MEPE antibody
- Known as:
- MEPE (anti-)
- Catalog number:
- orb30399
- Product Quantity:
- 20 ug(Trial size)
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- MEPE antibody
Related genes to: MEPE antibody
- Gene:
- MEPE NIH gene
- Name:
- matrix extracellular phosphoglycoprotein
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 4q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-19
- Date modifiied:
- 2016-10-05
Related products to: MEPE antibody
Related articles to: MEPE antibody
- Otosclerosis is a common cause of conductive hearing loss thought to result from dysregulated bone remodeling in the embryonic tissues of the globuli interossei. Both familial and sporadic cases have been reported. To date, 10 published loci and four genes ( (), (), , ) have been identified in autosomal dominant families. Using a combined genetic and genomics approach in five affected siblings, we identified a nonsense mutation in Karyopherin subunit α7 (, c.49C>T, p.R17X), the newest of the importin-α family of nuclear transporters. KPNA7 is a key maternal factor involved in the classical transport of NLS-containing cargo proteins, active during early embryonic cleavage events and zygotic genome activation. So far, 377 cargo proteins associated with KPNA7 have been identified. Recessive variants cause skeletal abnormalities, epilepsy, intellectual disabilities and preimplantation embryo arrest (PREMBA). A closer look at the genes reveals their involvement in endochondral ossification signaling pathways. We explore how KPNA7 haploinsufficiency in the embryonic tissues of the otic capsule may cause dysregulated bone remodeling. This study expands the phenotypic spectrum of KPNA7 and provides new insights into the pathobiology of otosclerosis. - Source: PubMed
Publication date: 2026/05/30
Benteau TammyAbdelfatah NellyGriffin AnnePenney CindyHu PingzhaoStanton Susan GZhai GuangjuMaheu MaximeFrench Curtis RYoung Terry-Lynn - Osteoporosis is a highly heritable metabolic bone disorder characterized by low bone mass and increased fracture risk. However, the causal genes underlying disease susceptibility remain incompletely understood. In this study, we employed a summary-data-based Mendelian randomization (SMR) framework to identify genes with potential causal effects on osteoporosis by integrating genome-wide association study summary statistics from the FinnGen consortium with multilayer molecular quantitative trait loci (xQTL) data, including expression, splicing, methylation, and protein QTLs across multiple tissues (106 xQTL datasets in total). The heterogeneity in dependent instruments (HEIDI) test was applied to distinguish pleiotropic associations from linkage disequilibrium-driven effects. Functional characterization was further conducted using Gene Ontology and KEGG pathway enrichment analyses, protein-protein interaction network construction, drug-gene enrichment analysis, and molecular docking. Using this integrative approach, we identified 15 high-confidence genes - CEP112, CKB, GID4, MEOX1, MEPE, PPP6R3, RGS9, RSPO3, SERPINA1, SFRP4, SOST, SPP1, SREBF1, TOM1L2, and ZBTB48 - showing evidence of causal associations with osteoporosis after stringent multiple-testing correction and HEIDI filtering. These genes included established regulators of bone metabolism as well as novel candidates involved in metabolic regulation and signal transduction. Enrichment analyses highlighted pathways related to Wnt and bone morphogenetic protein signaling, extracellular matrix organization, and metabolic processes, while network analysis revealed substantial functional connectivity among the prioritized genes. In addition, drug-gene enrichment analysis prioritized β-carotene, apocarotenal, and bezafibrate as potential therapeutic candidates, with molecular docking supporting stable interactions with key protein targets. Overall, this study provides robust genetic evidence for causal molecular regulators of osteoporosis and highlights potential therapeutic targets, offering a clinically relevant resource for future functional validation and translational research. - Source: PubMed
