Ask about this productRelated genes to: NKIRAS1 Blocking Peptide
- Gene:
- NKIRAS1 NIH gene
- Name:
- NFKB inhibitor interacting Ras like 1
- Previous symbol:
- -
- Synonyms:
- KBRAS1, kappaB-Ras1
- Chromosome:
- 3p24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-31
- Date modifiied:
- 2016-10-05
Related products to: NKIRAS1 Blocking Peptide
Related articles to: NKIRAS1 Blocking Peptide
- The transcriptional regulation of pyroptosis in acute pancreatitis (AP) remains poorly understood. This study aims to elucidate the role of the transcription factor ETS proto-oncogene 1 (ETS1) and its association with pyroptosis in AP. - Source: PubMed
Publication date: 2026/02/20
Xia WenwenSu HuilanHuang YisuWen CanZhou JianjunZhao Yan - The mammalian cornea is endowed with stem cells (SCs) that have lifelong regenerative activity. The niche for these cells is the limbus, and damage to it or its SCs results in limbal stem cell deficiency (LSCD). Despite the numerous studies that employ single-cell RNA sequencing, the identity of these cells remains an enigma principally because their spatial positioning is lost upon dissociation. These adversities were avoided via on-tissue spatial transcriptomics where Krt16 and Nkiras1 were differentially expressed. Krt16 was dynamically expressed in the developing limbus, correlated with slow-cycling label-retaining limbal epithelial SCs and was induced during corneal injury, observations consistent with marking functional SCs. Additionally, we established Nkiras1 as a novel maker of limbal neutrophils. Because current gold-standard treatments for LSCD include SC transplantation, our data will inform future studies in delivering a more reliable standard therapy that incorporates an identifiable SC population to improve clinical outcomes. - Source: PubMed
Publication date: 2026/02/05
Nureen LamiaSalerno AntoniettaD'Agostino StefaniaBarbaro VanessaFerrari StefanoPonzin DiegoVittorio OrazioDi Girolamo Nick - The NF-κB family of transcription factors and the Ras family of small GTPases are important mediators of proproliferative signaling that drives tumorigenesis and carcinogenesis. The κB-Ras proteins were previously shown to inhibit both NF-κB and Ras activation through independent mechanisms, implicating them as tumor suppressors with potentially broad relevance to human cancers. In this study, we have used two mouse models to establish the relevance of the κB-Ras proteins for tumorigenesis. Additionally, we have utilized a pan-cancer bioinformatics analysis to explore the role of the κB-Ras proteins in human cancers. Surprisingly, we find that the genes encoding κB-Ras 1 () and κB-Ras 2 () are rarely down-regulated in tumor samples with oncogenic Ras mutations. Reduced expression of human alone is associated with worse prognosis in at least four cancer types and linked to a network of genes implicated in tumorigenesis. Our findings provide direct evidence that loss of in human tumors that do not carry oncogenic mutations is associated with worse clinical outcomes. - Source: PubMed
Publication date: 2023/11/06
Postler Thomas SWang AnqiBrundu Francesco GWang PingzhangWu ZikaiButler Kelly EGrinberg-Bleyer YenkelKrishnareddy SuneetaLagana Stephen MSaqi AnjaliOeckinghaus AndreaRabadan RaulGhosh Sankar - Indoleamine 2,3-dioxygenase (IDO) is a tryptophan-degrading enzyme belonging to the kynurenine pathway. IDO activity has been suggested as a potential biomarker for early diagnosis of chronic kidney disease (CKD). The aim of this study was to perform coincident association analysis to gain genetic insights into the correlation between IDO activity and CKD. This study evaluated the association between IDO activity and CKD using the Korea Association REsource (KARE) cohort. Logistic and linear regression were used to analyze CKD and quantitative phenotypes such as IDO and estimated glomerular filtration rate (eGFR). Our results identified 10 single nucleotide polymorphisms (SNPs) that were coincidently associated with both IDO and CKD ( < 0.001). Among them, rs6550842, rs77624055, and rs35651150 were selected as potential candidates after excluding SNPs with insufficient evidence for having an association with IDO or CKD. Further expression quantitative trait loci (eQTL) analysis for variants at selected loci showed that rs6550842 and rs35651150 significantly affected the expression of and genes in human tissues, respectively. Additionally, we highlighted that the and genes were correlated with IDO activity and CKD through signaling pathways associated with inflammation. Our data suggest that , , and were potential causative genes affecting IDO activity and CKD through integrated analysis. Identifying these genes could aid in early detection and treatment by predicting the risk of CKD associated with IDO activity. - Source: PubMed
Publication date: 2023/04/10
Kim Hye-RimJin Hyun-SeokEom Yong-Bin - McNulty and colleagues describe the glomerular transcriptional landscape of subjects with APOL1 (the gene encoding apolipoprotein L1)-associated kidney disease, using bulk RNA sequencing. They found the following: APOL1 gene expression was higher in individuals with APOL1 high-risk genetic status; in glomeruli, STC1, encoding stanniocalcin, was the most upregulated gene, and CCL18, encoding C-C motif chemokine ligand 18, was the most downregulated gene; and nuclear factor kappa BNF-κB inhibitor-interacting Ras-like 1 (NKIRAS1) is the strongest hub gene. These findings identify disease pathways that might mediate or mitigate APOL1-associated nephropathies. - Source: PubMed
Kopp Jeffrey BHeymann Jurgen