Ask about this productRelated genes to: KPNA1 antibody
- Gene:
- KPNA1 NIH gene
- Name:
- karyopherin subunit alpha 1
- Previous symbol:
- -
- Synonyms:
- SRP1, RCH2, NPI-1, IPOA5
- Chromosome:
- 3q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-03-19
- Date modifiied:
- 2016-10-05
Related products to: KPNA1 antibody
Related articles to: KPNA1 antibody
- Asthma is a chronic inflammatory airway disease characterized by epithelial barrier dysfunction, mucus hypersecretion, and type 2-skewed immune responses. Macrophages play a critical role in shaping airway inflammation and tissue remodeling, yet the molecular mechanisms regulating macrophage activation in allergic asthma remain incompletely understood. The vitamin D receptor (VDR) is an immune-modulatory transcription factor expressed in macrophages, but its macrophage-specific function and regulatory mechanisms in allergic airway inflammation remain unclear. - Source: PubMed
Publication date: 2026/03/25
Wu CuiwenLin WeixianZou ZhanshengWei YuanhaoZhou ZiliLuo WangLuo CaihongLuo XujingLiang JiayuanZhou ZicongLiang ShixiuJiang LiYou YimingChi ZijunCai ShaoxiYu Changhui - Italy hosts a rich biodiversity of local goat breeds, shaped by its wide variety of climates, landscapes, and traditional farming systems, making the preservation of these locally adapted populations critical for maintaining genetic resources. This study aimed to explore the genomic biodiversity of Italian goats, track recent temporal changes through comparison with samples collected about two decades ago, and investigate the genomic mechanisms underlying environmental adaptation, as well as identify hotspots of possible climatic vulnerability. Demographic data over the last 15 years show that only five breeds are currently considered not at risk of extinction according to FAO criteria, while 22 breeds are classified as critical or formally extinct (no registered animals in 2024). Medium-density single-nucleotide polymorphism (SNP) data from 685 goats representing 31 populations were analysed for population structure, genomic background, and genetic diversity. Comparison with historical samples revealed changes over time, exemplified by Bianca Monticellana and Capestrina, which now display a highly similar and uniform genetic background and higher inbreeding. Genomic analyses revealed a clear separation between northern and central-southern breeds, with northern populations exhibiting more distinct genomic backgrounds while central-southern populations are generally more admixed. Landscape genomic analyses were conducted on a subset of 693 goats from 32 populations, using latent factor mixed model and partial redundancy analysis approaches together with present and projected (SSPs 2-4.5 and 5-8.5, 2080-2100) climatic variables from WorldClim 2.1. A total of 468 SNPs were identified as putatively adaptive, including five detected by both methods, encompassing genes such as KPNA1, PARP9, and LRP8. Genomic offset analyses highlighted vulnerable areas in the northern fringes of the Alpine region, the eastern Po Valley (unsampled due to limited presence of local goat populations), and the Murgia-Gargano region of Apulia, home to the Garganica breed. Overall, these results reveal the impact of breeding practices and environmental pressures on Italian goat genomes, provide insights into adaptive genetic variation of goat species, and identify populations and regions at greatest risk, emphasising the need for targeted conservation and management strategies to preserve this unique component of livestock biodiversity. - Source: PubMed
Publication date: 2025/12/08
