SMPDL3B Antibody (monoclonal) (M01)
- Known as:
- SMPDL3B Antibody (mab) (M01)
- Catalog number:
- AT3963a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- SMPDL3B Antibody (monoclonal) (M01)
Related genes to: SMPDL3B Antibody (monoclonal) (M01)
- Gene:
- GTF2H2B NIH gene
- Name:
- general transcription factor IIH subunit 2B (pseudogene)
- Previous symbol:
- -
- Synonyms:
- DKFZP686M0199
- Chromosome:
- 5q13.2
- Locus Type:
- pseudogene
- Date approved:
- 2008-07-04
- Date modifiied:
- 2015-11-09
- Gene:
- POLR1A NIH gene
- Name:
- RNA polymerase I subunit A
- Previous symbol:
- -
- Synonyms:
- DKFZP586M0122, FLJ21915, RPO1-4, RPA1
- Chromosome:
- 2p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-01
- Date modifiied:
- 2017-06-28
- Gene:
- SMPDL3B NIH gene
- Name:
- sphingomyelin phosphodiesterase acid like 3B
- Previous symbol:
- -
- Synonyms:
- ASML3B
- Chromosome:
- 1p35.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-20
- Date modifiied:
- 2016-01-25
- Gene:
- TDRP NIH gene
- Name:
- testis development related protein
- Previous symbol:
- C8orf42
- Synonyms:
- INM01, TDRP1, TDRP2
- Chromosome:
- 8p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-28
- Date modifiied:
- 2015-08-26
Related products to: SMPDL3B Antibody (monoclonal) (M01)
Related articles to: SMPDL3B Antibody (monoclonal) (M01)
- It remains unclear whether the observed heterogeneity in the burden of inflammatory bowel disease (IBD) across countries is associated with differences in population genetic structure. To address this problem, we performed a burden quantitative trait locus (bQTL) analysis, integrating epidemiological data (1990-2021) from the Global Burden of Disease (GBD) study with genotypes of 2 621 978 SNPs from 2414 unrelated individuals in the 1000 Genomes Project across 20 matched countries. We identified 1074 bQTLs of IBD, of which 384 were significantly associated with both the age-standardized prevalence rate and age-standardized incidence rate. rs7633471 (chr3:30698616:C>A) showed the strongest effect: each increase in centi-allele frequency (CAF) of the allele C was associated with a 10.00 decrease in age-standardized prevalence rate and a 1.02 decrease in age-standardized incidence rate. Pathway analysis revealed that bQTLs were primarily enriched in synaptic membrane, voltage-gated potassium channel complex, and potassium channel complex. Through fine-mapping, we further identified 800 putative causal variants for IBD, with significant findings located within genes related to the immune system (IGSF21 and CSMD2), inflammatory response (SMPDL3B and AOAH), and intestinal cancers (FHIT and CSMD2). Our study provides the first comprehensive characterization of the genetic architecture underlying the global burden of IBD. - Source: PubMed
Publication date: 2026/09/27
Sun ChenWei SiyuTao JunxianChen HaiyanYan ChiWang JiachengXu JingDuan LianZhan YuanboZou YupingLi RuilinYuan LinnaShe WeiLu SonglinWang NingRen QinduoGuo YanXu YuanWang ChangTian HongshengZhang ChenDong YuTang GuopingShang ZhenweiJiang YongshuaiLv WenhuaZhang MingmingLyu Hongchao - Ceramide-1-phosphate (C1P), once considered a minor metabolic intermediate, is now recognized as a relevant regulator of cell survival, inflammation, migration, oxidative stress, glucose uptake, and adipogenesis. These diverse functions are mediated by direct interactions between C1P and specific protein targets, including enzymes, lipid transfer proteins, and signaling effectors (typically proteins). While C1P was demonstrated to regulate a variety of signaling pathways, including phosphatidylinositol 3-kinase (PI3K)/Akt, mitogen-activated protein kinase kinase (MEK)/extracellularly regulated kinases (ERK) 1-2, or sphingomyelin synthase (SMS)/protein kinase-C-alpha (PKCα), this review namely focuses on the eight major proteins that directly interact with C1P: acidic sphingomyelinase (ASMase), serine palmitoyl transferase (SPT), Ca-dependent cytosolic phospholipase A-alpha (cPLAα), Gi protein-coupled receptors, C1P transfer protein (CPTP), sphingomyelinase phosphodiesterase like 3b (SMPDL3b), annexin A2-p11 (S100A10), and Kelch-like ECH-associated protein 1 (KEAP1). Understanding C1P-protein interactions provides a conceptual framework for targeting sphingolipid signaling in inflammation, cancer and metabolic diseases. Here, we summarize current evidence for C1P binding or functional modulation of these proteins, and highlight the implications of these interactions in inflammation, oxidative stress control, and disease pathogenesis. - Source: PubMed
Gomez-Muñoz AntonioBenito-Vicente AsierUribe Kepa BLarrea-Sebal AsierGomez-Larrauri AnaMartín César - Tumor-associated macrophages (TAMs) are implicated in the enhanced chemoresistance of ovarian cancer (OC), with extracellular vesicles (EVs) serving as important mechanism mediating intercellular communication. This study aimed to investigate the role of TAMs-derived EVs in OC chemoresistance. Chemoresistance of OC cell lines were evaluated after treated with cisplatin. EVs were isolated from TAMs, and OC cells were then co-cultured with TAMs or treated with TAMs-derived EVs. Cell viability was measured by CCK-8 and colony formation assays, while cell apoptosis was evaluated by TUNEL and flow cytometry. A xenograft model was employed to examine the interaction between OC cells and TAMs in vivo. Our results showed that co-culture with TAMs or incubation with TAMs-derived EVs increased chemoresistance in OC cells, as evidenced by increased IC values and colony formation numbers, as well as decreased