Ask about this productRelated genes to: SHROOM1 antibody
- Gene:
- SHROOM1 NIH gene
- Name:
- shroom family member 1
- Previous symbol:
- -
- Synonyms:
- APXL2, KIAA1960
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-07-20
- Date modifiied:
- 2014-11-18
Related products to: SHROOM1 antibody
Related articles to: SHROOM1 antibody
- Biological mechanisms underlying heterogeneous antipsychotic response in schizophrenia remain incompletely understood. In this exploratory cross-sectional study, we applied deep data-independent acquisition LC-MS/MS plasma proteomics to 56 adults initially enrolled (14 per group), including healthy controls and patients meeting TRRIP criteria for treatment-sensitive (TSS), treatment-resistant (TRS), and ultra-treatment-resistant schizophrenia (UTRS). Following proteomic quality control and exclusion of outliers, 52 individuals comprised the final analytical cohort. Proteomic data were analyzed using a layered strategy integrating covariate adjustment, variance partitioning, mediation analysis, monotonicity filtering, LASSO stability assessment, and redundancy reduction. More than 1400 plasma proteins were quantified; 450 differed across groups before adjustment, and 310 reviewed proteins remained significant after covariate modeling. A sensitivity-associated profile distinguishing TSS from controls (CRP, CCDC62, FBXW7, GULP1, CALD1, COPS6) was consistent with lower inflammatory tone and relative preservation of proteostatic and cytoskeletal regulation. In contrast, a resistance-associated profile separating TRS/UTRS from TSS (SHROOM1, MYH7, ABR, EZR, SERPINF2) converged on cytoskeletal organization, actin-membrane dynamics, and extracellular regulatory processes. Directionally concordant but quantitatively amplified changes were observed in UTRS relative to TRS, although multivariate separation between resistant subgroups was limited after full covariate adjustment. Several proteins enriched in resistant groups corresponded to intracellular or nuclear factors rarely detected in plasma and require cautious interpretation. Overall, these findings are compatible with a progression-like molecular pattern in which treatment sensitivity and resistance may reflect shifts in cellular adaptability and structural regulation. Replication in larger and longitudinal cohorts is required. - Source: PubMed
Publication date: 2026/04/27
de Oliveira Caio AndradeSoares Michelle Verde Ramode Pinho Carolina Saraiva NunesPinto Joel PorfírioFrota Annyta FernandesMoreira Ana Cristina de OliveiraSilva Maria Francilene SouzaBatista Tiago de OliveiraHallak Jaime Eduardo CecilioSheheryar SheheryarMoura Arlindo De Alencar Araripe NoronhaSanders Lia Lira OGallo Margareth Borges Coutinhode Sousa Felipe DomingosMacedo Danielle S - Lung adenocarcinoma (LUAD) is characterized by substantial genetic heterogeneity, making it challenging to identify reliable biomarkers for diagnosis and treatment. Tumor mutational burden (TMB) is widely recognized as a predictive biomarker due to its association with immune response and treatment efficacy. In this study, we take a different approach by treating TMB as a response variable to uncover its genetic drivers using multiomics data. We conducted a thorough evaluation of recent feature selection methods through extensive simulations and identified three top-performing approaches: projection correlation screening (PC-Screen), distance correlation sure independence screening (DC-SIS), and Wasserstein distance-based screening (WD-Screen). Unlike traditional approaches that rely on simple statistical tests or dataset splitting for validation, we adopt a method-based validation strategy, selecting top-ranked features from each method and identifying consistently selected genes across all three. Using The Cancer Genome Atlas (TCGA) dataset, we integrated copy number alteration (CNA), mRNA expression, and DNA methylation data as predictors and applied our selected methods. In the two-platform analysis (mRNA + CNA), we identified 13 key genes, including both previously reported LUAD-associated genes (, and ) and novel candidates (, and ). Expanding to a three-platform analysis (mRNA + CNA + methylation) further refined our findings, with and emerging as the robust candidates. These results highlight the complexity of multiomics integration and the need for advanced feature selection techniques to uncover biologically meaningful patterns. Our multiomics strategy and robust selection approach provide insights into the genetic determinants of TMB, offering potential biomarkers for targeted LUAD therapies and demonstrating the power of Wasserstein distance-based feature selection in complex genomic analysis. - Source: PubMed
