Recombinant Human ACVR2B Protein
- Known as:
- Recombinant Human ACVR2B Protein
- Catalog number:
- ac-720
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Proxinobio
- Gene target:
- Recombinant Human ACVR2B Protein
Related genes to: Recombinant Human ACVR2B Protein
- Gene:
- ACVR2B NIH gene
- Name:
- activin A receptor type 2B
- Previous symbol:
- -
- Synonyms:
- ActR-IIB
- Chromosome:
- 3p22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-03-19
- Date modifiied:
- 2016-10-05
Related products to: Recombinant Human ACVR2B Protein
Related articles to: Recombinant Human ACVR2B Protein
- In both sexes, fetal gonads are connected to the abdominal wall by caudal genital ligaments (CGLs). The male CGL (gubernaculum testis) drives testis descent under the influence of testicular hormones, whereas the fate of the female CGL is thought to result from the absence of these hormones. However, the process in humans has not been clearly demonstrated. We here examined the expression patterns of receptors and metabolizing enzymes of gonadal hormones in CGLs collected from male and female human first trimester fetuses and from boys with uni- or bilateral cryptorchidism by using RT-qPCR, in situ hybridisation, and when possible, immunostaining. We show that the CGLs of both sexes express receptors for insulin-like factor 3 (RXFP2), androgens, estrogens and for members of the transforming growth factor beta family during the first trimester of pregnancy. The expression of RXFP2 increased with fetal age in both sexes, was heterogeneous and unrelated to proliferation. Androgen receptor expression also tended to increase with age, particularly in males. Notably, five alpha reductase type 2 (SRD5A2) and estrogen receptor (ESR1) mRNA levels increased significantly with age in both sexes, but showed clear sexual dimorphism. In contrast, ACVR2B and BMPR1B mRNA decreased with age in both sexes, unlike stable levels of AMHR2 mRNA. In boys with cryptorchidism, gene expression remained consistent regardless of age, ligament position, or appearance. The expression of male hormone receptors and the increased expression of ESR1 in female CGLs raises questions about their physiological significance and susceptibility to xenoestrogens during early development. - Source: PubMed
Publication date: 2026/04/06
Desdoits-Lethimonier CCoiffec-Dorval IToupin MBey MGuinot ALavoué VFrémond BMazaud-Guittot SJégou B - Hedgehog (HH) signaling is essential in directing the fate determination of postmigratory cranial neural crest cells (CNCCs) to ensure proper craniofacial development. Gli transcription factors (TFs) are established as primary effectors of HH signaling, yet their distinct roles and regulatory mechanisms in governing cell commitment and differentiation of postmigratory CNCCs remain poorly understood. Here, using tooth root as a model, we combined transgenic mouse models with bioinformatic analyses to interrogate the functions of Gli2 and Gli3 in CNCC-derived root progenitor cells of the mouse molar. We revealed that loss of Gli3 alone in dental mesenchymal root progenitor cells caused shortened roots and that concurrent loss of Gli2 and Gli3 exacerbated root malformations, concomitant with profound impairments in cell proliferation and multilineage differentiation, suggesting a synergistic interaction between Gli2 and Gli3 during tooth root development. Mechanistically, Gli2 and Gli3 cooperatively regulated the transcription of Acvr2b, thereby modulating the activity of TGF-β/SMAD signaling within the dental mesenchyme. This Gli2/Gli3-TGF-β signaling cascade was critical for the lineage specification of tooth root progenitor cells during molar morphogenesis. Collectively, this work uncovers synergistic interactions of Gli2 and Gli3 in orchestrating tooth root morphogenesis and provides a novel insight into HH-TGF-β crosstalk in cell fate decisions of postmigratory CNCCs. - Source: PubMed
Publication date: 2026/03/12
