NUP160 antibody Polyclonal Antibodies Primary antibodies
- Known as:
- NUP160 (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100640
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- NUP160 antibody Polyclonal Antibodies Primary antibodies
Related genes to: NUP160 antibody Polyclonal Antibodies Primary antibodies
- Gene:
- NUP160 NIH gene
- Name:
- nucleoporin 160
- Previous symbol:
- -
- Synonyms:
- KIAA0197, FLJ22583
- Chromosome:
- 11p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-18
- Date modifiied:
- 2016-10-05
Related products to: NUP160 antibody Polyclonal Antibodies Primary antibodies
Related articles to: NUP160 antibody Polyclonal Antibodies Primary antibodies
- Sepsis arises from a dysregulated host response to infection, leading to multiorgan inflammatory injury. Early diagnosis and treatment necessitate the identification of reliable immune biomarkers. This study investigated the relationship between aging, immunity, and sepsis by analyzing six human aging-related gene sets (656 genes). We identified 16 aging-related differentially expressed genes (DEGs) in sepsis. Among these, ATP11B, RBBP7, DOCK10, and NUP160 demonstrated the strongest connectivity with other genes and exhibited significant predictive power. Functional enrichment analysis (GO and KEGG) revealed distinct signaling pathway profiles between high-risk and low-risk sepsis groups (stratified based on risk scores). These dysregulated pathways, associated with multiple immune cells, were primarily linked to transcriptional dysregulation in cellular processes and cancer-related pathways. Experimental validation assays corroborated the roles of ATP11B and RBBP7. Collectively, our bioinformatic and experimental findings indicate that ATP11B, RBBP7, DOCK10, and NUP160 are implicated in the pathogenesis and progression of sepsis. But their potential for sepsis biomarkers still requires further verification. - Source: PubMed
Publication date: 2025/12/04
Sun XueyiGeng ShaoleiWang ZeyuanChen Qingjiang - Congenital nephrotic syndrome of the Finnish type (CNF) is an autosomal recessive disorder resulting from mutations in the gene, which encodes nephrin, an essential protein in the podocyte slit diaphragm. Pathogenic mutations of cause substantial proteinuria detectable at birth. Variants of uncertain significance (VUS) are recognized mutations, but their effects on health are not yet understood. This uncertainty makes it challenging to identify specific types of VUS that may contribute to disease development. The association of CNF with VUS remains unclear. - Source: PubMed
Publication date: 2025/07/09
Zafar FarzinaAl-Obaide Mohammed AVasylyeva Tetyana L - Lung adenocarcinoma (LUAD), the predominant histological subtype of non-small cell lung cancer, demonstrates critical regulatory involvement of RNA-binding proteins (RBPs) and circular RNAs (circRNAs) in tumorigenic processes. Emerging evidence highlights the circRNA-autophagy regulatory axis as a crucial modulator of cancer progression. This study systematically investigates the functional interplay within the RBP-circRNA-autophagy network in LUAD pathogenesis. - Source: PubMed
Publication date: 2025/07/08
Ling LiqunHu TianqiZhou ChenkangDai YingjieHu LijuanChen YuxinHu ZhaotingHuang KateChen JieWang Yumin - Mutations in four genes encoding the outer ring complex of nuclear pore complexes (NPCs), NUP85, NUP107, NUP133 and NUP160, cause monogenic steroid-resistant nephrotic syndrome (SRNS). Knockout of NUP85, NUP107, or NUP133 in immortalized human podocytes activates CDC42, an important effector of SRNS pathogenesis. However, it is unknown whether or not loss of NUP160 dysregulates CDC42 in the podocytes. Here, we generated a podocyte-specific Nup160 knockout mouse model with double-fluorescent (mT/mG) Cre reporter genes using CRISPR/Cas9 and Cre/loxP technologies. We investigated nephrotic syndrome-associated phenotypes in the Nup160podo-/- mice, and performed single-cell transcriptomic and proteomic analysis of glomerular suspension cells and cultured primary podocytes, respectively. The Nup160podo-/- mice exhibited progressive proteinuria and fusion of podocyte foot processes. We found decreased Cdc42 protein and normal Cdc42 transcriptional level in the podocytes of the Nup160podo-/- mice using analysis of single-cell transcriptomes and proteomes. We subsequently observed that Cdc42 protein decreased in both kidney tissues and cultured primary podocytes of the Nup160podo-/- mice, although Cdc42 mRNA levels were elevated in the cultured primary podocytes of the Nup160podo-/- mice. We also found that Cdc42 activity was significantly reduced in the cultured primary podocytes of the Nup160podo-/- mice. In conclusion, loss of Nup160 dysregulated Cdc42 in the podocytes of the Nup160podo-/- mice with proteinuria and fusion of podocyte foot processes. Our findings suggest that the dysregulation of CDC42 may contribute to the pathogenesis of SRNS in patients with mutations in NUP160. - Source: PubMed
Liu DeyingLi JiaxinXu ChanLi YuanyuanChen XiaohanZhao FengTong HuajuanYang YonghuiQiu XiaojianYu Zihua - Nucleoporins, as major components of nuclear pore complex, have been recently discovered to participate in organ development. Here, we report a young female patient with nephrotic proteinuria resistant to immune suppressant treatment and congenital ovarian insufficiency. Renal pathology confirmed focal segmental glomerulosclerosis and whole-exome sequencing revealed compound heterozygous mutations in Nucleoporin 160 (), NM_015231.2 c.4154C>T (p.Pro1385Leu) and c.1102-9T>G. Notably, mutations have been associated with congenital nephropathy in four families. We also ruled out competing genetic variants implicated in focal segmental glomerulosclerosis and ovarian dysgenesis. Our identification of two novel mutations associated with congenital nephropathy and ovarian insufficiency simultaneously contributes to a deeper understanding of nuclear pore complex function in the urogenital system. - Source: PubMed
Publication date: 2024/12/14
Liu YuhaoHuang XiaoyingXu LubinCao YaqingNie MinLi Mingxi