Ask about this productRelated genes to: SPDYA antibody
- Gene:
- SPDYA NIH gene
- Name:
- speedy/RINGO cell cycle regulator family member A
- Previous symbol:
- SPDY1
- Synonyms:
- SPY1, Ringo3
- Chromosome:
- 2p23.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-07-05
- Date modifiied:
- 2016-10-05
Related products to: SPDYA antibody
Related articles to: SPDYA antibody
- Endometrial cancer, the most common gynecological malignancy with an annual increase of 1%-3%, lacks suitable noninvasive diagnostic tools, as current methods like hysteroscopy and biopsy are invasive and impractical for routine screening. We conducted a comprehensive, multilayered marker discovery workflow integrating whole-genome bisulfite sequencing and targeted methylation panels in tumor and control tissues, then prioritized and optimized candidates for detection in cervical exfoliated cells. Using a two-stage design, we built and tested a quantitative methylation-specific PCR (qMSP) model in ThinPrep Cytology Test (TCT) samples, with 148 samples for discovery/model construction and an independent cohort of 80 TCT samples for validation. We identified a three-gene methylation panel-ZNF626, GRIA4, and SPDYA-that demonstrated high accuracy for early endometrial cancer detection from cervical cytology. In the validation cohort, the model showed strong performance across menopausal subgroups: in premenopausal women, sensitivity was 90.91% and specificity for benign endometrial disease was 92.59%; in postmenopausal women, sensitivity and specificity were 96.55% and 84.62%, respectively. Notably, the approach achieved a 92.86% detection rate for stage I endometrial cancer. These results support a robust, noninvasive diagnostic strategy that leverages simple cervical cytology sampling to enable early detection, facilitate clinical decision-making, and potentially improve outcomes for patients at risk of endometrial cancer. - Source: PubMed
Publication date: 2026/03/07
Cai YanChen ShuchaoWu ZhenGuan JinxiaZhao JieYe JianweiDu BaochenHan XiaoliangShu TongZhou GuangpengZheng Hong - Populations of adult neural stem cells (NSCs) that reside in the mammalian brain aid in neurogenesis throughout life and can be identified by a type VI intermediate filament protein, Nestin. Cell cycle regulation plays an important role in maintaining a balance between self-renewal and differentiation and determining the fate of NSCs. Data from our group and others support that the atypical cyclin-like protein SPY1 (also called RingoA; gene SPDYA) plays a critical role in activating NSCs from a quiescent state. Elevated levels of Spy1 are found in aggressive human brain cancers, including glioblastoma. Using a conditional mouse model, we demonstrate that driving the expression of Spy1, in the Nestin-enriched NSC population of the brain, increases stemness characteristics, decreases differentiation, and increases susceptibility to oncogenic transformation. This study contributes to better understanding of intricate cell cycle mechanisms that lead to deviation from the homeostatic state, promoting aberrant changes in adult NSCs. - Source: PubMed
Publication date: 2026/01/02
Lubanska DorotaQemo IngridStringer Keith FranklinMahendran Hema PriyaFifield Bre-AnneCieslukowski AlanAlrashed SamiEl-Abed YoushaaBoujeke EmmanuelRodzinka AlexanderFidalgo da Silva ElizabethDinescu StephanieSorge AlexandraKandalam SrinathLiwanpo DaltonBrown JillianGhafoor HasanArshad MaheenPorter Lisa A - The identification of quantitative trait locus (QTL) or genes responsible for key agronomic traits has significantly enhanced genetic improvement through marker-assisted selection (MAS). However, the impacts of MAS on genetic parameters and subsequent selection processes have not been thoroughly characterised. Here, through genome-wide selective sweep analysis, we identified a diverse set of genes involved in oocyte meiosis, including PPP3CA, AR, PPP1CB, SPDYA, MAD1L1, and BMPR1B. The genome-wide association study (GWAS) further identified three genes UNC5C, BMPR1B, and PDLIM5 as being associated with lambing rate in Hu sheep. From these analyses, the FecB loci emerged as a potential molecular marker for lambing rate. with an increase of 0.5 