更新于：2024-11-01

SEMA4C

更新于：2024-11-01

基本信息

别名

KIAA1739、SEMA4C、Semacl1

+ [4]

简介

Cell surface receptor for PLXNB2 that plays an important role in cell-cell signaling. PLXNB2 binding promotes downstream activation of RHOA and phosphorylation of ERBB2 at 'Tyr-1248'. Required for normal brain development, axon guidance and cell migration (By similarity). Probable signaling receptor which may play a role in myogenic differentiation through activation of the stress-activated MAPK cascade.

关联

项与 SEMA4C 相关的药物

CN117343180

专利挖掘

靶点

SEMA4C

作用机制-

在研机构

北京志道生物科技有限公司初创企业

原研机构

北京志道生物科技有限公司初创企业

在研适应症

实体瘤

非在研适应症-

最高研发阶段药物发现

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 SEMA4C 相关的临床结果

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100 项与 SEMA4C 相关的转化医学

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0 项与 SEMA4C 相关的专利（医药）

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项与 SEMA4C 相关的文献（医药）

2024-09-01·Histology and histopathology

Altered expression of the Plexin-B2 system in tuberous sclerosis complex and focal cortical dysplasia IIb lesions.

Article

作者: Shen, Kai-Feng ; Wang, Zhong-Ke ; Zhang, Chun-Qing ; Zhang, Li ; Xu, Sen-Lin ; Liu, Shi-Yong ; Yang, Xiao-Lin ; Yang, Hui ; Zhu, Gang ; Dai, Lu ; Huang, Jun ; Liao, Xiang ; Li, Xing-Yi

Tuberous sclerosis complex (TSC) and focal cortical dysplasia (FCD) type IIb are the predominant causes of drug-refractory epilepsy in children. Dysmorphic neurons (DNs), giant cells (GCs), and balloon cells (BCs) are the most typical pathogenic profiles in cortical lesions of TSC and FCD IIb patients. However, mechanisms underlying the pathological processes of TSC and FCD IIb remain obscure. The Plexin-B2-Sema4C signalling pathway plays critical roles in neuronal morphogenesis and corticogenesis during the development of the central nervous system. However, the role of the Plexin-B2 system in the pathogenic process of TSC and FCD IIb has not been identified. In the present study, we investigated the expression and cell distribution characteristics of Plexin-B2 and Sema4C in TSC and FCD IIb lesions with molecular technologies. Our results showed that the mRNA and protein levels of Plexin-B2 expression were significantly increased both in TSC and FCD IIb lesions versus that in the control cortex. Notably, Plexin-B2 was also predominantly observed in GCs in TSC epileptic lesions and BCs in FCD IIb lesions. In contrast, the expression of Sema4C, the ligand of Plexin-B2, was significantly decreased in DNs, GCs, and BCs in TSC and FCD IIb epileptic lesions. Additionally, Plexin-B2 and Sema4C were expressed in astrocytes and microglia cells in TSC and FCD IIb lesions. Furthermore, the expression of Plexin-B2 was positively correlated with seizure frequency in TSC and FCD IIb patients. In conclusion, our results showed the Plexin-B2-Sema4C system was abnormally expressed in cortical lesions of TSC and FCD IIb patients, signifying that the Plexin-B2-Sema4C system may play a role in the pathogenic development of TSC and FCD IIb.

2024-07-01·Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis

miR-129–2-3p binds SEMA4C to regulate HCC development and inhibit the EMT

Article

作者: Pu, Chun ; Ma, Siyuan

BACKGROUNDAmong primary liver cancers, HCC is the most prevalent. Small noncoding RNAs called miRNAs control the expression of downstream target genes to take part in a variety of physiological and pathological processes, including those related to cancer.METHODSmiR-129-2-3p and SEMA4C expression levels were assessed using RT-qPCR. The CCK-8, invasion, and wound healing assays were used to confirm the capacity of HCC cells for proliferation, invasion and migration respectively. Serum SEMA4C levels were detected via ELISA. The RIP and dual-luciferase reporter assays were used to confirm the existence of intergenic binding sites. Cell apoptosis assay and cell cycle assay were performed to detect the apoptosis rate and cycle distribution of cells, and WB was performed to detect the protein expression of SEMA4C, RhoA, ROCK1, E-cadherin, N-cadherin, and vimentin. Furthermore, cancer-inhibiting role of miR-129-2-3p were further confirmed by animal tests.RESULTSmiR-129-2-3p expression was reduced in HCC tissues and cells. Overexpression of miR-129-2-3p decreased the proliferation, invasion, migration, and EMT in HCC cells, whereas inhibition of miR-129-2-3p had the opposite effects. Our research also showed that SEMA4C was increased in HCC tissues, serum and cells, and that SEMA4C knockdown prevented HCC cell invasion, migration, proliferation, and EMT. Overexpression of SEMA4C reversed the inhibitory effect of miR-129-2-3p on HCC.CONCLUSIONSOverall, we discovered that through binding to SEMA4C, miR-129-2-3p regulates HCC cell proliferation, invasion, migration, and EMT.

