Sema3C antibody Polyclonal Antibodies Primary antibodies
- Known as:
- Sema3C (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100559
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- Sema3C antibody Polyclonal Antibodies Primary antibodies
Related genes to: Sema3C antibody Polyclonal Antibodies Primary antibodies
- Gene:
- SEMA3C NIH gene
- Name:
- semaphorin 3C
- Previous symbol:
- SEMAE
- Synonyms:
- SemE
- Chromosome:
- 7q21.11
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-25
- Date modifiied:
- 2016-10-05
Related products to: Sema3C antibody Polyclonal Antibodies Primary antibodies
Related articles to: Sema3C antibody Polyclonal Antibodies Primary antibodies
- Transposable elements (TEs), which are under tight epigenetic control, have been co-opted as cis-regulatory elements to regulate gene expression during development and cancer. Among them, long interspersed element 1 (LINE-1) retrotransposons are the most abundant and exhibit high activity in embryonic stem cells. However, the precise role of LINE-1 in breast cancer stem cells (BCSCs) remains poorly understood. Here, using RNA sequencing, an enhancer dual-luciferase reporter assay, and a nuclease-dead Cas9 (dCas9)-based CRISPR activation (CRISPRa) assay, we show that the LINE-1 retrotransposon L1Md_T within Sema3c (Sema3c_L1Md_T) is derepressed and functions as a cis-regulatory enhancer that drives SEMA3C expression to sustain mouse BCSC survival. In mouse BCSCs, Sema3c_L1Md_T results in the formation of more phase-separated nuclear condensates with the transcriptional coactivator BRD4 under conditions of increased chromatin accessibility. BRD4 puncta coincide with regions marked by histone H3 lysine 27 acetylation (H3K27ac), enhancing the transcription of SEMA3C. Aberrant SEMA3C expression contributes to mouse BCSC survival and self-renewal via its receptor NRP1 and the coreceptors PlexinA2/PlexinD1. Importantly, we also demonstrate that this regulatory mechanism is conserved in human breast cancer, where SEMA3C is highly expressed in human BCSCs. A human LINE-1 element (SEMA3C_L1ME4a) exhibits enhancer activity and colocalizes with BRD4 condensates in human BCSCs. These findings confirm that the LINE1-BRD4-SEMA3C regulatory axis is present in both mouse and human BCSCs, underscoring its translational relevance. Notably, pharmacological degradation of BRD4 using the proteolysis-targeting chimaera (PROTAC) MZ1 reduces SEMA3C levels and decreases BCSC viability both in vitro and in vivo. Our study reveals an oncogenic role for a LINE-1-derived enhancer in regulating SEMA3C transcription and sustaining BCSC properties, highlighting BRD4 as a therapeutic vulnerability in BCSC-driven breast cancer progression. - Source: PubMed
Publication date: 2026/04/10
Xia QidongFeng JingweiPan JiayaoDeng WenWeng XiaoqiJiang JianhuiWang LinXie WenqianChen YiBi AiweiLi JiangLu YiwenSu Shicheng - The crucial role of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in regulating aneurysm formation, inflammation, and neural dysfunction has gradually been recognized. This study aimed to evaluate the effects of MALAT1 modification on pathological changes, inflammation, vascular smooth muscle cell (VSMC) phenotype switching, and the underlying mechanism in intracranial aneurysms (IAs). - Source: PubMed
Publication date: 2026/03/11
Kang JunlongLi WeiGao XinjieTian XinhuaFeng WeiYao XiangWei FengChen LuyueChen HongjinTong JunjiangChen EGu Yuxiang - This study aimed to identify novel signaling axes governing keloid pathogenesis by investigating the role of the semaphorin 3C (SEMA3C)/plexin D1 (PLXND1) pathway in fibrotic processes via transforming growth factor (TGF)-β1 signaling, using single-cell RNA sequencing (scRNA-seq) and experimental validation. scRNA-seq analysis was performed on eight keloid and eight normal skin samples from four public data sets, using Seurat and CellChat to map intercellular communication networks. Primary keloid fibroblasts were treated with recombinant SEMA3C, PLXND1-specific siRNA, or the TGF-β1 inhibitor SB431542. Transcriptome sequencing, real-time quantitative PCR, Western blot analysis, and immunofluorescence were used to assess changes in collagen I/III, fibronectin, and TGF-β1 expression. scRNA-seq revealed significantly enhanced intercellular communication in keloids, particularly among fibroblasts, with a 1.65-fold increase in interaction numbers and 17.79-fold stronger communication strength compared with normal skin. A critical ligand-receptor pair, SEMA3C (predominantly secreted by Schwann cells) and its receptor PLXND1 (overexpressed in keloid fibroblasts), was identified as the most prevalent in keloid samples. Experimental assays demonstrated that SEMA3C dose dependently up-regulated collagen I/III, fibronectin, and TGF-β1 expression, whereas PLXND1 knockdown or TGF-β1 inhibition (via SB431542) attenuated these effects, confirming that SEMA3C/PLXND1 drives fibrosis through TGF-β1 signaling. This study is the first to demonstrate that the SEMA3C/PLXND1 axis drives keloid fibrosis by activating TGF-β1, promoting collagen and extracellular matrix deposition. Targeting this axis holds promise for keloid therapy. - Source: PubMed
Publication date: 2026/03/13
Tang YanqiuWang SihuiXu YangYang YinCui XiaomeiHua HuiBu WenboZhou Bingrong - Pancreatic ductal adenocarcinoma (PDAC) remains a highly aggressive malignancy with a complex tumor microenvironment. Although the class-3 semaphorin (SEMA3) gene family has been implicated in tumor progression and immune regulation, its specific role and clinical relevance in PDAC are not yet fully understood. - Source: PubMed
Publication date: 2026/03/06
Jin XinGuan XiaoMu YongrunWang MinWang Chengfeng - Down syndrome (DS; trisomy 21) confers a ~100-fold increased risk of Hirschsprung disease (HSCR), yet the causal contributions of specific chromosome 21 genes remain unresolved. Here we show that increased dosage of SOD1 alone is sufficient to perturb enteric nervous system (ENS) development. We engineered a humanized trisomic mouse line by inserting a 28 kb human locus into ROSA26 and genetically profiled the distal colon at postnatal day 0 using single-cell RNA-seq and immunofluorescence. was elevated ~1.5X in the ENS but varied by cell type, with transcriptionally active progenitors showing the greatest increase. Cell composition shifted toward transcriptionally active cells and glia, with concomitant loss of excitatory and inhibitory motor neurons and interneurons. Genetically, trisomy downregulated synaptic and neuronal communication programs but upregulated DNA replication/cell-cycle and genome maintenance pathways, especially within glia. Consequently, key HSCR genes were dysregulated: , , and were decreased, while ,a negative guidance cue, was increased. was selectively reduced in inhibitory and excitatory motor neurons and progenitors, unchanged in glia, and reduced at the protein level . Within glia, Sod1/SOD1 was particularly elevated in proliferating/active glia with a glia-specific bias toward endogenous mouse expression. Taken together, these data support a dual mechanism whereby increased dosage suppresses -dependent neurogenesis while independently promoting reactive/proliferative glial states. Thus, is sufficient to alter ENS development significantly and provide the susceptibility substrate for HSCR with further reductions in gene expression leading to aganglionosis. - Source: PubMed
Publication date: 2026/01/28
Grullon GabrielRollins JarodWilkes LaurenZuberi AamirChakravarti AravindaChatterjee Sumantra