ACVR1C antibody Polyclonal Antibodies Primary antibodies
- Known as:
- ACVR1C (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb37443
- Product Quantity:
- 5
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- ACVR1C antibody Polyclonal Antibodies Primary antibodies
Related genes to: ACVR1C antibody Polyclonal Antibodies Primary antibodies
- Gene:
- ACVR1C NIH gene
- Name:
- activin A receptor type 1C
- Previous symbol:
- -
- Synonyms:
- ALK7, ACVRLK7
- Chromosome:
- 2q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-07-21
- Date modifiied:
- 2019-03-21
Related products to: ACVR1C antibody Polyclonal Antibodies Primary antibodies
Related articles to: ACVR1C antibody Polyclonal Antibodies Primary antibodies
- To elucidate the role and regulatory mechanisms of macrophage-derived cystatin C (CST3) in Crohn's disease (CD), focusing on colonic inflammation, macrophage-epithelial interactions, and barrier dysfunction. Colonic samples from CD patients, including inflamed and non-inflamed regions, were subjected to scRNA-seq. In vitro macrophage-epithelial co-culture models and untargeted metabolomics were employed, and the findings were validated using macrophage-specific CST3 knockout (KO) and overexpression mice under TNBS-induced and IL-10 KO colitis conditions. Mechanistic investigations included Co-IP, ChIP-qPCR, ubiquitination assays, rescue experiments, and functional analyses of efferocytosis, macrophage polarization, and barrier integrity. CST3 expression was considerably reduced in macrophages from inflamed CD tissues through suppressor of SMAD5-dependent transcriptional repression and MYCBP2-mediated K48-linked ubiquitination and degradation. Loss of CST3 impaired efferocytosis and M2 polarization by inhibiting the ACVR1C/TGF-β/SMAD pathway. CST3 deficiency also disrupted intestinal epithelial proliferation, compromised barrier function, and increased apoptosis via enhanced NAMPT-INSR signaling and accumulation of the inflammatory cytokines. In mice, macrophage-specific CST3 deletion exacerbated colitis, whereas its overexpression alleviated inflammation and restored epithelial integrity. These findings establish macrophage CST3 as a key regulator of immune-metabolic-epithelial crosstalk in CD, and indicate that restoring CST3 function or targeting its regulatory axis may represent a novel therapeutic strategy for CD. - Source: PubMed
Publication date: 2026/05/05
Wang HonggangJiao ChenyangXing HailinCheng ChaoCheng ShaoqiJiang WenliangXu ZiweiYang JianboSun JingZhao Jie - - Source: PubMed
Publication date: 2026/01/24
Zhou HuaixiangJin QunlongFu ZhangYang YanmingGao YunfeiWang NiuZhao BoGui LongLi JiangZhu ZijingZhang YingHe YulongZhang YingLuo ShouqingFu LiWu XudongWang GuihuaXu ZhimingLi HuiliangZhang JunjingShen XuetongWang TaoJiang YouhengLi Ningning - Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) is an RNA-binding protein known to play critical roles in metabolism, cell proliferation, and tumorigenesis. Although its involvement in muscle development has been documented in several species, the function of goose IGF2BP2 remains largely unexplored. In this study, we cloned and characterized the full-length cDNA and genomic DNA sequences of goose IGF2BP2. The cDNA is 2957 bp in length and contains a 1662 bp open reading frame encoding a 553-amino acid protein with five conserved RNA-binding domains. The genomic sequence spans 12,183 bp and consists of 12 exons and 11 introns. A total of 60 genetic variants were identified, including a deletion of a G base at position 2299 (g.2299delG) that results in a frameshift mutation. Expression analysis revealed high levels of IGF2BP2 mRNA in the liver, heart, and muscle tissues of female geese across embryonic (E25d), growing (A70d), and laying (L270d) stages, consistent with a potential role in muscle development ( < 0.05). Functionally, overexpression of IGF2BP2 in skeletal muscle satellite cells (SMSCs) was associated with significant changes in the expression of several genes linked to muscle development and signaling pathways, including upregulation of IGF1, EGFR, FGF19, BMP6, BMP2, ACVR1C and WNT5A and downregulation of MYBPC3, NODAL, HOXD13, TNXB, and ADD2 ( < 0.01). Furthermore, protein-protein interaction (PPI) network analysis of these genes suggests that IGF2BP2 may coordinate key genes, contributing to its potential role in skeletal muscle development in geese. - Source: PubMed
Publication date: 2025/12/24
Wang CuiLiu YiDai JiuliChen ShufangHe Daqian - Makorin ring finger protein 3 (MKRN3) acts as a "pubertal brake." MKRN3 loss-of-function mutations are the most common genetic cause of central precocious puberty, and its expression in the brain drops significantly towards puberty, yet the drivers responsible for this reduction remain unclear. We aimed here to identify factors responsible for repressing expression across the pubertal transition, initially through bioinformatic analysis of developmental RNA-seq datasets from rodent tissues. Genes whose expression correlated significantly with , and are linked to puberty and signaling, were identified. Notably, these included , whose knockout was shown previously to delay puberty in mice. Experimentally, we show that activation suppresses via Smad2/3 signaling, involving recruitment of Kap1 and repressive histone modifications. These findings provide mechanistic explanation for the reduction in Mkrn3 required for pubertal onset, while underscoring the value of integrating high-throughput gene expression analyses with experimental validation to uncover novel regulatory pathways. - Source: PubMed
Publication date: 2025/03/25
Shalev DorGolan GilPnueli LilachKahan AnatMandel-Gutfreund YaelMelamed Philippa - Delayed wound recovery is a major health issue affecting people with diabetes. Histone lactylation is involved in tissue repair. However, it is not clear whether protocatechuic aldehyde (PCA) promotes diabetic wound healing through histone lactylation. In this study, a diabetic wound mouse model was constructed to delve into the role of PCA in vivo. Chromatin immunoprecipitation sequencing (ChIP-seq) was used to determine genes affected by H3K18 lactylation (H3K18la) under PCA treatment. The effects and mechanisms of PCA on histone lactylation and angiogenesis were investigated through cellular experiments. We found that PCA accelerated wound healing and angiogenesis in diabetic mice, and significantly reduced the inflammatory response in wound tissues. Lactate and H3K18la levels were augmented in the model group in comparison with the control group, however, PCA treatment remarkably reversed their levels. ChIP-seq analysis revealed a significant enrichment of H3K18la at the Acvr1c locus, and this histone modification was downregulated by PCA treatment. PCA remarkably enhanced Acvr1c expression through H3K18la in HUVECs. Moreover, PCA treatment markedly elevated cell viability, migration and tube formation in comparison with the control group. However, this effect was counteracted by Acvr1c knockdown. In conclusion, PCA promoted HUVEC angiogenesis by increasing H3K18la-mediated Acvr1c expression, thereby promoting diabetic wound healing. This could offer a new treatment approach to enhance the effectiveness of healing diabetic wounds. - Source: PubMed
Publication date: 2025/09/30
Fan WeijingYou YangQu YinLiu Guobin