Anti_Human, mab EDA_A2 Source Mouse
- Known as:
- Anti_Human, mab EDA_A2 Source Mouse
- Catalog number:
- 101-M384
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Human mab EDA_A2 Source Mouse
Related genes to: Anti_Human, mab EDA_A2 Source Mouse
- Gene:
- EDA2R NIH gene
- Name:
- ectodysplasin A2 receptor
- Previous symbol:
- -
- Synonyms:
- XEDAR, EDA-A2R, EDAA2R, TNFRSF27
- Chromosome:
- Xq12
- Locus Type:
- gene with protein product
- Date approved:
- 2004-08-17
- Date modifiied:
- 2016-10-05
Related products to: Anti_Human, mab EDA_A2 Source Mouse
Related articles to: Anti_Human, mab EDA_A2 Source Mouse
- The aim of this study was to investigate the mediating role of immune cells in the relationship between plasma proteins and the risk of major depressive disorder (MDD). Using a two-step, two-sample Mendelian randomization (MR) approach, we systematically assessed whether immune cells mediate the causal effects of plasma proteins on MDD. We found that eleven plasma proteins (TRABD, CACNB4, EDA, SAR1A, GLRX, COTL1, STOM, CRP, FGF22, and EDA2R) were positively associated with MDD risk, while one protein (SPTLC1) exhibited a negative association. Additionally, seven immune cell phenotypes-including CD14 on CD33dim HLA DR + CD11b + , memory B cells (% of B cells), IgD⁻ CD24⁻ % B cells, CD20 on B cells, CD27 on IgD⁺ CD24⁺, CD27 on IgD⁻ CD38dim, and CD62L on CD62L⁺ DCs-showed potential causal effects on MDD. Further mediation analysis revealed that three immune cell types mediated the effects of four plasma proteins on MDD: CD27 on IgD⁺ CD24⁺ cells mediated the effects of both COTL1 and RNF122 (mediation proportions: 5.13% and 4.50%, respectively); IgD⁻ CD24⁻ % B cells mediated the effect of EDA (12.1%); and CD62L on CD62L⁺ DCs mediated the effect of GLRX (-9.46%). The negative mediation proportion suggests a protective pathway. Sensitivity analyses supported the robustness of these findings.These results provide novel insights into immune-mediated mechanisms linking plasma proteins to MDD and may inform future research into targeted immunotherapeutic strategies. - Source: PubMed
Publication date: 2025/11/13
Jia RuolingNie MingkunWang XunYang Yang - Tooth agenesis (TA), the congenital absence of one or more teeth, is the most common manifestation of defective dental morphogenesis in humans. TA can occur as an isolated (non-syndromic) condition or as part of a broader syndromic presentation. In this review, we analyzed a total of 73 manuscripts to provide a comprehensive update on the genetic landscape of TA. To investigate the genes, variants, and associated phenotypes, we reviewed data from curated databases including Human Phenotype Ontology (HPO), OMIM, ClinVar and MalaCards. Based on the current evidence, the genes most frequently implicated in TA are , , and . However, chromosomal abnormalities, such as those seen in Down syndrome and Williams syndrome, along with structural variations (e.g., deletions and duplications), also contribute significantly to TA etiology. The most involved pathways include TNF receptor binding, encompassing genes such as , , , and , and the mTOR signaling pathway, which includes , , , , and . The aim of this review is to provide an critical synthesis of the genetic mechanisms underlying TA, highlighting the contribution of major signaling pathways, regulatory networks, and emerging molecular insights that may inform diagnostic and therapeutic advances. - Source: PubMed
Publication date: 2025/10/28
Fallea AntonioVinci MirellaL'Episcopo SimonaBartolone MassimilianoMusumeci AntoninoRagalmuto AldaTreccarichi SimoneCalì Francesco - Sperm capacitation, a prerequisite for fertilization, is regulated not only by intrinsic signaling but also by paracrine factors within the female tract. Analysis of previously published RNA-seq datasets identified the ectodysplasin-A2 receptor (EDA2R), an X-linked member of the TNF-receptor superfamily, as a candidate regulator of this process. This study was conducted to test the hypothesis that the EDA-A2/EDA2R axis is a regulator that directly regulates sperm capacitation during fertilization process. Western blotting and immunofluorescence showed that EDA2R was localized in late spermatogenic cells and in the midpiece of epididymal sperm. Incubation of mouse sperm in HTF medium containing the corresponding ligand EDA-A2 (0-1 µg/mL) resulted in a dose-dependent improvement in the amplitude of lateral head displacement and curvilinear velocities. Ligand exposure promoted the appearance of capacitation hallmarks: tyrosine phosphorylation level was elevated within 30 min and the proportion of FITC-PNA positive, acrosome-reacted cells increased at 30 and 60 min (p < 0.05). The EDA-A2 treated sperm yielded a higher cleavage rate (78.5% vs. 48.3%) and a higher blastocyst formation rate (97.6% vs. 88.4%) after in vitro fertilization. qPCR in hormonally synchronized females revealed transient ovarian and prolonged oviductal Eda-a2 upregulation surrounding ovulation, suggesting that the ligand is present at the site of sperm-oocytes fertilization. These results clarify that EDA-A2/EDA2R is a rapid physiological driver of sperm capacitation. This provides a tractable cytokine axis for optimizing assisted reproduction. - Source: PubMed
Publication date: 2025/07/21
Anjorin Oluwakemi IYamanaka TakahiroShimada Masayuki - Tumour-induced skeletal muscle wasting in the context of cancer cachexia is a condition with profound implications for patient survival. The loss of muscle mass is a significant clinical obstacle and is linked to reduced tolerance to chemotherapy and increased frailty. Understanding the molecular mechanisms driving muscle atrophy is crucial for the design of new therapeutics. - Source: PubMed
Publication date: 2024/07/13
Agca SametDomaniku-Waraich AylinBilgic Sevval NurSucuoglu MelisDag MericDogan Sukru AnilKir Serkan - Skeletal muscle is essential in generating mechanical force and regulating energy metabolism and body temperature. Pathologies associated with muscle tissue often lead to impaired physical activity and imbalanced metabolism. Recently, ectodysplasin A2 receptor (EDA2R) signaling has been shown to promote muscle loss and glucose intolerance. Upregulated EDA2R expression in muscle tissue was associated with aging, denervation, cancer cachexia, and muscular dystrophies. Here, we describe the roles of EDA2R signaling in muscle pathophysiology, including muscle atrophy, insulin resistance, and aging-related sarcopenia. We also discuss the EDA2R pathway, which involves EDA-A2 as the ligand and nuclear factor (NF)κB-inducing kinase (NIK) as a downstream mediator, and the therapeutic potential of targeting these proteins in the treatment of muscle wasting and metabolic dysfunction. - Source: PubMed
Publication date: 2024/03/04
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