apoptosis. Additionally, SMPDL3B protein levels were upregulated by TAMs co-culture or EVs treatment. However, pretreatment with the EVs secretion inhibitor GW4869 reversed the effect of TAMs co-culture on OC cell chemoresistance. Mechanistically, SMPDL3B upregulation in OC cells increased chemoresistance by inhibiting the cGAS/STING pathway, and the pathway activator ADU-S100 reversed its effect. Notably, TAMs co-cultured with OC cells overexpressing SMPDL3B were induced toward an M2-associated macrophage phenotype, which was reversed by ADU-S100 pretreatment. Finally, the xenograft model showed that TAMs co-injection promoted tumor progression, whereas SMPDL3B knockdown in TAMs abolished this effect. Collectively, this study demonstrates that TAMs-derived EVs transfer SMPDL3B to OC cells, where it inhibits the cGAS/STING pathway and thereby enhances chemoresistance. - Source: PubMed
Publication date: 2026/09/07
Liang XinYang HanluHong Lan - BACKGROUNDS: Neoadjuvant chemoradiation (nCRT) is a standard treatment for rectal carcinoma that reduces tumor size and local recurrence while improving the rate of sphincter preservation. However, many patients remain insensitive to nCRT, with some exhibiting tumor progression. To date, there is still a lack of clinically available prognostic models to differentiate the sensitivity of patients with rectal carcinoma to nCRT. This study aimed to develop a genetic predictive model that predicts the effectiveness of nCRT in patients with rectal carcinoma, offering guidance for future treatments and studies on the underlying mechanisms. METHODS: Based on the NCBI GEO database datasets, key hub genes affecting the efficacy of neoadjuvant chemoradiotherapy in rectal carcinoma were identified using WCGNA. Subsequently, a consistency analysis of 101 model combinations constructed using ten different machine learning algorithms was performed in two independent cohorts, and a prognostic model (chemoradiation resistance score, CRTR score) was developed and validated. Moreover, the clinical applicability of CRTR in immunotherapy and drug selection was investigated using multi-omics analysis and public databases. Finally, the effect of KIF14 on the radiosensitivity of rectal carcinoma cells was studied using in vitro experiments. RESULTS: The CRTR model was composed of 13 genes impacting nCRT sensitivity, whereas six genes (KIF4, DBF4, UBL4A, SLC10A3, PRRG4, and PAPSS2) acted as protective factors and seven (BMS1, DSC2, PROM2, MNAT1, PPID, SMPDL3B, and TNFRSF14) served as risk factors. The CRTR model showed a significant negative correlation with the prognosis of patients with rectal carcinoma undergoing nCRT. Furthermore, patients with higher CRTR values displayed an increased potential to benefit from immunotherapy. Drug sensitivity analysis indicated that aurora kinase inhibitors, telomerase inhibitors, JAK1 inhibitors, and others may enhance the efficacy of nCRT. Finally, we identified KIF14 as the gene that contributed the most to the model and performed preliminary validation. Radiation significantly upregulated the expression of KIF14, and overexpression of KIF14 increased the radiosensitivity of rectal carcinoma cells. CONCLUSION: The CRTR score, based on 13 genes, was able to predict the prognosis of patients with rectal carcinoma undergoing neoadjuvant chemoradiotherapy and demonstrated immense potential in providing personalized risk assessments and recommendations for targeted immunotherapy. The core gene, KIF14, in the CRTR model may serve as a potential predictive biomarker of radiosensitivity in rectal carcinioma. - Source: PubMed
Publication date: 2026/03/21
Gao ZhanhuaQiu MinghanYang ZhenFang XinyueYin GuoxingZhang QiaonanLiu JinpuLiu RuxueWang YayunLiu YuyaZhang MengZhang HaiyangZheng XiangqianWang HuiHao JieGao Ming - Sirtuin 1 (Sirt1), a member of the sirtuin family, is integral to the regulation of energy homeostasis, cellular metabolism, and stress responses. While Sirt1 has been intensively studied in mammals, studies on this gene in aquatic animals, especially turbot, is relatively limited. In this study, the sirt1 gene was cloned. The open reading frame (ORF) of the Sirt1 consists of 2187 base pairs, encoding a 728-amino-acid protein that contains a SIR2 domain. Compared with the siRNA-NC group, Sirt1 knockdown resulted in a significant downregulation of mRNA expression levels of the tight junction proteins occludin, tricellulin, claudin3, and zo1, as well as protein levels of Occludin and ZO1, within the intestinal tissue of turbot. Concurrently, it markedly inhibited the expression of genes associated with ceramide synthesis (sptlc2, kdsr, cers1, cers2, cers3, smpdl3a, smpdl3b, neu1, glb1, gba1, and sgpp2) and ceramide catabolism (sgms1a, ugcg, b4galt, and sphk1) in the same tissue. Conversely, compared to the pcDNA3.1 group, Sirt1 overexpression significantly enhanced the mRNA expression levels of occludin, tricellulin, claudin3, claudin7, and zo1, along with the protein level of Occludin. Furthermore, Sirt1 overexpression significantly elevated the expression of genes involved in ceramide synthesis (cers2, cers3, smpd3, smpdl3b, neu1, glb1, gba1, sgpp2) and ceramide catabolism (sgms1a, galt, b4galt, and sphk1). These results suggest that Sirt1 may influence the intestinal mechanical barrier by acting on the metabolic balance of ceramide and altering the expression of intestinal tight junction proteins, thus playing a crucial role in maintaining the intestinal health of turbot. - Source: PubMed
Publication date: 2026/03/18
Ma XiuhuaLiu QianhuiMai KangsenZhang Yanjiao