Ask about this productRelated genes to: MFAP2 Blocking Peptide
- Gene:
- MFAP2 NIH gene
- Name:
- microfibril associated protein 2
- Previous symbol:
- -
- Synonyms:
- MAGP, MAGP-1
- Chromosome:
- 1p36.13
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-22
- Date modifiied:
- 2017-05-16
Related products to: MFAP2 Blocking Peptide
Related articles to: MFAP2 Blocking Peptide
- Gastric cancer (GC) is a leading cause of cancer mortality worldwide, and dietary factors like mycotoxins play a significant role in its etiology. Zearalenone (ZEN), a widespread grain contaminant, is a suspected carcinogen; however, its molecular mechanisms in GC remain unclear. This study used an integrated systems toxicology approach to identify key targets and pathways of ZEN-induced GC and validate the findings. - Source: PubMed
Publication date: 2026/03/31
Zheng HangbinChen ShunLin GuoHuang WenxinGuo YihuiZhang HaoJin ZiyiLin JiaLin YaoChen Liwu - Advanced paternal age compromises male fertility and correlates to a decline of the deacetylase SIRT1 activity, a central regulator of germline homeostasis and chromatin dynamics. Acetylation imbalance has been pointed out as a driver of testicular aging. We therefore asked whether SIRT1 insufficiency reproduces aging-associated shifts in the acetylation landscape and how these might propagate to sperm function, fertilization capacity and embryo development. To address this, we combined acetylomic profiling of / and naturally aged mice with functional assays of sperm quality and in vitro fertilization (IVF). Both and aged wild type (WT) testes shared a distinct acetylation signature absent in young WT controls, including nuclear regulators (ZNF638, MORC4), proteins involved in sperm structure and motility (Rootletin, Kinectin, CFAP58), and phosphoinositide signaling mediators such as PLCη1, which regulate intracellular Ca release. Conversely, 22 proteins displayed acetylation exclusively in WT controls but were absent in and aged testes, encompassing modules related to flagellar organization (CEP170, CEP350, AKAP13), meiotic control (ANAPC7, PDS5B, ESCO1, CENPE), signaling and metabolism (SHIP1, GAK, ABCD4), chromatin regulation (BRD4, MAGEB4), and testicular architecture (MFAP2). This differential acetylomic profile persisted in mature sperm, with / males showing elevated acLys levels and, more specifically, midpiece-restricted α-tubulin hyperacetylation, a pattern particularly shared with aged cohorts. Notably, this tubulin hyperacetylation remained after capacitation and correlated with mitochondrial dysfunction, elevated reactive oxygen species, reduced acrosome responsiveness, and diminished fertilization capacity. IVF assays further revealed decreased cleavage and blastocyst developmental rates, indicating defective paternal support of early embryogenesis despite preserved blastocyst quality. Together, these findings indicate that testicular SIRT1 contributes to germline acetylation patterns and that midpiece-restricted α-tubulin hyperacetylation is a shared feature of SIRT1 insufficiency and natural aging, correlating with the mitochondrial dysfunction and impaired sperm performance. Overall, our work broadens current understanding by integrating acetylomic and functional evidence within a model that reflects the physiological, age-related reduction of SIRT1. - Source: PubMed
Publication date: 2026/03/25
Iniesta-Cuerda MaríaValentova IvetaMoravec JiříLiška FrantišekKrálíčková MilenaKrapf DarioNevoral Jan - Head and neck squamous cell carcinoma (HNSCC) continues to be a deadly cancer with heterogeneous molecular characteristics and poor survival outcomes, particularly in HPV- patients. This study aimed to identify key overexpressed genes that drive HNSCC progression, evaluate their prognostic value, and explore associations with HPV status, promoter methylation, and changes in the immune microenvironment. - Source: PubMed
Publication date: 2026/03/03
Yang YifanWang LingwaWang RuLi HaiyangZhu SiyuFang JugaoFeng Ling - Colorectal cancer (CRC) is a prevalent condition, with metastasis spread as the primary cause of mortality. However, MFAP2 function in CRC progression and its regulatory mechanisms in metastasis remain poorly understood. To investigate the status of MFAP2, an extensive analysis was conducted using multiple clinical databases and transcriptomic data from CRC metastasis patients' tissues and several CRC cell lines. The efficacy of standard first-line chemotherapy drugs (5-fluorouracil, irinotecan, and oxaliplatin) were evaluated for any potential drug resistance. Virtual screening and molecular docking were used to identify potential inhibitory compounds that could be effective against CRC. Moreover, MFAP2 expression was found to be significantly higher in CMS4 CRC patients compared to those with other subtypes. This elevation in MFAP2 correlated with both tumor stromal score and tumor purity. Reducing MFAP2 expression led to a significantly decline in the functional capabilities of CRC cells and heightened their sensitivity to standard chemotherapy treatments. Results have identified MFAP2 as a key regulator in the metastasis of CRC, influencing processes like epithelial-to-mesenchymal transition through the EGFR-AKT-STAT3 signaling pathway. Therefore, MFAP2 emerges as a promising therapeutic target for anti-tumor efforts. Notable, three compounds were discovered that effectively bind and down-regulate MFAP2, which significantly impairs tumor cells migration. These findings revealed new functions of MFAP2, suggesting it plays a vital role in driving epithelial-to-mesenchymal transition, metastasis, and chemotherapy resistance in CRC. This provides a fresh perspective for developing treatment strategies. Overall, targeting MFAP2 may offer a more effective therapeutic option for CRC patients with CMS4. - Source: PubMed
Publication date: 2025/08/12
He ZhichengChen YuanzhiYang ShutingChen ChengHe YingyingLiu Shubai - Colorectal cancer (CRC) ranks among the most prevalent malignancies of the digestive system, with the intricate tumor immune microenvironment (TIME) emerging as a key determinant of poor prognosis. Cancer-associated fibroblasts (CAFs), a central constituent of the tumor microenvironment, critically influence tumorigenesis and progression by orchestrating immunosuppression through cytokine secretion and other mechanisms. This study investigates the multifaceted interplay between CAFs and the immune system to identify novel therapeutic targets and improve prognostic outcomes for CRC patients. Through comprehensive analyses of clinical samples and public database data, we identified elevated MFAP2 expression in both CRC tissues and fibroblasts. Mechanistically, we established that CAFs-derived MFAP2 interacts with integrin β8 (ITGB8) on cancer cell surfaces, activating the integrin-FAK-ERK1/2 signaling cascade to drive CRC progression. Furthermore, ERK1/2 phosphorylates and activates the transcription factor ETS2, which upregulates the expression of CYP27A1, an enzyme that modulates lipid metabolism and suppresses CD8 T cell function via liver X receptor beta (LXRβ) signaling. These findings elucidate a novel MFAP2-ITGB8-FAK-ERK1/2-ETS2-CYP27A1-LXRβ signaling axis, significantly activated by CAFs-derived MFAP2 in both in vitro and in vivo models, contributing to immune exhaustion and tumor progression. This axis offers significant therapeutic and prognostic potential for CRC, providing critical insights into CAF-mediated immune modulation and paving the way for targeted immunotherapeutic strategies. - Source: PubMed
Publication date: 2026/01/30
Zhang XuFei YuxiangXie ChunqiLi TaoNiu BenYang ZihaoSong MengweiMeng FanjunDiao HongtingJi JingDu QianmingLiu Chao