C14orf129 Antibody
- Known as:
- C14orf129 Antibody
- Catalog number:
- XW-7787
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- C14orf129 Antibody
Related genes to: C14orf129 Antibody
- Gene:
- GSKIP NIH gene
- Name:
- GSK3B interacting protein
- Previous symbol:
- C14orf129
- Synonyms:
- -
- Chromosome:
- 14q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-28
- Date modifiied:
- 2012-09-25
Related products to: C14orf129 Antibody
Related articles to: C14orf129 Antibody
- Gastric cancer (GC) is one of the most common malignant neoplasms. This study aims to explore the effects of miR-181b-5p on the proliferation and metastasis of GC and its potential molecular mechanisms. 5-Ethynyl-2'-deoxyuridine (EdU), cell counting kit-8 (CCK8), and flow cytometry assay were used to assess the proliferation. Transwell and wound-healing assay were performed to evaluate the migration ability. Dual luciferase reporter assay, quantitative real-time PCR (qRT-PCR) and western blotting were used to validate that Glycogen synthase kinase 3β interaction protein (GSKIP) was the target gene of miR-181b-5p. Tumor formation in NTG mice was applied to determine the effects of miR-181b-5p on cell proliferation in vivo. In this study, we showed that miR-181b-5p promoted the proliferation and migration in vitro and facilitated GC growth in vivo. Mechanistically, we confirmed that miR-181b-5p accelerated tumor progression by targeting GSKIP. Furthermore, we found that miR-181b-5p overexpression activated the Erk/AKT signaling pathway through downregulating GSKIP. Taken together, miR-181b-5p had a role in causing cancer, which suggested that it could be used as a target for treatment in GC. - Source: PubMed
Publication date: 2026/05/28
Tu FeiLi ZhiyuanZhang YiqiuZhou QingyuanHe FengyuanJia YiqingWang LingzhuLv ShumingZhao TiesuoGuo ShengZhong JiatengJin YanYang Zhijun - Meat quality traits, particularly WHC and tenderness, are pivotal for consumer satisfaction and economic value in the sheep industry. However, their genetic regulatory mechanisms remain unclear. We used RNA-Seq and WGCNA to identify genes regulating WHC and tenderness. Sixty longissimus thoracis samples were classified into high/low WHC (HWHC vs. LWHC) and high/low tenderness (HTN vs. LTN) groups. Comparative transcriptomics identified 270 differentially expressed genes (DEGs) linked to WHC, enriched in pathways like the regulation of the ATP metabolic process and the inhibition of canonical Wnt signaling. Key DEGs (e.g., , , , ) correlated significantly with WHC-associated traits. For tenderness, 165 DEGs were identified, including , , , and , enriched in PPAR signaling, fat cell differentiation, and cAMP signaling pathways. WGCNA revealed modules associated with WHC and tenderness, with hub genes (, , , , ) involved in ATP metabolism, lipid biosynthesis, and myofibril assembly. Tissue-specific gene integration prioritized muscle-enriched candidates ( and ) with strong trait correlations. Our findings unveil interconnected gene networks governing WHC and tenderness, highlighting some candidate genes as potential biomarkers for precision breeding. This study provides novel insights into the molecular determinants of meat quality, offering actionable targets to enhance mutton production sustainability and consumer appeal. - Source: PubMed
Publication date: 2025/05/27
Zhao LimingLi FadiZhang XiaoxueTian HuibinMa ZongwuYang XiaobinZhang QiPu MengruCao PeiliangZhang DeyinZhang YukunZhao YuanCheng JiangboXu QuanzhongXu DanLi XiaolongWang Weimin - Genome-Wide Association Studies (GWAS) have been decisive in elucidating the genetic predisposition of neuroblastoma (NB). The majority of genetic variants identified in GWAS are found in non-coding regions, suggesting that they can be causative of pathogenic dysregulations of gene expression. Nonetheless, pinpointing the potential causal genes within implicated genetic loci remains a major challenge. In this study, we integrated NB GWAS and expression Quantitative Trait Loci (eQTL) data from adrenal gland to identify candidate genes impacting NB susceptibility. We found that ZMYM1, CBL, GSKIP and WDR81 expression was dysregulated by NB predisposing variants. We further investigated the functional role of the identified genes through computational analysis of RNA sequencing (RNA-seq) data from single-cell and whole-tissue samples of NB, neural crest, and adrenal gland tissues, as well as through in vitro differentiation assays in NB cell cultures. Our results indicate that dysregulation of ZMYM1, CBL, GSKIP, WDR81 may lead to malignant transformation by affecting early and late stages of normal program of neuronal differentiation. Our findings enhance the understanding of how specific genes contribute to NB pathogenesis by highlighting their influence on neuronal differentiation and emphasizing the impact of genetic risk variants on the regulation of genes involved in critical biological processes. - Source: PubMed
Publication date: 2024/08/27
Tirelli MatildeBonfiglio FerdinandoCantalupo SuevaMontella AnnalauraAvitabile MariannaMaiorino TeresaDiskin Sharon JIolascon AchilleCapasso Mario - [This retracts the article DOI: 10.2147/OTT.S245254.]. - Source: PubMed
Publication date: 2024/08/08
- GSK3β interacting protein (GSKIP) is a small A-kinase anchor protein previously reported to mediate the N-cadherin/β-catenin pool for differentiation in SH-SY5Y cells through overexpression of GSKIP to present the neuron outgrowth phenotype. To further investigate how GSKIP functions in neurons, CRISPR/Cas9 technology was utilized to knock out GSKIP (GSKIP-KO) in SH-SY5Y. Several GSKIP-KO clones resulted in an aggregation phenotype and reduced cell growth without retinoic acid (RA) treatment. However, neuron outgrowth was still observed in GSKIP-KO clones treated with RA. The GSKIP-KO clones exhibited an aggregation phenotype through suppression of GSK3β/β-catenin pathways and cell cycle progression rather than cell differentiation. Gene set enrichment analysis indicated that GSKIP-KO was related to epithelial mesenchymal transition/mesenchymal epithelial transition (EMT/MET) and Wnt/β-catenin/cadherin signaling pathways, suppressing cell migration and tumorigenesis through the inhibition of Wnt/β-catenin mediated EMT/MET. Conversely, reintroduction of GSKIP into GSKIP-KO clones restored cell migration and tumorigenesis. Notably, phosphor-β-catenin (S675) and β-catenin (S552) but not phosphor-β-catenin (S33/S37/T41) translocated into the nucleus for further gene activation. Collectively, these results suggested that GSKIP may function as an oncogene to form an aggregation phenotype for cell survival in harsh environments through EMT/MET rather than differentiation in the GSKIP-KO of SH-SY5Y cells. GSKIP Implication in Signaling Pathways with Potential Impact on SHSY-5Y Cell Aggregation. - Source: PubMed
Publication date: 2023/05/03
Tsai Cheng-YuKo Huey-JiunChiou Shean-JawLin Xin-YiChuang Tsung-HsienCheng Jiin-TsueySu Yu-FengLoh Joon-KhimHong Yi-Ren