Ask about this productRelated genes to: MS4A12 antibody
- Gene:
- MS4A12 NIH gene
- Name:
- membrane spanning 4-domains A12
- Previous symbol:
- -
- Synonyms:
- Ms4a10, FLJ20217
- Chromosome:
- 11q12
- Locus Type:
- gene with protein product
- Date approved:
- 2002-11-26
- Date modifiied:
- 2016-01-20
Related products to: MS4A12 antibody
Related articles to: MS4A12 antibody
- This study aimed to evaluate tissue-associated circulating cell-free DNA (cfDNA) as indicators of radiotherapy-related effects and treatment-associated toxicity in prostate cancer. In addition, inter-individual variability in these markers and their responses to radiotherapy-induced cystitis and rectitis were investigated. The DNA methylation status of six tissue-associated genes representing the prostate (,), colon (,), and bladder (,) was analyzed in serum-derived cfDNA using methylation-sensitive melting curve analysis (MS-MCA). Five of the six analyzed genes demonstrated significantly higher relative DNA levels in patients with prostate cancer compared with controls. Radiotherapy did not significantly alter the relative DNA levels of these tissue-associated genes. However, cfDNA fragmentation was significantly increased in the post-treatment group compared to the pre-treatment group. Notably, 79-bp DNA fragments were significantly more abundant than 230-bp fragments. In the post-treatment group, no significant correlations were observed between cfDNA fragmentation and the relative DNA levels of most targets, except for an association between the 230-bp fragment and relative DNA levels. These findings suggest limited coupling between cfDNA fragmentation patterns and tissue-associated cfDNA release. Marked inter-individual variability in cfDNA methylation signatures was observed across all examined CpG-containing regions except . This variability did not change significantly following radiotherapy and may therefore limit the utility of these assay regions for monitoring individual radiation-induced tissue damage. Furthermore, no significant changes in methylation profiles of colon- or bladder-associated genes were detected in patients who developed radiotherapy-induced rectitis or cystitis. Overall, increased cfDNA fragmentation following radiotherapy and substantial inter-individual variability in methylation profiles across tissue-associated regions may mask tissue-associated cfDNA signals, thereby complicating the assessment of radiation-induced tissue damage. - Source: PubMed
Publication date: 2026/03/06
Bahtiyar NurtenMermut OzlemFirtina SinemOzaydin AhmetSuleymanova AishaIsikgil BegumOnaran İlhan - In individuals presenting with locally advanced rectal cancer, the therapeutic strategy of neoadjuvant concurrent chemoradiotherapy (CCRT) aims to enhance tumor downstaging; however, only a subset of patients exhibit a favorable response. Molecular stratification, combined with the traditional tumor staging system (TNM), is a promising approach for predicting treatment efficacy and patient outcomes. Therefore, we intend to better grasp the molecular basis of CCRT resistance and guide therapeutic strategies with greater precision. - Source: PubMed
Publication date: 2025/08/09
Chen Chih-IKao Yi-KaiYang Po-WenChen Pin-ChunYang Ching-ChiehLi Wan-ShanTsai Hsin-HwaWang Yu-JenLai Hong-Yue - Vulvovaginal candidiasis (VVC) affects 75% of women worldwide at least once in their lifetime, with up to 9% of women experiencing recurrent episodes (RVVC). Genetic differences may play a role in women developing recurrent VVC infections. Thus, we investigated genetic host factors that may increase the risk of RVVC in women from an African population. We conducted a case-control study in women in Nairobi Kenya, to identify genetic risk factors for RVVC. Our genome-wide association study compared women with RVVC (n = 174) to those with acute VVC (n = 157), and with controls (n = 347). The control group included both symptomatic but uninfected women (n = 246) and asymptomatic/healthy women (n = 101). We identified several genomic variants linked to increased RVVC susceptibility (P < 10), with the key ones being SNP rs8181503 found near the MS4A12 gene (P = 9.28 × 10, odds ratio (OR) = 0.46), and SNP rs58936172 located near the TMEM39A gene (P = 8.96 × 10, OR = 2.42). Pathway enrichment analysis revealed enrichment of genetic variants linked to increased risk of RVVC in genes involved in metabolic, disease signalling, and cell adhesion pathways. These included pathways related to gluconeogenesis, fatty acid metabolism, linoleic acid metabolism, pentose phosphate, chemotaxis, and fibroblast growth factor signalling pathways. The genes and pathways identified in our study may help to understand the susceptibility to RVVC in African populations, to improve patient care. - Source: PubMed
