Mouse polyclonal to SLC25A18, Host Mouse
- Known as:
- Mouse pab SLC25A18, Host Mouse
- Catalog number:
- YF-PA26695
- Product Quantity:
- 50 uL
- Category:
- -
- Supplier:
- Abfron
- Gene target:
- Mouse polyclonal SLC25A18 Host
Related genes to: Mouse polyclonal to SLC25A18, Host Mouse
- Gene:
- SLC25A18 NIH gene
- Name:
- solute carrier family 25 member 18
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 22q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-31
- Date modifiied:
- 2016-10-05
Related products to: Mouse polyclonal to SLC25A18, Host Mouse
Related articles to: Mouse polyclonal to SLC25A18, Host Mouse
- 22q11.2 Microduplication syndrome is a genomic disorder characterized by extreme phenotypic variability and reduced penetrance. While minor ear anomalies are common, severe malformations like microtia and aural atresia are rarely reported. We present a unique case of maternally inherited 22q11.2 microduplication with severe external ear defects but superior neurodevelopment. - Source: PubMed
Publication date: 2026/04/28
Kim Hyun HoJang WooriKim NamsuPark Joonhong - Hepatocellular carcinoma (HCC) typically develops from liver cirrhosis (LC), however early diagnosis is difficult due to a lack of reliable biomarkers. The goal of this study was to use SomaScan proteomics technology to find plasma protein profiles that differentiated LC and HCC from healthy controls in order to develop novel biomarkers for HCC early detection and targeted therapy. - Source: PubMed
Publication date: 2026/06/01
Huang LingyuGuo JunjunLiu WeiXie ShenpingYan QiangPu WenjunZeng ZhipengLai LiushengWang BaoyaoDai YongTang DongeChen Huaizhou - Preeclampsia (PE) is a serious complication of pregnancy that affects the offspring and mothers. Those with a history of PE are at higher risk of future cardiometabolic diseases, the etiology of which remains uncertain. - Source: PubMed
Publication date: 2026/02/19
Cheng Yu-ChunLai Yun-JuLian Wei-ShiungTsai Ching-ChangCheng Hsin-HsinYu Hong-RenTiao Mao-MengSheen Jiunn-MingHsu Ying-LunWang Feng-ShengLin I-Chun - Heart failure (HF) represents the end stage of cardiovascular disease and is the leading cause of mortality. The objective of this study was to identify potential biomarkers and elucidate the mechanisms underlying the development of HF across diverse populations and among different genders. - Source: PubMed
Publication date: 2025/10/14
Yu YueXue ChentianJi DongSheng WeiGao XiangWu XizeWu Chengyan - Musculoskeletal diseases are the leading cause of disability-adjusted life years. Mitochondria, often referred to as the "powerhouses" of cells, are believed to play a role in regulating cellular metabolism and differentiation, potentially influencing the occurrence and progression of musculoskeletal diseases. However, the exact causal relationships remain to be defined. This study aimed to investigate the causal relationships between mitochondrial biological functions and musculoskeletal diseases (including osteoarthritis (OA), osteoporosis, rheumatoid arthritis (RA), and ankylosing spondylitis through Mendelian randomization (MR) analysis). We systematically summarized data related to mitochondrial functional proteins and musculoskeletal diseases from the IEU OpenGWAS and UK Biobank databases. We used single nucleotide polymorphisms significantly associated with musculoskeletal diseases as instrumental variables. The inverse variance weighting method performed the main MR analysis. We used Mendelian randomized residual sum of pleiotropy and outliers, MR-Egger regression, Cochran Q statistic, Rucker Q statistic, Radial-MR, weighted median, simple mode, weighted mode, and leave-one-out analysis methods as supplementary analyses. First, 14 positive mitochondrial functional proteins were screened out. After Bonferroni correction, COA3 and COX4I2 were found to be causally related to OA and act as protective factors. We identified a causal relationship between SLC25A18 and RA as a risk factor. This study provides genetic support and offers new evidence regarding the roles of COA3, COX4I2, and SLC25A18 in the pathophysiology of OA and RA. This study paves the way for a deeper understanding of the pathological mechanisms of musculoskeletal diseases and provides information for their prevention strategies and treatments. - Source: PubMed
Li Jia-ChenHuang Wei-ShengYang Da-HangHe Qi-FeiSun Wei