Yu FeiWan XiwenQiu Jiaxuan - Wound healing is a complicated process, so it's critical to identify efficient ways to hasten recovery. Platelet-rich plasma (PRP) and zinc oxide nanoparticles (ZnO NPs) have demonstrated potential in improving cutaneous wound healing in a variety of species. But little is known about their combined effects, especially in dogs. Therefore, this study determined how topical infiltration of PRP and ZnO NPs ointment, both separately and in combination, affect the healing of dogs' cutaneous wounds. Thirty-six full skin wounds were induced in the chest of six adult mongrel dogs. These wounds were randomly divided into six equal groups (6 wounds each) according to treatment protocol: group 1 served as a control and the wounds were dressed daily with normal saline only, group 2: the wounds were dressed daily with lanolin only, group 3: the wounds were infiltrated once with PRP, group 4: the wounds were treated with PRP single infiltration combined with lanolin ointment daily dressing, group 5: the wounds were dressed daily with ZnO NPs ointment, and group 6: the wounds were infiltrated once with PRP and daily dressed with ZnO NPs ointment. Wound healing progress was monitored; epithelialization, wound contraction, and overall healing were assessed. Total antioxidant capacity (TAC), malondialdehyde (MDA) and the concentration of platelets derived growth factor beta (PDGFβ) were measured on wound fluid. Gene expression of matrix extracellular phosphoglycoprotien (MEPE), transforming growth factor beta (TGF-β) and tumor necrosis factor alpha (TNF-α) were also evaluated on skin biopsies at day 0, 5, 10 and 20. Histopathology, immunohistochemistry and staining of collagen bundles were performed on skin biopsies at 5, 10 and 20 days of wound induction. All data were statistically analyzed. There was a significant interaction between the group and time across all parameters (P < 0.001). The PRP-ZnO NPs group consistently has a great effect on wound size reduction, contraction, healing, epithelialization, and antioxidant activity, along with higher MEPE and PDGFβ expression and arranged parallel collagen bundles, indicating enhanced regeneration. While PRP alone showed the strongest TGF-β increase and anti-inflammatory effect (lowest TNF-α). PRP-ZnO NPs provided the best overall balance between regeneration and inflammation control. All treatments surpassed the control and lanolin groups, which showed minimal improvement. PRP-Lanolin and ZnO NPs offered moderate benefits but were less effective than PRP-ZnO NPs or PRP. ZnO NPs and PRP work together to improve skin wound healing in dogs; PRP promotes regenerative signaling, while ZnO NPs reduce oxidative stress and microbial load. - Source: PubMed
Publication date: 2026/06/02
Wafy Mona NHassan Elham ASaeed SamarKhattab Marwa SAbuBakr Huda OAbu-Seida Ashraf M - The mechanisms underlying sex differences in calcific aortic valve stenosis (CAVS) are poorly understood. We aimed to uncover sex-specific gene expression signatures of CAVS, including genes located on sexual chromosomes. - Source: PubMed
Publication date: 2026/05/22
Houessou UrsulaZamani PardisManikpurage Hasanga DLi ZhonglinGaudreault NathalieDahmene ManelDagenais FrançoisCouture ChristianClavel Marie-AnnickPibarot PhilippeMathieu PatrickBossé YohanThériault Sébastien - The increasing prevalence of bone-related diseases and the desire to improve patient outcomes are driving research into bone replacement materials that overcome the limits of current bone substitutes. Molybdenum (Mo) is a promising candidate as an implant and degradable bone replacement material because it combines three key properties: mechanical strength, biocompatibility, and resorbability. However, little is known about the cellular mechanisms induced by Mo on bone regeneration. This study exposed a complex in vitro bone model as quadruple culture with primary human osteoblasts, osteocytes, osteoclasts, and endothelial cells, to Mo powder extracts to understand cell-material interactions in a multicellular system. Extracts with a final concentration of 1 mM Mo in quadruple cultures induced osteogenic differentiation by stimulation of gene expression and ALP activity, and gene expression, as well as enhanced calcium deposition of osteoblasts. Furthermore, expression of osteoblasts increased significantly and network formation of HUVEC with stimulated expression occurred. However, CD31 () expression and endothelial network density were reduced, indicating a complex, mixed angiogenic response. In contrast, Mo inhibited osteoclast formation and slowed down osteocyte differentiation, reducing , , and gene expression. Additionally, the RANKL ()/OPG () ratio of osteocytes was shifted toward OPG after Mo treatment. Cellular effects are most likely caused by the presence of molybdate anions. In summary, Mo extracts stimulated early bone healing factors involved in osteogenesis, vascularization, and mineralization, while osteoclastogenesis was inhibited. These dual effects in vitro provide mechanistic evidence supporting the potential of Mo as a growth factor-free bone replacement material and establish a cellular foundation for further preclinical development. - Source: PubMed
Publication date: 2026/05/07
Wirsig KatharinaBernhardt Anne