Bionda ANegro ABarbato MLiotta LGrande SCrepaldi P - Abnormal expression of kinesins has been observed in several types of cancer. The present study provided the first evidence that KIF26B could induce RNA mC modification in bladder cancer (BCa). Detailly, KIF26B interacted with NSUN2 and recruited ubiquitinase STUB1 to promote K63-linked ubiquitination of NSUN2 at K511 site. K63-linked ubiquitination enabled NSUN2 to bind to KPNA1 and translocate into nucleus where it drove RNA mC modification. Furthermore, KIF26B induced liquid-liquid phase separation (LLPS) of YBX1 and upregulated IL-6 expression through NSUN2/mC/YBX1 axis. Secreted IL-6 then activated STAT3 signaling to promote transcription of kif26b through direct binding between STAT3 and kif26b promoter. IL-6 also recruited DLAT to acetylate NSUN2 at K229 site and increased association affinity between NSUN2 and KIF26B. Together, these established a KIF26B/NSUN2/mC/IL-6 positive feedback loop, suggesting that targeting KIF26B may be a promising therapeutic strategy for BCa. - Source: PubMed
Publication date: 2025/12/22
Wang Jia-MingXie Hai-YunZhang Feng-HaoShu XuanLuo Jin-DanXie Li-PingLi Jiang-Feng - Human bocavirus 1 (HBoV1), first identified in human nasopharyngeal specimens in 2005, is a relatively recent member of the respiratory virus family and is primarily associated with respiratory tract infections. Despite this, the mechanisms underlying HBoV1 pathogenesis remain poorly understood, primarily due to the lack of suitable cell lines and animal models, as well as the complicating factor of co-infections with other pathogens. In this study, we demonstrate that the non-structural protein 1 (NP1) of HBoV1 antagonizes the type I interferon (IFN-I) signaling pathway. NP1 interacts with the DNA-binding domain (DBD) of signal transducer and activator of transcription 1 (STAT1) and the importing β-binding (IBB) domain of karyopherin subunit alpha-1 (KPNA1), thereby disrupting the formation of the STAT1/KPNA1/KPNB1 complex and subsequently inhibiting STAT1 nuclear translocation, a critical step in IFN-I signaling. Furthermore, we show that HBoV1 NP1 facilitates the replication of influenza A virus (IAV) and respiratory syncytial virus (RSV). These findings suggest a novel mechanism by which bocavirus proteins antagonize the host's innate immune response and provide new evidence that bocavirus may exacerbate the symptoms of clinical respiratory viral infections. - Source: PubMed
Publication date: 2025/10/15
Xue MinfeiHuang ChenxiaoJiang XiaohuiZhou ShimengYan YongdongDong ChunshengChen ZhengrongDai Jianfeng - Leukodystrophies are inherited disorders characterized by progressive degeneration of white matter in the central nervous system. Here, we investigate a previously uncharacterized autosomal recessive leukodystrophy which is associated with the homozygous missense variant in ZNF319 (c.800T>C; p.Phe267Ser) in an 18-year-old male presenting with spasticity, ataxia, cognitive decline, and white matter abnormalities on MRI. The variant was absent in population databases (gnomAD, ClinVar) and predicted to be pathogenic by multiple in silico tools. Molecular dynamics simulations revealed that F267 is a stabilizing residue within a β-strand of the zinc finger domain, forming π-stacking and hydrophobic interactions that are lost upon substitution with serine, leading to structural instability, increased flexibility, and protein unfolding. Despite normal transcript and protein expression, ZNF319-F267S mislocalized to the cytoplasm due to disruption of its bipartite nuclear localization signal (NLS), resulting in impaired interaction with importin α1 (KPNA1). Functional analysis confirmed that the mutation disrupts nuclear transport and prevents transcriptional activation of genes involved in myelination. Protein interaction network and gene ontology analysis highlighted ZNF319's role in transcriptional regulation and its localization in the CHOP-C/EBP transcriptional complex. Expression profiling demonstrated ZNF319 enrichment in oligodendrocytes and white matter regions, correlating with the observed leukoencephalopathy. Our study identifies ZNF319 as a novel gene implicated in human leukodystrophy and highlights how a single-point mutation can compromise nuclear import and transcriptional function, leading to white matter degeneration. These findings expand the genetic landscape of leukodystrophies and provide mechanistic insights into transcriptional regulation in myelin maintenance. - Source: PubMed
Publication date: 2025/08/18
Ahmad S RehanZeyaullah MdZahrani YousefAltijani Abdelrhman A GDawria AdamSalih Ahmed