - Hypoxia-inducible factor 1α (HIF1α) is the master transcriptional regulator of cellular adaptation to low oxygen microenvironment, essential for oxygen homeostasis and promoting tumorigenesis. We report that AKAP17A, an A-kinase anchoring protein, activates HIF1α signaling through a protein kinase A (PKA)-independent mechanism. Depletion of AKAP17A in mammalian cells reduced HIF1α abundance and attenuated the transcriptional activation of HIF target genes. Consistently, akap17a-null zebrafish exhibited compromised HIF signaling, impaired hypoxia tolerance, and diminished hypoxia-induced erythropoiesis. Functionally, knocking out AKAP17A suppressed cancer cell proliferation in vitro and impeded tumor growth in vivo. Mechanistic investigations revealed that AKAP17A augments HIF1α protein synthesis. Collectively, this work identifies AKAP17A as a pivotal regulator of the HIF1α, providing novel insights into its role in hypoxic adaptation and oncogenesis. - Source: PubMed
Publication date: 2025/12/13
Zhang BoqiWang ZifanTang YanfeiMa GuanboLiu YunzhangLi YunHao JiejieYe JunliSun XiangrongLu Ling - All genomes have mobile genetic segments called transposable elements (TEs). Here we describe a system, which we term SOS splicing, that protects Caenorhabditis elegans and human genes against DNA-transposon-mediated disruption by excising these TEs from host mRNAs. SOS splicing, which seems to operate independently of the spliceosome, is a pattern-recognition system triggered by the base-pairing of inverted terminal repeat elements, which are a defining feature of DNA transposons. We identify three factors required for SOS splicing in both C. elegans and human cells: AKAP17A, which binds TE-containing mRNAs; the RNA ligase RTCB; and CAAP1, which bridges RTCB and AKAP17A to allow RTCB to ligate mRNA fragments generated by TE excision. We propose that SOS splicing is a previously undescribed conserved and RNA-structure-directed mode of mRNA splicing, and that an identified function of SOS splicing is to genetically buffer animals from the deleterious effects of DNA-transposon-mediated gene perturbation. - Source: PubMed
Publication date: 2025/12/10
Zhao Long-WenNardone ChristopherChang CindyPaulo Joao AElledge Stephen JKennedy Scott - All genomes harbor mobile genetic parasites called transposable elements (TEs). Here we describe a system, which we term SOS splicing, that protects and human genes from DNA transposon-mediated disruption by excising these TEs from host mRNAs. SOS splicing, which operates independently of the spliceosome, is a pattern recognition system triggered by base-pairing of inverted terminal repeat elements, which are a defining feature of the DNA transposons. We identify three factors required for SOS splicing in both and human cells; AKAP17A, which binds TE-containing mRNAs; the RNA ligase RTCB; and CAAP1, which bridges RTCB and AKAP17A, allowing RTCB to ligate mRNA fragments generated by TE excision. We propose that SOS splicing is a novel, conserved, and RNA structure-directed mode of mRNA splicing and that one function of SOS splicing is to genetically buffer animals from the deleterious effects of TE-mediated gene perturbation. - Source: PubMed
Publication date: 2025/02/17
Zhao Long-WenNardone ChristopherPaulo Joao AElledge Stephen JKennedy Scott - Melatonin is synthesized in multiple tissues and organs of pigs, and existing studies have shown the presence of the melatonin-synthesizing enzyme ASMT protein. However, the genomic information for the gene has been lacking. The aim of this study was to locate the genomic information of the gene in pigs using comparative genomics analysis and then obtain the coding region information through molecular cloning. First, using the NCBI Genome Data Viewer, we found that in most animals, the gene is often located next to the gene, with both genes arranged in the same direction. Similarly, the gene is commonly adjacent to the gene, also in the same orientation. We also discovered that the gene is frequently adjacent to the ASMT gene and arranged in the opposite direction. Using the "three-point localization" principle, we inferred the position of the gene based on the coordinates of and in pigs. Our results revealed that on the pig X chromosome, a gene called LOC110258194 is located next to the and genes, and its arrangement aligns with the gene in other species. Additionally, Ensembl contains a gene, ENSSSCG00000032659, at the same position, with completely overlapping exons, though it is not annotated as . Further analysis using the TreeFam tool from EMBL-EBI and the CDD tool from NCBI revealed that LOC110258194 and ENSSSCG00000032659 do not contain the typical Maf domain of and, thus, should not be annotated as , but rather as the gene. Using a slow-down PCR method for high-GC content genes, we successfully cloned the full CDS region of the pig gene and identified a new transcript missing Exon 6 and Exon 7. This transcript was submitted to NCBI and assigned the GenBank accession number MW847601. Our results represent the first successful localization of the gene in pigs, the first cloning of the gene's coding region, and the first discovery of a new transcript of the pig gene. - Source: PubMed
Publication date: 2025/01/13
Yan LaiqingLi GuangdongDeng ShoulongWang LikaiWang YiweiShen ZixiaYin DepengJi PengyunWang BingyuanLiu Guoshi