Mammalian Genome最新文献

{"title":"Draft nuclear and complete mitochondrial genome assemblies of the flare-horned markhor (Capra falconeri): genomic resources for conservation and phylogenetics.","authors":"Javeria Wali, Muhammad Waqas, Azhar Hussain Shah, Inam Ullah, Asif Mir, Zunnan Huang, Amjad Ali","doi":"10.1007/s00335-026-10261-0","DOIUrl":"10.1007/s00335-026-10261-0","url":null,"abstract":"<p><p>The flare-horned markhor (Capra falconeri), a near-threatened mountain ungulate endemic to the Western Himalayas, remains vulnerable to habitat fragmentation, human disturbance, and environmental change. Although localized conservation efforts have stabilized some populations, genomic resources for this species remain limited. Here, we report nuclear and mitochondrial genome assemblies for C. falconeri, including a nuclear genome assembly (GCA_038502695.1) and a complete mitochondrial genome (OR799853.1), and place these data within an ecological context derived from field surveys. A structured winter survey conducted between 2020 and 2022 documented 225 individuals across 14 sites, indicating a demographically stable population with marked spatial heterogeneity. Genome-completeness assessment with BUSCO indicated that the short-read nuclear assembly is a fragmented draft (49.4% complete), and should be regarded as a preliminary genomic resource rather than a reference-quality genome. The complete mitochondrial genome is 16,639 bp in length and exhibits conserved gene organization and pronounced AT bias; comparison with the reference mitogenome identified high-confidence coding-region substitutions, exclusively transitions, distributed across the major mitochondrial protein-coding gene groups. Codon usage analyses revealed moderate bias, whereas Ka/Ks ratios across the mitochondrial protein-coding genes were consistently below one, indicating pervasive purifying selection. Comparative phylogenetic analyses based on mitochondrial and nuclear data resolved the evolutionary placement of C. falconeri within the genus Capra. Together, these results provide genomic assemblies supported by ecological context and establish a foundation for future comparative, population, and conservation genomics studies of this species.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"37 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148584594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypoxia-induced mechanism of TNBC promoting tumour cell proliferation through exosomal miRNA.","authors":"Xiangxin Zheng, Peng Yang, Sai Zhou, Xiaochao Zhu, Xiaoqing Guan, Guoqin Jiang","doi":"10.1007/s00335-026-10260-1","DOIUrl":"10.1007/s00335-026-10260-1","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC), characterized by the absence of ER, PR, and HER2 expression, is associated with aggressive clinical behavior and limited treatment options. Hypoxia in the tumor microenvironment (TME) may influence intercellular communication through exosomes. In this study, we investigated whether hypoxia-derived exosomes regulate malignant phenotypes of TNBC cells through exosomal miRNAs. Exosomes derived from hypoxic TNBC cells increased proliferation, migration, and invasion of recipient TNBC cells compared with normoxia-derived exosomes. Small RNA sequencing and RT-qPCR validation showed enrichment of miR-4791 in hypoxia-derived exosomes. Functional assays indicated that miR-4791 overexpression promoted TNBC cell proliferation, whereas miR-4791 inhibition reduced proliferative capacity. Mechanistically, miR-4791 directly targeted the 3'UTR of CTCFL and was associated with reduced PTEN expression. Rescue experiments suggested that restoration of CTCFL or PTEN partially attenuated miR-4791-associated malignant phenotypes in vitro and in vivo. Analysis of GSE19536 showed higher miR-4791 expression in breast cancer tissues than in normal tissues; however, the number of normal samples was limited. Survival analysis using GSE19783 indicated that higher miR-4791 expression was associated with poorer survival, although the prognostic ROC performance was weak-to-modest. Overall, these findings suggest that hypoxia-derived exosomal miR-4791 may contribute to TNBC progression, at least in part, through a CTCFL/PTEN-related mechanism.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"37 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148497622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Semi-supervised ensemble learning with interval type-2 fuzzy-rough sets for Parkinson's disease prediction from multi-omics.","authors":"Ambika Hazarika, Ansuman Kumar, Anindya Halder","doi":"10.1007/s00335-026-10256-x","DOIUrl":"10.1007/s00335-026-10256-x","url":null,"abstract":"<p><p>Parkinson's disease (PD) is a disorder involving progressive degeneration of the nervous system. Its clinical signs typically become noticeable only after substantial impairment has occurred in the substantia nigra, a brain region involved in motor control. Therefore, early and accurate prediction of PD based on molecular alterations is essential for proper diagnosis and improved patient outcomes. In this context, feature-level multi-omics integration has become a useful strategy because it combines molecular information from multiple biological levels and may support a broader understanding of disease progression. This study proposes a novel technique called Semi-supervised Ensemble Learning with Interval Type-2 