2024-01-01·Heliyon

Comparison of the efficacy of combined budesonide and fexofenadine versus combined fluticasone propionate and fexofenadine on the expression of class-4 semaphorins and their receptors in the peripheral blood cells of patients with allergic rhinitis

Article

作者: Gorgin Karaji, Ali ; Asadi, Gelayol ; Faryadi, Elham ; Rezaei Varmaziar, Fatemeh ; Feizollahi, Parisa ; Salari, Farhad ; Rajabinejad, Misagh ; Rezaiemanesh, Alireza ; Falahi, Sara

BackgroundAllergic rhinitis (AR) is a common immunoglobulin (Ig) E-mediated disease. This study aimed to evaluate the gene expression levels of class 4 semaphorins and their receptors in AR patients before and after treatment with budesonide and fexofenadine (B/F) compared to fluticasone propionate and fexofenadine (FP/F).MethodsIn this study, 29 AR patients (age 34.4 ± 1.2 years, 18 men and 11 women) were treated with B/F, and 24 AR patients (age 32.8 ± 1.9 years, 15 men and 9 women) were treated with FP/F for one month. Before and after treatment, peripheral blood samples were taken from patients. The expression levels of SEMA4A, SEMA4C, SEMA4D, Plexin-B2, and Plexin-D1 genes were measured using the qPCR method. In addition, the serum levels of IgE were measured using an enzyme-linked immunosorbent assay (ELISA).ResultsThe expression levels of SEMA4A (P = 0.011), 4C (P = 0.017), Plexin-B2 (P = 0.0005), and Plexin-D1 (P = 0.008) remarkably increased in AR patients treated with B/F. Our results show a significant reduction in the gene expression levels of SEMA4A (P = 0.002), 4C (P = 0.014), 4D (P = 0.003), Plexin-B2 (P = 0.033), and Plexin-D1 (P = 0.035) after treatment with FP/F. The serum levels of IgE increased in FP/F treated group (P = 0.017) and conversely decreased in the treated group with B/F (P = 0.019). Moreover, the percentages of eosinophils were reduced in both FP/F and B/F groups (P = 0.015 and P = 0.0001, respectively).ConclusionIn conclusion, concomitant use of fexofenadine and fluticasone propionate reduced SEMA4A, 4C, 4D, Plexin-B2, and Plexin-D1, while the SEMA4A, 4C, Plexin-B2, and Plexin-D1 gene expression levels were increased in the patient group treated with B/F.

项与 SEMA4C 相关的新闻（医药）

2022-05-30

·生物谷

Molecular Therapy Nucleic Acids: Nlgn环状RNA介导阿霉素诱导的心脏重构和纤维化

尽管阿霉素作为一种化疗药物被广泛用于治疗各种类型的癌症，但由于其心脏毒性，它会产生严重的副作用。阿霉素的心脏毒性可能导致反应性氧化应激，改变DNA功能和基因表达，阻止DNA复制，诱导细胞凋亡。尽管阿霉素作为一种化疗药物被广泛用于治疗各种类型的癌症，但由于其心脏毒性，它会产生严重的副作用。阿霉素的心脏毒性可能导致反应性氧化应激，改变DNA功能和基因表达，阻止DNA复制，诱导细胞凋亡。广泛的细胞功能障碍和死亡导致心脏重构，伴随着I型和III型胶原的异常堆积，以及转化生长因子β(TGF-β)信号的失调。随着时间的推移，心脏重构会导致心肌纤维化、肥大、扩张、心肌病，以及无法满足心脏容量和压力需求的收缩强度下降。这种重构是不可逆转的，会导致心肌功能障碍和心力衰竭。其机制还不是很清楚。研究者最近发现，当表达CircNlgn的转基因小鼠表现出心脏重构、心脏纤维化和心力衰竭时，似乎与介导阿霉素的作用有关。图片来源: https://doi.org/10.1016/j.omtn.2022.03.007 近日，来自加拿大桑尼布鲁克健康科学中心的研究者们在Molecular Therapy: Nucleic Acids杂志上发表了题为“The circular RNA circNlgn mediates doxorubicin-induced cardiac remodeling and fibrosis”的文章，该研究对减轻癌症患者阿霉素治疗的副作用具有治疗意义。阿霉素是一种化疗药物，通常用于治疗许多类型的癌症，但它有副作用，包括呕吐、皮疹、脱发和骨髓抑制。最危险的副作用是心肌病、心肌纤维化和心力衰竭，因为阿霉素会产生细胞毒性并阻止DNA复制。目前还没有治疗方法来阻止这些副作用。研究者已经建立了一个高表达CircNlgn环状RNA的转基因小鼠系，并表明CircNlgn是阿霉素诱导的心肌纤维化的介质。CircNlgn基因的高表达通过上调Gadd45b、Sema4C和Rad50，激活p38和pJNK，从而降低心功能，诱导心肌纤维化。沉默Nlgn可减少阿霉素对心肌细胞活动的影响，并阻止阿霉素诱导的纤维化相关分子的表达。由CircNlgn翻译的蛋白(Nlgn173)能结合并激活H_2AX，产生gH_2AX，导致IL-1b、IL-2Rb、IL-6、EGR1和EGR3表达上调。研究者发现，沉默信号通路中的这些分子可以阻止阿霉素诱导的心肌细胞凋亡，提高心肌细胞活力，减少心脏成纤维细胞的增殖，并抑制胶原的产生。 CircNlgn表达加重阿霉素诱导的心脏纤维化和心功能损害图片来源: https://doi.org/10.1016/j.omtn.2022.03.007 该研究表明，EGR1和EGR3被阿霉素诱导，并被CircNlgn表达上调。由于EGR是组织重塑和纤维化的主要调节者，并且它们是介导CircNlgn效应的下游信号分子，这些分子可能成为减少癌症患者阿霉素副作用的潜在靶点。（生物谷 Bioon.com）参考文献 Jindong Xu et al. The circular RNA circNlgn mediates doxorubicin-induced cardiac remodeling and fibrosis. Mol Ther Nucleic Acids. 2022 Mar 9;28: 175-189. doi: 10.1016/j.omtn.2022.03.007.