Zhou TaoHuang LinyangXie YaxinYin YijiaYao YufeiMei LiCooper Paul RZhao HuHan XianglongJing Junjun - Non-coding RNAs (ncRNAs) have emerged as promising biomarkers for prostate cancer (PCa), yet evidence remains dispersed across heterogeneous studies and their regulatory context is seldom analyzed in an integrated manner. This study systematically maps ncRNAs reported as diagnostic biomarkers for PCa and characterizes their molecular interactions through in silico analyses. A comprehensive evidence-mapping strategy across major bibliographic databases identified 693 studies, of which 58 met eligibility criteria. Differentially expressed ncRNAs were extracted and classified by RNA type. Subsequently, miRNA-target prediction, miRNA-protein interaction network construction, and functional enrichment analyses were performed to explore the regulatory landscape of miRNA-associated proteins. Results: The final dataset included 4500 participants (2871 PCa cases and 2093 controls) and reported 94 differentially expressed miRNAs, eight lncRNAs, and several circRNAs, snoRNAs, snRNAs, and piRNAs. In silico analyses predicted 13,493 miRNA-mRNA interactions converging on 4916 unique target genes, with an additional 2481 prostate tissue-specific targets. The miRNA-protein network comprised 845 nodes and 2335 edges, revealing highly connected miRNAs (e.g., hsa-miR-16-5p, hsa-miR-20a-5p) and protein hubs (QKI, YOD1, TBL1XR1; prostate-specific CDK6, ACVR2B). Enrichment analysis showed strong overrepresentation of metabolic process-related GO terms and cancer-associated KEGG pathways. Conclusions: These findings refine the list of promising ncRNA biomarkers and highlight candidates for future clinical validation. - Source: PubMed
Publication date: 2026/01/08
Albarracín-Navas LorenaLara-Salas Nicolás IAlarcon-Roa Javier HAlmonte-Becerril MaylinGuerrero EnmanuelRiffo-Campos Ángela L - Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis is an immune-mediated neurological disorder driven by dysregulated neuroimmune interactions, yet the molecular architecture linking tumor-associated immune activation, peripheral immunity, and neuronal dysfunction remains insufficiently understood. In this study, we established an integrative computational framework that combines multi-tissue transcriptomic profiling, weighted gene co-expression network analysis, immune deconvolution, and machine learning-based feature prioritization to systematically characterize the regulatory landscape of the disease. Joint analysis of three independent GEO datasets spanning ovarian teratoma tissue and peripheral blood transcriptomes identified 2001 consistently dysregulated mRNAs, defining a shared tumor-immune-neural transcriptional axis. Across multiple feature selection algorithms, and were reproducibly prioritized as immune-associated candidate genes and were consistently downregulated in anti-NMDAR encephalitis samples, showing negative correlations with neutrophil infiltration. Reconstruction of an integrated mRNA-miRNA-lncRNA regulatory network further highlighted a putative core axis (-hsa-miR-22-3p-), proposed as a hypothesis-generating regulatory module linking non-coding RNA regulation to immune-neuronal signaling. Pathway and immune profiling analyses demonstrated convergence of canonical immune signaling pathways, including JAK-STAT and PI3K-Akt, with neuronal communication modules, accompanied by enhanced innate immune signatures. Although limited by reliance on public datasets and small sample size, these findings delineate a systems-level neuroimmune regulatory program in anti-NMDAR encephalitis and provide a scalable, network-based multi-omics framework for investigating immune-mediated neurological and autoimmune disorders and for guiding future experimental validation. - Source: PubMed
Publication date: 2026/01/21
Fang KechiLi XinmingWang Jing - This review summarizes recent advances in ligand trap therapies targeting activin type II receptors [ActRIIA/ACVR2A and ActRIIB/ACVR2B], which serve as shared receptors for members of the TGF-β family, including activins, GDF11, and myostatin [MSTN]. These receptors mediate Smad2/3 signaling and play critical roles in hematopoiesis, vascular homeostasis, and muscle regulation. Two peptide-based ligand traps have recently received clinical approval: luspatercept [ActRIIB-Fc], an erythroid maturation agent, and sotatercept [ActRIIA-Fc], a novel therapeutic agent for pulmonary arterial hypertension [PAH]. Luspatercept primarily inhibits activin B and GDF11, thereby promoting late-stage erythropoiesis and demonstrating efficacy in anemia associated with conditions such as myelodysplastic syndromes [MDS] and β-thalassemia. Sotatercept binds activins and GDFs to rebalance Smad2/3 and Smad1/5/8 signaling, thereby improving vascular remodeling in PAH. Although both agents have failed to increase skeletal muscle mass in clinical trials consistently, they represent significant advances in the treatment of hematopoietic and vascular disorders. Future studies should focus on optimal dosing strategies, long-term safety, and potential synergistic effects when combined with other therapeutic modalities. - Source: PubMed
Publication date: 2026/01/02
Tsuchida Kunihiro