Fuzzy-Rough Sets (SSEnIT2FRS) for PD prediction from multi-omics data, which leverages interval type-2 fuzzy-rough sets to achieve early and accurate prediction. The type-2 fuzzy-rough set enhances the handling of uncertainty and vagueness present in real-world biological datasets, while the ensemble approach improves predictive robustness by combining the decisions of multiple base classifiers. Furthermore, the inclusion of semi-supervised learning addresses the scarcity of labeled samples. The experimental findings indicate that the proposed method outperforms nine existing methods across all evaluation metrics, achieving the highest accuracy of 98.49%, with precision 0.9820, recall 0.9865, macro [Formula: see text]-score 0.9836, micro [Formula: see text]-score 0.9842, kappa 0.9672, specificity 0.9953, and AUC of 0.9969 on the multi-omics dataset. Boxplots, paired t-test results, confidence interval analysis, and SHAP-based explanations further justify the superior performance, robustness, statistical significance, and interpretability of the proposed method. Therefore, the proposed method could be an effective computational technique for identifying PD at an early stage from multi-omics data.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"37 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148422282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Persistent homology of blood gene co-expression networks reveals reduced cycle structure in autism spectrum disorder: a multi-cohort analysis.","authors":"Mehmet Ali Balcı, Ömer Akgüller","doi":"10.1007/s00335-026-10259-8","DOIUrl":"10.1007/s00335-026-10259-8","url":null,"abstract":"<p><p>Autism spectrum disorder (ASD) exhibits substantial molecular heterogeneity that challenges traditional gene-centric analyses. We applied persistent homology of the graph 1-skeleton to characterize co-expression cycle structure in mutual information-based gene networks in ASD. Using transcriptomic data from brain tissue and peripheral blood, we constructed MI networks from the 500 most variable genes, computed Betti-1 numbers across 30 filtration steps, and assessed significance via 10,000-permutation testing. We note that this approach computes first homology on the 1-skeleton, not the full flag/clique complex; this distinction is made explicit throughout. ASD peripheral blood networks exhibited nominally significant topological reorganization relative to neurotypical controls, with a 20.4% reduction in the area under the Betti-1 curve. After excluding 44 redundant SNORD115-family probes to address microarray probe-redundancy concerns, the finding strengthened substantially to [Formula: see text], which we consider the primary result. This indicates that regulatory cycle structure accumulates less readily in ASD blood co-expression networks across the full filtration range. Brain cortex networks showed no significant topological differences; however, a post-hoc power analysis indicates the brain cohort has only ∼ 36% power to detect the blood-magnitude effect, so this null result should not be interpreted as evidence of preserved brain topology or tissue specificity. After SNORD115 probe exclusion, ASD hub genes form a ribosomal protein gene cluster consistent with translational dysregulation in ASD. To validate the blood finding, we applied the identical TDA pipeline to two independent blood transcriptome datasets: GSE42133 and GSE25507. Both independent cohorts exhibited the same ASD < control direction. Stouffer meta-analysis combining the z-scores from all three blood datasets, demonstrating robust directional replication of the reduced-cycle-structure signal across independent cohorts (spanning two Affymetrix platforms, Human Gene 1.0 ST and U133 Plus 2.0). These findings demonstrate that graph-filtration cycle-rank analysis detects reduced co-expression cycle structure in ASD peripheral blood, independently replicated across three blood transcriptome cohorts. The Stouffer meta-analysis substantially exceeds conventional significance thresholds and supports the potential utility of topological biomarkers in neurodevelopmental disorders.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"37 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148422231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deciphering genetic diversity and selection footprints in Rathi cattle through ddRAD-based genome-wide analysis.","authors":"Nishu Bharia, Anal Bose, Sonali Sonejita Nayak, Divya Rajawat, Vijay Kumar, Triveni Dutt, Manjit Panigrahi","doi":"10.1007/s00335-026-10254-z","DOIUrl":"10.1007/s00335-026-10254-z","url":null,"abstract":"<p><p>Rathi cattle, an indigenous Bos indicus breed of north-western India, represent a valuable genetic resource due to their adaptation to arid environments, heat tolerance and dairy potential. However, genomic information on this breed remains limited. This study provides the first double-digest restriction-site associated DNA sequencing (ddRAD) based genome-wide assessment of Rathi cattle using a large sample size. A total of 96 animals were genotyped, generating 78,193 high-quality SNPs with 96.52% alignment to the Bos taurus (ARS-UCD2.0) reference genome, guaranteeing dependable variant identification. The population exhibited moderate genetic diversity with nucleotide diversity (π = 0.33 ± 0.09) and heterozygosity (Ho = 0.291 ± 0.084; He = 0.329 ± 0.104). Runs of homozygosity (ROH) made up 5.43% of the genome, and most of them were short segments (< 2 Mb), which shows that there hasn't been much inbreeding lately (F_ROH = 0.0512). Effective population size (Ne) declined from 1454 (150 generations ago) to 94 at present, highlighting the impact of demographic bottlenecks and genetic drift. The declining Ne suggests a risk of future genetic erosion, highlighting the need for effective conservation and breeding strategies. Population structure analyses (PCA, ADMIXTURE and STRUCTURE) revealed clear genetic distinctness of Rathi from other indigenous dairy breeds, despite its composite origin. Selection signature analyses (Tajima's D, CLR, ROH islands and iHS) identified candidate regions harboring genes associated with immunity (IL2RB, USP18), reproduction (INHBA, MEI4, HBA), lactation (LRRC8D, TRERF1, CCND3) and stress adaptation (CARHSP1, ITGAV). These findings are highlighting the valuable insights about diversity, demographic history and adaptive potential of rathi and offering genomic resources for conservation, sustainable utilization and genetic improvement programs.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"37 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148411865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of shared hub genes CTNNB1, TJP1, PTK2, and TP53 associated with endothelial proliferation in infantile hemangioma and glioblastoma.","authors":"Yanli Niu, Jing Li, Liang Wang, Duoduo Li","doi":"10.1007/s00335-026-10252-1","DOIUrl":"10.1007/s00335-026-10252-1","url":null,"abstract":"<p><p>Infantile hemangioma (IH) and glioblastoma multiforme (GBM) are clinically distinct but share vascular and proliferative characteristics. This study aimed to identify common transcriptional and regulatory mechanisms between IH and GBM to uncover potential hub genes driving disease progression. Transcriptomic datasets GSE127487 (IH) and GSE108476 (GBM) were analyzed using the limma package in R. Differentially expressed genes (DEGs) were overlapped to identify shared signatures. Protein-protein interaction networks were built using STRING and analyzed in Cytoscape to determine hub genes via CytoHubba. Gene expression, promoter methylation, mutation, and CNV data were validated using OncoDB, GEO2R, UALCAN, and cBioPortal. Functional enrichment and drug sensitivity analyses were performed using DAVID and GSCA. Experimental validation included siRNA knockdown or overexpression of target genes in HemSCs, HemECs, U87-MG, and LN229 cells, followed by RT-qPCR, western blot, proliferation, colony formation, and wound-healing assays. A total of 142 common DEGs were identified, with four hub genes, including TP53, CTNNB1, TJP1, and PTK2 showing consistent dysregulation. TP53 and CTNNB1 were upregulated, while TJP1 and PTK2 were downregulated in both IH and GBM. Methylation, mutation, and CNV analyses supported their regulatory involvement. Functional assays confirmed that CTNNB1 knockdown and TJP1/PTK2 overexpression suppressed proliferation and migration. This integrative study identifies CTNNB1, TJP1, PTK2, and TP53 as shared hub genes, highlighting common molecular regulators of endothelial proliferation and tumor-associated phenotypes in IH and GBM, and suggesting potential therapeutic targets.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"37 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148405154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroinflammation in glaucoma: a myriad of cellular pathways and players.","authors":"Michael MacLean, Sean D Lydon, Cátia Gomes, Elizabeth M Pizzi, Cory A Diemler, Sarah E R Yablonski, Gareth R Howell, Jason S Meyer, Richard T Libby","doi":"10.1007/s00335-026-10253-0","DOIUrl":"10.1007/s00335-026-10253-0","url":null,"abstract":"<p><p>Glaucoma is a complex neurodegenerative disease with multiple subtypes, yet all are characterized by the progressive dysfunction and loss of retinal ganglion cells (RGCs), which ultimately results in vision impairment and blindness. Elevated intraocular pressure (IOP) is a major risk factor for glaucoma; however, it is neither necessary nor sufficient for glaucomatous neurodegeneration, as patients can exhibit high IOP without developing glaucoma and patients can develop glaucoma with normal IOP. Yet FDA-approved treatment options are largely limited to approaches to minimize risk and reduce IOP. Thus, there is a critical need to target other aspects of glaucoma pathophysiology. Neuroinflammation is broadly defined here as immune-relevant responses, often involving microglia and astrocytes, within the central nervous system which may include peripheral immune cell infiltration. Burgeoning evidence has implicated glia in the development and progression of glaucoma in human tissues and mouse models. Most mouse models of glaucoma to date have shown that microglia and astrocytes are reactive in early stages of glaucomatous neurodegeneration prior to overt RGC loss. However, there is growing evidence that human and mouse glia adopt distinct phenotypes in response to neurodegeneration. Thus, there is critical need to expand our studies to include the new generations of human cell culture models. In this review, we discuss: 1) the evidence of neuroinflammatory processes in human glaucoma; 2) models of glaucoma relevant neuroinflammation; and the evidence specifically for 3) innate immune cell-driven and 4) macroglia-driven processes.