Publication date: 2025/06/25
Zhao ShaofeiHuang SimingYang LingliZhou WeiyuLi KexuanWang Shige - Homologous recombination (HR) is often used to achieve targeted gene integration because of its higher precision and operability compared with microhomology-mediated end-joining (MMEJ) or non-homologous end-joining (NHEJ). It appears to be inefficient for gene integration in animal cells and embryos due to occurring only during cell division. Here we developed genome-wide high-throughput screening and a subsequently paired crRNA library screening to search for genes suppressing homology-directed repair (HDR). We found that, in the reporter system, HDR cells with knockdown of were enriched as much as 4.7-fold than those with control. Down regulating significantly promoted gene integration in human and mouse cells after cleavage by clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein-9 nuclease (Cas9), regardless of the donor types. The knock-in efficiency of mouse embryos could also be doubled by the application of siRNA during micro-injection. The increased HDR efficiency of deletion in HEK293T cells could be counteracted by YU238259, an HDR inhibitor, but not by an NHEJ inhibitor. These results indicated that was an HDR-suppressed gene and that the knockdown strategy may be useful for a variety of applications, including gene editing to generate cell lines and animal models for studying gene function and human diseases. - Source: PubMed
Publication date: 2020/08/13
Zhao ZhihuaZhang HanshuoXiong TuanlinWang JunyiYang DiZhu DanLi JuanYang YeSun ChanghongZhao YutingXi Jianzhong Jeff - Metal nanoparticles from industries contaminate the environment and affect the normal development of fish even human health. However, little is known about their biological effects on fish embryogenesis and the potential mechanisms. In this study, zebrafish embryos exposed to/injected with silver nanopaticles (AgNPs) exhibited shorter body, reduced heartbeats, and dysfunctional movements. Less, loose, and unassembled myofibrils were observed in AgNPs-treated embryos, and genes in myofibrillogenesis and sarcomere formation were found to be down-regulated in treated embryos. Down-regulated calcium (Ca) signaling and loci-specific DNA methylation in specific muscle genes, such as bves, shroom1, and arpc1a, occurred in AgNPs-treated embryos, which might result in the down-regulated expression of myofibrillogenesis genes and muscle dysfunctions in the treated embryos. Our results for the first time reveal that through down-regulating Ca signaling and myogenic loci-specific DNA methylation in zebrafish embryos, AgNPs might induce defects of myofibril assembly and sarcomere formation via their particles mostly, which may subsequently cause heartbeat reduction and behavior dysfunctions. - Source: PubMed
Publication date: 2018/04/30
Xu Qin-HanGuan PengPengZhang TingLu ChangLi GuoLiangLiu Jing-Xia - Neural tube defects (NTDs), which include spina bifida and anencephaly, are the second most common form of human structural congenital malformations. While it is well established that SHROOM3 plays a pivotal role in the complex morphogenetic processes involved in neural tube closure (NTC), the underlying genetic contributions of SHROOM gene family members in the etiology of human NTDs remain poorly understood. Herein, we systematically investigated the mutation patterns of SHROOM1-4 in a Chinese population composed of 343 NTD cases and 206 controls, using targeted next-generation sequencing. Functional variants were further confirmed by western blot and the mammalian two-hybrid assays. Loss of function (LoF) variants were identified in SHROOM3. We observed 1.56 times as many rare [minor allele frequency (MAF) < 0.01] coding variants (p = 2.9 × 10) in SHROOM genes, and 4.5 times as many rare D-Mis (deleterious missense) variants in SHROOM2 genes in the NTD cases compared with the controls. D-Mis variants of SHROOM2 (p.A1331S; p.R1557H) were confirmed by Sanger sequencing, and these variants were determined to have profound effects on gene function that disrupted their binding with ROCK1 in vitro. These findings provide genetic and molecular insights into the effects of rare damaging variants in SHROOM2, indicating that such variants of SHROOM2 might contribute to the risk of human NTDs. This research enhances our understanding of the genetic contribution of the SHROOM gene family to the etiology of human NTDs. - Source: PubMed
Publication date: 2018/02/08
Chen ZhongzhongKuang LeleFinnell Richard HWang Hongyan