Ask about this productRelated genes to: MXRA7 antibody
- Gene:
- MXRA7 NIH gene
- Name:
- matrix remodeling associated 7
- Previous symbol:
- -
- Synonyms:
- FLJ46603, TMAP1, PS1TP1
- Chromosome:
- 17q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-06-15
- Date modifiied:
- 2016-05-13
Related products to: MXRA7 antibody
Related articles to: MXRA7 antibody
- Whiplash-associated disorder grade II (WADII) is characterised by persistent pain in the absence of frank nerve injury, yet its molecular mechanisms remain unclear. - Source: PubMed
Publication date: 2026/07/31
Fundaun JoelRidehalgh ColetteDilley AndrewSchmid Annina BBaskozos Georgios - Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by persistent colorectal mucosal damage, in which colonic epithelial cell pyroptosis and imbalanced macrophage M1 polarization serve as core pathological features, yet their interaction mechanism remains elusive. Matrix remodeling-associated 7 (MXRA7) has been implicated in inflammatory immune responses and tissue repair, but its role in UC progression is still unclear. In this study, we performed bioinformatics and cell-cell communication analyses using the GSE214695 single-cell RNA sequencing dataset, collected clinical colonic tissues from UC patients, and established a dextran sulfate sodium (DSS)-induced mouse colitis model, complemented by in vitro cell co-culture, gene knockdown/overexpression and molecular biological assays. The results showed that pyroptosis levels, the degree of macrophage M1 polarization, and MXRA7 expression were all significantly upregulated in the colonic tissues of both UC patients and model mice. Mechanistically, macrophage M1 polarization can directly trigger colonic epithelial cell pyroptosis, whereas MXRA7 may, on the one hand, reduce macrophage M1 polarization by inhibiting the NF-κB signaling pathway, and on the other hand, alleviate epithelial cell pyroptosis induced by M1-polarized macrophages. Collectively, MXRA7 may attenuate colonic tissue damage through these dual regulatory mechanisms, thereby serving as a potential regulatory factor or therapeutic target in UC. - Source: PubMed
Publication date: 2026/07/31
Zhu XueyingTang KunyangKang JianCui NingXiang HongyuSu WenhaoHe YangGuo YingyunXiao MinZhou ZhongyinDong Weiguo - Exercise-induced fatigue (EIF) is closely associated with male reproductive dysfunction, but the underlying mechanism remains unclear. This study aimed to explore whether EIF induces oxidative stress and epididymal inflammation, and to clarify the protective role and regulatory pathway of matrix remodeling-associated 7 (MXRA7). Clinical samples from EIF volunteers and an EIF mouse model were used to detect oxidative stress, inflammation, and sperm quality. Mouse caput epididymal PC-1 cells and cauda epididymal DC-2 cells were cultured to establish inflammatory injury models. MXRA7 expression, localization, and function were analyzed by transcriptomic analysis, gene knockdown/overexpression, Western blotting, immunofluorescence, co-immunoprecipitation, and in vitro phosphorylation assays. The results showed that EIF significantly elevated systemic and epididymal oxidative stress and inflammatory responses in both humans and mice, accompanied by impaired sperm motility and epididymal dysfunction. MXRA7 was highly expressed in epididymal epithelial cells, especially in the cauda epididymis, and its expression was negatively correlated with the severity of inflammation. MXRA7 knockdown aggravated inflammatory injury in DC-2 cells, whereas MXRA7 overexpression suppressed oxidative stress, inflammatory factor release, and NF-κB signaling activation. Mechanistically, protein kinase C alpha (PKCα) mediated the expression and phosphorylation of MXRA7, and MXRA7 further inhibited the NF-κB pathway to alleviate epididymal inflammation. In addition, MXRA7 expressed by cauda epididymal epithelial cells directly protected sperm from inflammatory damage. In conclusion, EIF impairs sperm function by triggering epididymal oxidative stress and inflammatory injury. MXRA7, regulated by PKCα-mediated phosphorylation, serves as a key protective factor that attenuates EIF-induced epididymal inflammation via inhibiting the NF-κB signaling pathway. This study provides a novel target for the prevention and treatment of reproductive damage caused by excessive exercise. - Source: PubMed
Publication date: 2026/07/14
Tang KunyangJiang XiaocuiZhou YanyanHu XinLiu JiasenHuang DonghuiYu XiaomingZhao MinLiu YingCao JigangFang ZhipengXiao Min - Marrow senescence contributes to overall organismal aging and involves functional alterations in both the mesenchymal and hematopoietic compartments of bone marrow. Although matrix remodeling-associated 7 () has been demonstrated to modulate mesenchymal function and megakaryocyte differentiation in mice, this study aimed to investigate the potential role of in marrow senescence. Single-cell RNA sequencing was performed on bone marrow cells from young and aged wild-type and -knockout mice. Comparative analysis of 2-month-old and 2-year-old mice revealed that aging significantly altered the cellular proportions within the bone marrow niche, and deficiency markedly increased Macro1 macrophages in aged mice, likely driven by the dysregulation of the axis. deficiency altered Mid1 expression and the macrophage migration inhibitory factor (), , and Von Willebrand factor signaling pairs (), all of which are closely associated with cell status in the bone marrow microenvironment. In summary, these findings underscore 's role in cellular profile shifts during bone marrow aging, offering novel insights into how coordinates hematopoietic and immune homeostasis in the bone marrow. - Source: PubMed
Publication date: 2026/05/28
Qin YuzhenZhao ZiyanChen YihanZheng YudanMa KunpengLin DandanLiu XinWang Yiqiang - Frailty, a clinical state of increased vulnerability to stressors with aging, imposes significant strain on healthcare systems. Its genetic underpinnings remain incompletely explored, highlighting the need to identify novel therapeutic targets for aging. - Source: PubMed
Publication date: 2026/04/01
Zhong JiaYuYuan MingHaoZhou EnHu Shuo