KIAA1199 Blocking Peptide
- Known as:
- KIAA1199 Blocking Peptide
- Catalog number:
- 33r-7080
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- KIAA1199 Blocking Peptide
Related genes to: KIAA1199 Blocking Peptide
- Gene:
- CEMIP NIH gene
- Name:
- cell migration inducing hyaluronidase 1
- Previous symbol:
- KIAA1199
- Synonyms:
- IR2155535, TMEM2L, HYBID
- Chromosome:
- 15q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-29
- Date modifiied:
- 2018-02-26
Related products to: KIAA1199 Blocking Peptide
Related articles to: KIAA1199 Blocking Peptide
- It is documented that antigens can induce immune responses able to regulate complex diseases. Conversely, the dysregulated inflammatory response in leprosy increases morbidity and leads to reactional episodes, impairing the disease pathogenesis. The goal of this study was to evaluate the potential of the (Sm29) antigen in regulating the immune response in leprosy through a transcriptome study across clinical reactional forms: reversal reaction (RR), and erythema nodosum leprosum (ENL), and without reaction (WR). - Source: PubMed
Publication date: 2026/06/01
Karoline Silva Joycede Farias Lucas NevesLago TainãCardoso Luciana Dos SantosKhouri RicardoMachado Paulo RobertoCastellucci Léa Cristina - Disruption of cation homeostasis is increasingly recognized as a driver of breast cancer (BC) progression, yet a clinically actionable gene signature that quantifies this disturbance has been lacking. This study aims to systematically explore the value of cation homeostasis-related genes in the prognosis assessment of BC through bioinformatics analysis, construct and validate a prognostic model based on these genes, and integrate immune mechanism and drug sensitivity analyses to provide novel biomarkers and potential therapeutic targets for precise prognosis evaluation and individualized treatment of BC. - Source: PubMed
Publication date: 2026/04/29
Xu MingxingYe ZhihaoHong WeiminZhu LiquanHe ChaoqiYang ZhuotaoHu JunsiQian DaMeng XuliRen Zhuozhuo - Sepsis-induced acute lung injury (ALI) is a life-threatening condition associated with high mortality rates. While emerging evidence suggests that KIAA1199 (also known as cell migration-inducing protein, CEMIP) contributes to the pathogenesis of bacterial infections, its specific role in sepsis-induced ALI remains largely unexplored. In this study, we find that serum levels of KIAA1199 are significantly elevated in sepsis patients compared to healthy individuals, demonstrating a positive correlation with the SOFA scores. Additionally, we observe the expression of KIAA1199 increased in the lung tissue of septic mice, particularly in alveolar epithelial Type II (AT2) cells. We further generate AT2-specific KIAA1199 knockout mice on a male C57BL/6 J background and establish LPS-induced ALI model. The results indicate that KIAA1199-deficient mice exhibit improved survival rates, reduced lung injury, and decreased levels of proinflammatory cytokines. Transcriptomic analysis and functional validation reveal that KIAA1199 promotes pulmonary complement activation by downregulating complement factor H (CFH), a critical regulator of the alternative complement pathway. Mechanistically, KIAA1199 downregulates CFH expression by enhancing the ubiquitinated degradation of its transcription factor of p53. In conclusion, our data demonstrate that KIAA1199 exacerbates sepsis-induced ALI via promoting local complement activation through CFH suppression, which may serve as a potential therapeutic target for sepsis-induced ALI. - Source: PubMed
Publication date: 2026/05/08
Qin YangZhang JianiZhang YanwenLing SunwangRen WeikangLiu LiJin ShengweiWang JianguangYang Xinyu - To generate a single-cell atlas of colorectal cancer (CRC) development in Lynch syndrome (LS), and to delineate the associated cellular reprogramming and intercellular communication networks. - Source: PubMed
Chen ShangxiangFeng JishenFang ZhengkaiJiang YuhaoDuanmu JinzhongYu XinWang JunfuJiang Qunguang - Myocardial infarction (MI) remains one of the leading causes of mortality and morbidity worldwide. Cardiac remodeling is a key process following MI, involving changes in cellular composition and extracellular matrix (ECM) to adapt to injury. However, maladaptive remodeling can worsen cardiac function, leading to cardiac fibrosis and heart failure. In the context of MI, Cell migration inducing protein (CEMIP) has come into focus and its ability to modulate hyaluronan (HA) turnover has raised critical questions about its role in post-MI healing. - Source: PubMed
Publication date: 2026/04/22
Rebekka SchneckmannTheresa HubeViktoria DarakchievaAria ZardkouhiMirela BalanTobias LautweinAnne PetzSimone GorreßenDan J GorskiKatharina BottermannJens W Fischer