lambs per G allele. The heritability of the lambing rate was estimated to be 0.19 (±0.02). Moreover, based on 10-fold cross-validation, the accuracy of genomic selection (GS) was found to be 0.30. Simulated MAS resulted in a reduction of the additive genetic variance components, with estimated heritability dropping to 0.14 (±0.02) and GS accuracy decreasing to 0.18-representing a decline of 26.42% and 34.81%, respectively. To address the reduced GS accuracy, we performed GWAS on the reference set to identify weighted single nucleotide polymorphisms (SNPs). This method has the potential to increase accuracy by 13.8%. Our study found that MAS has a negative impact on GS. To address this issue, we integrated prior information on SNPs from GWAS, which exhibit pleiotropic genetic architecture. This integration enables us to utilise genetic markers for complex traits more effectively, thereby improving the accuracy and efficiency of GS. - Source: PubMed
Publication date: 2025/12/08
Zhao YuanZhang XiaoXueLi FaDiTian HuibinZhang DeYinLi XiaolongZhang YuKunCheng JiangBoMa ZongWuLin ChangChunZeng XiWenZhao LiMingWang WeiMin - In mouse early pachytene spermatocytes, the X and Y chromosomes undergo rapid non-homologous (NH) synapsis and desynapsis, but the functional significance remains unknown. Here, we report that pachynema-specific knockout of Speedy A (SpdyA) from telomeres caused persistent Y-X NH synapsis, with the entire Y axis synapsed onto the X axis. This persistent Y-X NH synapsis did not interrupt meiotic sex chromosome inactivation, recombination, or sex body formation, but it disrupted X-Y loop-axis organization and homologous X-Y desynapsis, leading to spermatocyte death. Similarly, persistent Y-X NH synapsis was also observed in pachytene spermatocytes lacking TRF1, where SpdyA was frequently lost from the X-Y non-pseudoautosomal region (non-PAR) telomeres. Mechanistic studies revealed that Serine 48 of SUN1 is a key SpdyA/CDK2 phosphorylation site required for Y-X NH desynapsis. We propose that SpdyA governs Y-X NH desynapsis by stabilizing the linkage between the X-Y non-PAR telomeres and their LINC complexes, and that this process is regulated independently from other aspects of pachynema progression. Our findings suggest a key role for Y-X NH desynapsis in establishing proper X-Y loop-axis organization. - Source: PubMed
Publication date: 2025/08/18
Liu DongtengZhang YuxiangLi DongliangJiang BinjieZhao XudongLi YanyanLin ZexiongZhao YuHu ZheDeng ShuziLi ZhengLu HaonanChan Karen K LYeung William S BKaldis PhilippYao ChenchengWang HengbinChow Louise TLiu Kui - Vincristine-induced peripheral neuropathy is a common and highly debilitating toxicity from vincristine treatment that affects quality of life and often requires dose reduction, potentially affecting survival. Although previous studies demonstrated genetic factors are associated with vincristine neuropathy risk, the clinical relevance of most identified variants is limited by small sample sizes and unclear clinical phenotypes. A genome-wide association study was conducted in 1100 cases and controls matched by vincristine dose and genetic ancestry, uncovering a statistically significant (p < 5.0 × 10) variant in MCM3AP gene that substantially increases the risk of neuropathy and 12 variants protective against neuropathy within/near SPDYA, METTL8, PDE4D, FBN2, ZFAND3, NFIB, PAPPA, LRRTM3, NRG3, VTI1A, ARHGAP5, and ACTN1. A follow-up pathway analysis reveals the involvement of four key pathways, including nerve structure and development, myelination, neuronal transmission, and cytoskeleton/microfibril function pathways. These findings present potential actionable genomic markers of vincristine neuropathy and offer opportunities for tailored interventions to improve vincristine safety in children with cancer. This study is registered with ClinicalTrials.gov under the title National Active Surveillance Network and Pharmacogenomics of Adverse Drug Reactions in Children (ID NCT00414115, registered on December 21, 2006). - Source: PubMed
Publication date: 2024/11/05
Mufti KheireddinCordova MiguelScott Erika NTrueman Jessica NLovnicki Jessica MLoucks Catrina MRassekh Shahrad RRoss Colin J DCarleton Bruce C