Ask about this productRelated genes to: KIAA0020 antibody
- Gene:
- PUM3 NIH gene
- Name:
- pumilio RNA binding family member 3
- Previous symbol:
- KIAA0020
- Synonyms:
- XTP5, PEN, PUF6, hPUF-A, HA-8
- Chromosome:
- 9p24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-06
- Date modifiied:
- 2015-11-05
Related products to: KIAA0020 antibody
Related articles to: KIAA0020 antibody
- Maternal recognition of pregnancy (MRP) in the mare requires coordinated adaptations of both the conceptus and the endometrium during the peri-recognition interval; however, integrated transcriptomic analyses of both compartments within the same biological window remain limited. Here, we analyzed conceptus RNA-seq data across embryonic age (Days 8 and 12 post ovulation) and endometrial RNA-seq data across pregnancy status (pregnant versus non-pregnant mares sampled between Days 8 and 12 post ovulation). In pregnant mares, conceptus recovery and endometrial biopsy collection were performed within the same gestation, allowing biological integration of embryo and maternal transcriptomes while preserving tissue-specific statistical contrasts. - Source: PubMed
Publication date: 2026/06/18
Da Silva Álvarez EvaOrtiz-Rodríguez José MMartín-Cano Francisco EÁlvarez-Barrientos AlbertoBecerro-Rey LauraGil María CRedondo EloyMasot JavierAparicio Inés MPeña Fernando JOrtega-Ferrusola Cristina - The beet leafhopper (BLH), Neoaliturus tenellus, is a major agricultural pest and vector of beet curly top virus (BCTV), a pathogen responsible for severe economic losses in vegetable and field crops in the Western U.S. Despite its economic importance, the genetic basis of BLH survival, reproduction, and virus-vector interactions remains unexplored mainly due to the lack of functional genomics tools in this species. In this study, we assessed the feasibility of RNA interference (RNAi) in BLHs by targeting two genes, protein gustavus isoform X2 (Gus) and pumilio homolog 3 (Pum3), which were previously identified as differentially expressed following BCTV infection. Double-stranded RNA (dsRNA) targeting conserved domains of each gene was delivered via microinjection or star polycation nanoparticle-mediated topical spray. Our results show that microinjection of dsRNA resulted in >90% knockdown of both Gus and Pum3 by 5 days post-treatment. Silencing Pum3 significantly reduced BLH survival and fecundity, whereas silencing Gus reduced fecundity without affecting adult survival, suggesting gene-specific fitness consequences. Nanoparticle-mediated dsRNA spray resulted in 88% reduction in Gus and 62% reduction in Pum3 expression, yet both produced biological effects on survival and/or reproduction, comparable to those observed with microinjection. To our knowledge, this study provides the first demonstration of the effectiveness of microinjection and nanoparticle-mediated RNAi in the BLH. Together, these findings demonstrate the critical roles of Gus and Pum3 in vector fitness and establish microinjection and nanoparticle-based dsRNA spray as robust platforms for functional genomics and developing potential scalable, non-invasive RNAi strategies for sustainable vector and disease management. - Source: PubMed
Publication date: 2026/06/29
Han JinlongAlonzo Maria Paula MejiaCui MeihuaPuffer Katherine OWolff Anna MMiyake Garret MNeher Oliver TNalam Vamsi JNachappa Punya - Previous genomic efforts on chromosome 9p deletion and duplication syndromes have utilized low-resolution strategies (i.e., karyotypes, chromosome microarrays). These studies have provided important initial insights into these syndromes. This current study is the first large-scale whole-genome sequencing (WGS) study of 100 individuals from families with chromosome 9p syndromes. - Source: PubMed
Publication date: 2025/10/24
Wang YingxiSams Eleanor ISlaugh RachelCrocker SandraHurtado Emily CordovaTracy SophiaHou Ying-Chen ClaireMarkovic ChristopherValle KostandinTate VictoriaBelhassan KhadijaAppelbaum ElizabethAkinwe TitilopeStarosta Rodrigo TCao YangNeilson AmberLiu YuJensen NathanielGhasemi RezaLindsay TinaManuel JuanaCouteranis SophiaKremitzki MilinnUstanik JackAntonacci ThomasNg Jeffrey KEmory AndrewMetz LauraDeLuca TracieLyons Katherine NSinnwell ToniThomeczek BrianneWang KymmeSisneros NickMuraleedharan MeghaKethireddy AnanthaCorbo MarcoGowda HarshaKing Katherine AGurnett Christina ADutcher Susan KGooch CatherineLi Yang EMitchell Matthew WPeterson Kevin AHorani AmjadRosenfeld Jill ABi WeiminStankiewicz PawelChao Hsiao-TuanPosey Jennifer EGrochowski Christopher MDardas ZainPuffenberger Erik GPearson Christopher EKooy FrankAnnear DaleInnes A MicheilHeinz MichaelHead RichardFulton