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"37 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13310235/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148339247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: THBS1: a biomarker for PCOS and its role in pathogenesis via the PI3K/AKT signaling pathway.","authors":"Jie Zhang, Luhongyuan Jin, Chi Chi, Wenjie Hou, Jinhua Zhou","doi":"10.1007/s00335-026-10255-y","DOIUrl":"10.1007/s00335-026-10255-y","url":null,"abstract":"","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"37 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148330506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elucidating the therapeutic targets and multi-target mechanisms of salvianolic acid A for diabetic nephropathy.","authors":"Tongfei Fu, Zhili Xiong, Hongwu Tao, Yongli Zhan","doi":"10.1007/s00335-026-10246-z","DOIUrl":"10.1007/s00335-026-10246-z","url":null,"abstract":"<p><p>Diabetic nephropathy (DN) is a leading cause of chronic kidney disease. Salvianolic acid A (SAA) has shown promising therapeutic potential against DN, yet its underlying mechanisms and precise molecular targets remain incompletely elucidated. Potential targets of SAA were predicted using SwissTargetPrediction and SuperPred, with its drug-like properties evaluated by ADMET analysis. Diabetic nephropathy (DN)-related targets were collected from GEO, CTD, and GeneCards databases. Shared targets underwent GO and KEGG enrichment analyses. Core targets were identified through topological analysis in Cytoscape, machine learning, and Mendelian randomization validation. Molecular docking and dynamics simulations assessed the binding affinity and stability between SAA and core targets. Single-cell RNA sequencing data revealed their cell type-specific expression in kidney tissues. Experimental validation was performed using an in vitro high glucose-induced podocyte injury model analyzed by RT-qPCR. The intersection of 212 drug targets with 5,097 disease targets yielded 134 potential therapeutic targets for salvianolic acid A in DN. Machine learning and Mendelian randomization further identified eight targets with causal relationships to DN. Molecular docking demonstrated strong binding affinities of salvianolic acid A to the domains of FYN, AKR1B1, TNF, GALK1, HMGCR, MAP2K2, SCN4A, and ITGA5. Single-cell analysis revealed distinct expression patterns across different renal cell types. In vitro experiments demonstrated that SAA effectively protected podocytes from HG-induced injury. SAA alleviates diabetic nephropathy through multi-target mechanisms, influencing key genes involved in disease progression. This study provides a systematic elucidation of the therapeutic basis for SAA and supports its further clinical development.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"37 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148317940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DeepDisSNP: Predicting disease-associated SNPs by representation learning on disease and SNP linkage disequilibrium networks.","authors":"Duc-Hau Le","doi":"10.1007/s00335-026-10250-3","DOIUrl":"10.1007/s00335-026-10250-3","url":null,"abstract":"<p><p>Genome-wide association studies (GWAS) have identified numerous disease-associated single nucleotide polymorphisms (SNPs), yet many potential disease-SNP associations remain undiscovered due to the high dimensionality and sparsity of genomic data. Computational approaches that integrate biological network information can complement existing GWAS resources by prioritizing candidate disease-associated SNPs for downstream investigation. In this study, we propose DeepDisSNP, a deep learning framework for disease-SNP association prediction that integrates disease similarity networks and chromosome-specific SNP linkage disequilibrium (LD) networks through graph attention network (GAT)-based representation learning. Disease similarity networks were constructed from MeSH-based disease relationships, while SNP LD networks were generated from Phase 1 and Phase 3 datasets of the 1000 Genomes Project under multiple LD thresholds. DeepDisSNP independently learns disease and SNP embeddings using weighted GAT encoders and subsequently predicts disease-SNP associations using a multilayer perceptron classifier. Extensive experiments across all 22 autosomal chromosomes demonstrated that DeepDisSNP consistently outperformed the state-of-the-art DisSNPNet framework under multiple experimental settings. Under the best-performing configuration, DeepDisSNP achieved AUROC and AUPRC values of approximately 0.96 and 0.95, respectively. Additional analyses demonstrated robustness across LD thresholds, 1000 Genomes Project phases, and increasingly imbalanced negative sampling settings. External GWAS resources, including NHGRI-EBI GWAS Catalog, PhenoScanner, and OpenGWAS, provided supportive biological evidence for many highly ranked predicted associations. Functional enrichment analyses further suggested biological relevance of the predicted SNP-associated genes. Overall, DeepDisSNP provides an effective network-based framework for large-scale disease-SNP association prioritization and may facilitate downstream genomic and translational research.</p>","PeriodicalId":18259,"journal":{"name":"Mammalian Genome","volume":"37 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148283838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}