AMICA1
- Known as:
- AMICA1
- Catalog number:
- 001525A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- AMICA1
Related genes to: AMICA1
- Gene:
- JAML NIH gene
- Name:
- junction adhesion molecule like
- Previous symbol:
- AMICA1
- Synonyms:
- Gm638, AMICA
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-09-12
- Date modifiied:
- 2016-11-16
Related products to: AMICA1
Related articles to: AMICA1
- This study demonstrates that gamma-aminobutyric acid (GABA) ameliorates diabetic kidney disease (DKD) by modulating macrophage-driven inflammation and podocyte injury through the JAML/FPR2 signaling axis. In streptozotocin (STZ)-induced DKD mice, GABA administration significantly improved renal function by reducing serum creatinine, urea nitrogen, 24-hour urine protein, attenuated glomerular hypertrophy/mesangial expansion, and suppressed pro-inflammatory cytokine production (TNF-α, IL-1β, iNOS) in renal tissue and serum. GABA inhibited glomerular macrophage infiltration (CD68 cells) and M1 polarization while mitigating renal apoptosis and podocyte injury by restoring nephrin and podocin. In a high glucose (HG)-stimulated macrophage-podocyte co-culture model, GABA reduced HG-induced podocyte apoptosis in a macrophage ratio-dependent manner by reversing M1 polarization and inflammatory cytokine overproduction. Mechanistically, GABA normalized DKD-elevated JAML expression in renal tissues and podocytes, while JAML overexpression abolished GABA's renoprotective effects by reactivating inflammation, macrophage recruitment, and podocyte apoptosis. Co-IP confirmed JAML interacted with receptor formyl peptide receptor 2 (FPR2), which mediated DKD-driven macrophage infiltration, as FPR2 knockdown abrogated JAML-induced CD68 cell accumulation. Collectively, GABA alleviated DKD progression by disrupting the JAML/FPR2 axis to suppress macrophage-mediated inflammation and podocyte injury, highlighting its therapeutic potential for diabetic kidney disease. - Source: PubMed
Publication date: 2026/10/01
Zhuang YiboFu ChenluGuo ZhengXu YanZhou JunNi HuipingZhang Aihua - Primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disease with progressive peribiliary inflammation and fibrosis. Disease-modifying therapies are lacking, and the cell-type-specific mechanisms linking genetic susceptibility to pathogenic immune states remain incompletely understood. - Source: PubMed
Publication date: 2026/09/04
Du ZhongyanXu ZhihaoYang ChenxiaoZhang YuanyuanJiang QuanWang Xiaolan - Non-small cell lung cancer (NSCLC) remains a major cause of cancer-related mortality worldwide, and the identification of novel prognostic biomarkers associated with tumor immunity is urgently needed. Junctional adhesion molecule-like (JAML), a member of the junctional adhesion molecule family, participates in leukocyte adhesion, migration, and T-cell activation. Although JAML has been implicated in immune regulation and tumor progression in other cancers, its expression pattern, prognostic significance, and association with the immune microenvironment in NSCLC remain unclear. This study aimed to investigate the clinical and immunological significance of JAML in NSCLC. - Source: PubMed
Publication date: 2026/09/02
Tian QinZhang FuchengHan Chunyan - Left ventricular lead position is a key determinant of optimal biventricular pacing for heart failure. Observational data indicate better outcomes in patients with late myocardial activation at the left ventricular lead site. We aimed to test whether targeting the left ventricular lead at site of latest electrical activation improves outcomes. - Source: PubMed
Publication date: 2026/08/31
Nielsen Jens CosedisSvendsen Jesper HastrupJohansen Jens BrockLarsen Jacob MoesgaardLarroudé Charlotte EllenPoulsen Steen HvitfeldtEiskjær HansNørgaard Bjarne LindeRisum NielsKøber LarsKristensen JensØvrehus KristianSommer Anders MunckSchou MortenSøgaard PeterPoulsen Mikael KjærKofoed Klaus FHansen Thomas FritzGraff ClausSkals Regitze GyldenholmFrausing Maria Hee Jung ParkFrandsen Emil AntonJensen Jesper MøllerVinther MichaelJensen Henrik KjærulfHaarbo JensZaremba TomasViezelis MindaugasPhilbert BeritHjort JakobGerdes ChristianKronborg Mads Brix - To establish a doxorubicin (DOX)-resistant acute myeloid leukemia (AML) cell line and explore the mechanisms of its drug resistance. - Source: PubMed
Feng Lu-LuWang Yu-TingHuang Chao-FanSun Cong-YongJun Ya-LiZhang Li