RobertToutain Stephan Antonacci-Fulton LucindaCui XiaoxiaMitra Robi DCole F SessionsNeidich JulieDickson Patricia IMilbrandt JeffreyTurner Tychele N - Topoisomerases are essential for resolving topological stress in DNA during key cellular processes. In human cells, six topoisomerases perform specialized yet overlapping functions to manage these challenges. To investigate their distinct and shared roles, as well as their involvement in DNA damage repair, we conducted a comprehensive analysis of the human topoisomerase-associated protein landscape. Using tandem affinity purification coupled with mass spectrometry, we mapped the protein-protein interaction networks of five human topoisomerases under both normal and stressed conditions. Our analysis identified several key interactions that may regulate topoisomerase function. Notably, TOP1 interacts with PUM3, which undergoes a similar relocalization from nucleoli to nucleoplasm following treatment with a TOP1 poison. In addition, we uncovered novel interactions of TOP3A with NSMCE4A, YTHDC2, and NDUFAF7, as well as a previously uncharacterized interaction between TOP3B and the mitochondrial membrane protein TDRKH (TDRD2). We further examined dynamic changes in these interactomes in response to TOP1 and TOP2 poisons and replication stress, distinguishing between interactions in chromatin and soluble fractions. These findings provide new insights into the regulation and functional coordination of human topoisomerases, offering potential biomarkers or therapeutic targets for topoisomerase inhibitors in cancer treatment. - Source: PubMed
Publication date: 2025/10/01
Zhang HuiminXiong YunChen ZhenChen Junjie - Previous genomic efforts on chromosome 9p deletion and duplication syndromes have utilized low resolution strategies (i.e., karyotypes, chromosome microarrays). We present the first large-scale whole-genome sequencing (WGS) study of 100 individuals from families with 9p-related syndromes including 85 unrelated probands through the 9P-ARCH (dvanced esearch in hromosomal ealth: Genomic, Phenotypic, and Functional Aspects of -Related syndromes) research network. We analyzed the genomic architecture of these syndromes, highlighting fundamental features and their commonalities and differences across individuals. This work includes a machine-learning model that predicts 9p deletion syndrome from gene copy number estimates using WGS data. Two Late Replicating Regions (LRR1 [a previously un-named human fragile site], LRR2) were identified that contain most structural variant breakpoints in 9p deletion syndrome pointing to replication-based issues in structural variant formation. Furthermore, we show the utility of using WGS information to obtain a comprehensive understanding of 9p-related variation in an individual with complex structural variation where chromothripsis is the likely mechanism. Genes on 9p were prioritized based on statistical assessment of human genomic variation. Furthermore, through application of spatial transcriptomics to embryonic mouse tissue we examined 9p-gene expression in craniofacial and brain development. Through these strategies, we identified 24 important genes for the majority (83%) of individuals with 9p deletion syndrome including , , , , , , , and . Two genes (, ) are involved in mitochondrial function and testing of the mitochondrial genome revealed excess copy number in individuals with 9p deletion syndrome. This study presents the most comprehensive genomic analysis of 9p-related syndromes to date, with plans for further expansion through our 9P-ARCH research network. - Source: PubMed
Publication date: 2025/03/30
Wang YingxiSams Eleanor ISlaugh RachelCrocker SandraHurtado Emily CordovaTracy SophiaHou Ying-Chen ClaireMarkovic ChristopherValle KostandinTate VictoriaBelhassan KhadijaAppelbaum ElizabethAkinwe TitilopeTzovenos Rodrigo StarostaCao YangNeilson AmberLiu YuJensen NathanielGhasemi RezaLindsay TinaManuel JuanaCouteranis SophiaKremitzki MilinnUstanik JackAntonacci ThomasNg Jeffrey KEmory AndrewMetz LauraDeLuca TracieLyons Katherine NSinnwell ToniThomeczek BrianneWang KymmeSisneros NickMuraleedharan MeghaKethireddy AnanthaCorbo MarcoGowda HarshaKing KatherineGurnett Christina ADutcher Susan KGooch CatherineLi Yang EMitchell Matthew WPeterson Kevin AHorani AmjadRosenfeld Jill ABi WeiminStankiewicz PawelChao Hsiao-TuanPosey JenniferGrochowski Christopher MDardas ZainPuffenberger ErikPearson Christopher EKooy FrankAnnear DaleInnes A MicheilHeinz MichaelHead RichardFulton RobertToutain Stephan Antonacci-Fulton LucindaCui XiaoxiaMitra Robi DCole F SessionsNeidich JulieDickson Patricia IMilbrandt JeffreyTurner Tychele N