Ask about this productRelated genes to: SNX7 antibody
- Gene:
- SNX7 NIH gene
- Name:
- sorting nexin 7
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-10
- Date modifiied:
- 2016-10-05
Related products to: SNX7 antibody
Related articles to: SNX7 antibody
- Glaucoma trabecular meshwork (GTM) cells cultured in vitro retain many characteristics of their in situ phenotype. Here, we used isobaric tandem mass tags (TMTpro) to label peptides from glaucomatous and non-glaucomatous TM (NTM) cells to identify differentially regulated proteins. Confluent NTM ( = 5) and GTM ( = 5) cells were lysed, proteins were trypsin digested, and peptides were labeled with 18-plex TMTpro. TMT-labeled peptides were fractionated on an Orbitrap Fusion mass spectrometer and data were processed using the PAW/Comet pipeline and EdgeR with Benjami–Hochberg multiple correction testing. Isobaric multiplexed quantitative proteomics identified 206 proteins that were significantly (FDR < 0.1) upregulated in GTM cells, 42 proteins that were downregulated, with 5270 non-candidates. Significant regulated pathways included extracellular matrix (DCN, COL4A1, CHI3L1), Wnt signaling (FZD1, FZD7, GSK3B), cytoskeletal regulation (ROCK2, MSN, TPM2, VIM, NF2), protein degradation (USP9X, LAMP1, SYNV1, UBE2L3), and nuclear proteins (LMNA, DFFA, CHMP3, RAD21). Western immunoblotting studies confirmed the TMTpro data. Immunofluorescence showed that the SNX7-stained nucleoli of GTM cells were significantly ( < 0.05) larger, and the DIAPH2 immunostaining was more distended into the cytosol than in NTM cells. This study identified many significantly regulated proteins in cultured GTM cells, and the results revealed several new avenues for developing clinical therapies for glaucoma patients. - Source: PubMed
Publication date: 2026/03/18
Holden PaulSun Ying YingZientek KeithWilmarth Phillip AReddy Ashok PKeller Kate E - Radiotherapy is a primary treatment for intermediate and advanced cervical cancer (CC). Resistance to radiotherapy is a principal reason for treatment failure in synchronous applications, yet the molecular mechanisms remain poorly understood. Identifying reliable prognostic markers to predict and evaluate patient outcomes is essential for advancing therapeutic strategies. This study aims to address this need by developing a prognostic prediction model for concurrent radiotherapy in CC, utilizing both single-cell RNA sequencing (scRNA-seq) and bulk RNA sequencing data. - Source: PubMed
Publication date: 2025/10/31
Yang SiqiLiu LitingSu QiuyueWang JiananXia JingqiZhao XinyaoSun YajuanYang Shanshan - Prostate cancer (PC) is a major health concern among men worldwide, yet its underlying molecular mechanisms remain incompletely understood. Identifying key regulatory genes and signaling pathways involved in PC progression is essential for improving diagnosis and developing targeted therapies. - Source: PubMed
Publication date: 2025/08/29
Qin LiangYang FanGuo ZhuifengLu XuweiWu JiawenJiang DongzhenYang Ning - Glioblastoma is a highly aggressive and invasive brain tumor with an extremely poor prognosis. The aims of the present study are to investigate the pathogenesis of glioblastoma and identify potential therapeutic targets. - Source: PubMed
Publication date: 2024/12/28
Zhang YuanlongChen BinghongLiu RenfuMei WenzhongLin Yuanxiang - Poor intrauterine environments increase the prevalence of chronic metabolic diseases in offspring, whereas maternal exercise is an effective measure to break this vicious intergenerational cycle. Placenta is increasingly being studied to explore its role in maternal-fetal metabolic cross-talk. The association between placental miRNA and offspring development trajectories has been established, yet the specific role and mechanism thereof in maternal exercise-induced metabolic protection remain elusive. Here, C57BL/6 female mice were subjected to either a normal control or a high-fat diet (HFD), half of the HFD-fed dams were housed with voluntary wheel running for 3 weeks before and during gestation. At embryonic day 18.5, we sacrificed parturient mice and then conducted miRNA-seq, transcriptomic, and metabolomic profiling of the placenta. Our data revealed that maternal HFD resulted in significant alterations in both miRNA and gene expressions, as well as metabolic pathways of the placenta, whereas prenatal exercise negated these perturbations. The common differentially expressed transcripts among three groups were enriched in multiple critical pathways involving energy expenditure, signal transduction, and fetal development. Through integrated analysis of multiomics data, we speculated that maternal exercise reversed the suppression of miR-495-5p induced by HFD, thereby inhibiting miR-495-5p-targeted Snx7 and modulating kynurenic acid production. These datasets provided novel mechanistic insight into how maternal exercise positively affects the metabolic homeostasis of offspring. The discovered important miRNAs, mRNAs, and metabolites could be promising predictive and therapeutic targets for protecting offspring metabolic health. - Source: PubMed
Publication date: 2024/12/06
Li ShunhuaZhou LiyuanRen JingZhang QianXiao Xinhua