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)
- Cardiovascular-kidney-metabolic (CKM) syndrome reflects complex pathobiological interactions among metabolic disorders, kidney injury, and cardiovascular disease (CVD). Stages 2 and 3 represent critical phases of disease progression characterised by high pathological heterogeneity. This study aimed to develop a CVD protein risk score (PRS) for this population and evaluate its incremental predictive value over the PREVENT model. - Source: PubMed
Publication date: 2026/06/01
Han XuefeiDing JiachengLi JingqianGao YiyinLi Yunqian - Approximately one in five patients undergoing coronary artery bypass graft (CABG) surgery will develop post-operative acute kidney injury (AKI). We sought to determine whether biomarkers of kidney tubule dysfunction and injury are associated with long-term risk of acute kidney injury (AKI) after coronary artery bypass graft (CABG) surgery. - Source: PubMed
Publication date: 2026/06/01
Shingler LaurenTamhane AshutoshChu Ching-MinFrey Jennifer ALevitan Emily BJudd Suzanne EBullen Alexander LSiew Edward DBonventre Joseph VShlipak Michael GJaeger ByronSeegmiller Jesse CKeister AlexanderGutierrez Orlando MIx Joachim HWang Henry E - Former studies indicate, that urinary Vascular Non-Inflammatory Molecule 1 (Vanin-1) may be an early biomarker of acute tubular necrosis. We evaluated the diagnostic performance of Vanin-1 regarding the detection of acute kidney injury (AKI) and the differentiation of prerenal from intrinsic AKI compared to other known biomarkers. - Source: PubMed
Publication date: 2026/05/28
Markakis KonstantinosZgoura PanagiotaSeidel MaximilianKolodziej Jonas FranzRieckmann SonjaBertram SebastianDoevelaar AdrianRohn BenjaminBabel NinaWesthoff TimmSeibert Felix - Delirium is an acute brain dysfunction syndrome with high morbidity and mortality, however its mechanisms remain poorly understood. Although multiple risk factors have been identified, directly targeting them is challenging. Proteins may provide new insights into this challenge. - Source: PubMed
Publication date: 2026/05/28
Wang XiaoxiaoLiu KaixiGuo XiangyangLi NanLi Zhengqian - Contrast-induced nephropathy (CIN), now more accurately referred to as contrast-induced acute kidney injury (CI-AKI), remains a major cause of hospital-acquired acute kidney injury (AKI) and is associated with increased morbidity and mortality, particularly in high-risk patients. This condition occurs following the intravascular administration of iodinated radiocontrast media (RCM), especially in individuals with pre-existing chronic kidney disease (CKD), diabetes mellitus, heart failure, advanced age, or exposure to high contrast volumes. The pathophysiology of CI-AKI is multifactorial and involves renal hemodynamic alterations, direct tubular toxicity, oxidative stress, inflammatory activation, and endothelial dysfunction, ultimately leading to tubular injury and reduced glomerular filtration rate (GFR). Traditional diagnostic markers such as serum creatinine (sCr) and estimated glomerular filtration rate (eGFR) are limited by low sensitivity and delayed response, prompting growing interest in novel biomarkers, including cystatin C (CysC), β-2 microglobulin (β-2M), Interleukin-18 (IL-18), Kidney Injury Molecule-1 (KIM-1), Neutrophil Gelatinase-Associated Lipocalin (NGAL), and osteopontin (OPN), which allow earlier detection and risk stratification. Preventive strategies remain the cornerstone of management and include optimizing hydration protocols, minimizing contrast dose, selecting low- or iso-osmolar agents, and individualized risk assessments. Despite extensive research into pharmacological and procedural interventions, no effective treatment for established CI-AKI exists, underscoring the critical importance of prevention and ongoing investigation into safer contrast agents and innovative prophylactic approaches. - Source: PubMed
Publication date: 2026/05/13
Carullo NazarenoTripodi LoredanaMichael AshourFaga TeresaBolignano DavideCoppolino GiuseppeBattaglia YuriIelapi NicolaCosta DavideSerra RaffaeleAndreucci Michele