Publication date: 2025/04/09
Omosa-Manyonyi Gloria SPonce Isis RicanoRosati DilettaBruno MariolinaKamau Nelly WObimbo Moses MJaeger Martinvan der Ven Andre J A MNetea Mihai GKumar VinodOever Jaap Ten - MS4A (membrane-spanning 4-domain, subfamily A) molecules are categorized into tetraspanins, which possess four-transmembrane structures. To date, eighteen MS4A members have been identified in humans, whereas twenty-three different molecules have been identified in mice. MS4A proteins are selectively expressed on the surfaces of various immune cells, such as B cells (MS4A1), mast cells (MS4A2), macrophages (MS4A4A), Foxp3CD4 regulatory T cells (MS4A4B), and type 3 innate lymphoid cells (TMEM176A and TMEM176B). Early research confirmed that most MS4A molecules function as ion channels that regulate the transport of calcium ions. Recent studies have revealed that some MS4A proteins also function as chaperones that interact with various immune molecules, such as pattern recognition receptors and/or immunoglobulin receptors, to form immune complexes and transmit downstream signals, leading to cell activation, growth, and development. Evidence from preclinical animal models and human genetic studies suggests that the MS4A superfamily plays critical roles in the pathogenesis of various diseases, including cancer, infection, allergies, neurodegenerative diseases and autoimmune diseases. We review recent progress in this field and focus on elucidating the molecular mechanisms by which different MS4A molecules regulate the progression of tumors, Alzheimer's disease, and autoimmune diseases. Therefore, in-depth research into MS4A superfamily members may clarify their ability to act as candidate biomarkers and therapeutic targets for these diseases. Eighteen distinct members of the MS4A (membrane-spanning four-domain subfamily A) superfamily of four-transmembrane proteins have been identified in humans, whereas the MS4A genes are translated into twenty-three different molecules in mice. These proteins are selectively expressed on the surface of various immune cells, such as B cells (MS4A1), macrophages (MS4A4A), mast cells (MS4A2), Foxp3CD4 regulatory T cells (MS4A4B), type 3 innate lymphoid cells (TMEM176A and TMEM176B) and colonic epithelial cells (MS4A12). Functionally, most MS4A molecules function as ion channels that regulate the flow of calcium ions [Ca] across cell membranes. Recent studies have revealed that some MS4A proteins also act as molecular chaperones and interact with various types of immune receptors, including pattern recognition receptors (PRRs) and immunoglobulin receptors (IgRs), to form signaling complexes, thereby modulating intracellular signaling and cellular activity. Evidence from preclinical animal models and human genetic studies suggests that MS4A proteins play critical roles in various diseases (2). Therefore, we reviewed the recent progress in understanding the role of the MS4A superfamily in diseases, particularly in elucidating its function as a candidate biomarker and therapeutic target for cancer. - Source: PubMed
Publication date: 2024/12/09
Luo XuejiaoLuo BinFei LeiZhang QinggaoLiang XinyuChen YongwenZhou Xueqin - Detection of appropriate receptor proteins and drug agents are equally important in the case of drug discovery and development for any disease. In this study, an attempt was made to explore colorectal cancer (CRC) causing molecular signatures as receptors and drug agents as inhibitors by using integrated statistics and bioinformatics approaches. - Source: PubMed
Publication date: 2023/03/29
Horaira Md AbuIslam Md ArifulKibria Md KaderiAlam Md JahangirKabir Syed RashelMollah Md Nurul Haque