Mouse KIM1 (4X96T)
- Known as:
- Mouse KIM1 (4X96T)
- Catalog number:
- LF-EK50618
- Product Quantity:
- 4
- Category:
- -
- Supplier:
- Abfron
- Gene target:
- Mouse KIM1 (4X96T)
Related genes to: Mouse KIM1 (4X96T)
- Gene:
- HAVCR1 NIH gene
- Name:
- hepatitis A virus cellular receptor 1
- Previous symbol:
- -
- Synonyms:
- HAVCR-1, TIM-1, TIM1, HAVCR, TIMD1, CD365, KIM1
- Chromosome:
- 5q33.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-12-04
- Date modifiied:
- 2018-07-06
Related products to: Mouse KIM1 (4X96T)
Related articles to: Mouse KIM1 (4X96T)
- Urosepsis is a kind of sepsis resulting from urogenital infections, marked by a significant prevalence of organ failure and mortality. This study sought to examine the preventive effect and possible mechanism of butyrate against multi-organ damage caused by urosepsis. - Source: PubMed
Publication date: 2026/09/01
Liu YanLiu ZhenyuXu HaoZhou YuChen YafengWang LinZhao FuhanGao LeiPan Tiejun - Kidney injury molecule 1 (KIM-1), encoded by HAVCR1, was initially identified as one of the most highly induced proteins in injured proximal tubule epithelial cells and subsequently established as a sensitive tissue, urinary, and circulating biomarker of kidney injury. Yet KIM-1 is not just a marker of epithelial damage. It is a phosphatidylserine receptor that enables injured proximal tubule cells to recognize and internalize apoptotic cells and luminal cargo. This process engages intracellular trafficking, autophagy-related processing, and immune regulatory pathways, with consequences that are highly context-dependent. Transient KIM-1 expression can promote debris clearance and limit inflammation after acute injury, whereas sustained expression and uptake of protein- and lipid-rich cargo can contribute to cellular stress, maladaptive repair, inflammation, and fibrosis. Beyond kidney injury, KIM-1 is expressed and shed by renal cell carcinomas, in which circulating levels carry diagnostic, prognostic, and potentially treatment-stratifying information. KIM-1 is also emerging as both a molecular address for targeted therapeutic delivery and a candidate for functional inhibition or degradation. This review traces how KIM-1 evolved from an injury-induced transcript to a biomarker, signaling receptor, disease mediator, and therapeutic target. We propose a framework in which expression duration, cargo identity, receptor processing, intracellular trafficking, and disease context determine whether KIM-1 supports repair or promotes pathology, highlighting unresolved questions essential for translating its complex biology into more precise diagnostic and therapeutic strategies. - Source: PubMed
Publication date: 2026/09/14
Soliman AhmedIchimura TakaharuBonventre Joseph V - To identify plasma protein biomarkers associated with incident non-fatal major adverse cardiovascular events (MACE) in diabetic kidney disease (DKD) patients. - Source: PubMed
Publication date: 2026/08/27
Jiang LiChien ChiehLi TianliZhang HaojunZhao TingtingWu Xiai - The DrugMatrix database contains systematically generated toxicogenomics data from short-term in vivo studies for over 600 chemicals. However, most potential endpoints are missing due to a lack of experimental measurements. Therefore, we leveraged matrix factorization and machine learning methods to predict the missing values, which includes gene expression across eight tissues on two expression platforms along with paired clinical chemistry, hematology, and histopathology. We propose a method, ToxCompl, that applies systematic hybrid sampling guided by Bayesian optimization in conjunction with low-rank matrix factorization to predict the missing values. In-depth validation of the ToxCompl predicted data from machine learning, biological, and toxicological perspectives shows that the predicted differential gene expression aligns well with what would be anticipated. This includes examining the connectivity pattern of predicted gene expression responses, characterizing molecular pathway-level responses from sets of differentially expressed genes, evaluating known transcriptional biomarkers of tissue toxicity, and characterizing predicted apical endpoints. For example, we identified kidney toxicants using the transcriptional biomarker Havcr1. All measured and predicted DrugMatrix data (i.e., gene expression, clinical chemistry, hematology, and histopathology) are available to the public (https://rstudio.niehs.nih.gov/toxcompl/). Notably, predicted clinical chemistry of subtle effects and histopathological prediction are two areas we will continue to improve. The main advantage of the ToxCompl approach is that it drastically extends the toxicogenomic landscape into many data-poor tissues in the absence of acquiring additional experimental data, thereby allowing researchers to formulate mechanistic hypotheses about effects in tissues that have been underrepresented in the literature. - Source: PubMed
Publication date: 2026/09/04
Word Laura JCong GuojingPatton Robert MChao FrankSvoboda Daniel LCasey Warren MSchmitt Charles PErickson Jeremy NCombs ParkerAuerbach Scott S - Autoimmune kidney diseases can cause glomerulonephritis and tubulointerstitial nephritis, which if unresolved, lead to progressive glomerulosclerosis and tubulointerstitial fibrosis. The IL-1 receptor (IL-1R1) is known to have divergent and cell-specific effects in kidney injury. We hypothesized that IL-1R1 would dampen pro-inflammatory activation of myeloid cells such that deletion of myeloid cell IL-1R1 would exacerbate autoimmune nephritis. Mice with myeloid cell-specific deletion of IL-1R1 (LysMCre(+) / Il1r1fl/fl - MKO) and littermate controls (LysMCre(-) / Il1r1fl/fl - MWT) were subjected to nephrotoxic serum (NTS) nephritis. MKO mice demonstrated worsened glomerular and tubular injury as indicated by increased albuminuria, glomerular injury scores, and kidney mRNA levels of kidney injury molecule (KIM)-1 (Havcr1) and neutrophil gelatinase-associated lipocalin (NGAL/Lcn2). We further found that myeloid IL-1R1 deficiency resulted in increased myeloid cell ER stress and expression of the heterodimeric cytokine Ebi3/Il27a (IL-27). IL-27 then induced increased type I IFN expression by kidney endothelial cells. In turn, anti-IL-27 limited type I IFN expression in endothelial cells and NTS nephritis, and anti-IFNAR1 therapy ameliorated glomerular and tubular injury in MKO mice. Thus, we demonstrated a myeloid cell-endothelial cell immunoregulatory axis whereby myeloid IL-1R1 activity constrained endothelial type I IFN generation to limit chronic kidney damage. - Source: PubMed
Publication date: 2026/09/01
Chen YantingLi YuRen JiafaWu Chia-ChunLu XiaohanInumarty AchintyaCrowley Steven DPrivratsky Jamie R