Ask about this productRelated genes to: EMID2 antibody
- Gene:
- COL26A1 NIH gene
- Name:
- collagen type XXVI alpha 1 chain
- Previous symbol:
- EMID2
- Synonyms:
- Emu2, EMI6
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-10
- Date modifiied:
- 2016-07-20
Related products to: EMID2 antibody
Related articles to: EMID2 antibody
- Junctophilin 3 (JPH3) acts as a tumor suppressor in several cancers; however, the role of JPH3 in anaplastic thyroid cancer (ATC) is still unknown. - Source: PubMed
Wang XiuyanLuan ShaSun LeiLian LixinQi Ming - Asymptomatic Alzheimer's Disease (AsymAD) is a preclinical stage of Alzheimer's Disease (AD) identified by amyloid plaques and neurofibrillary tangles in cognitively normal individuals and offers essential understanding for early diagnosis and treatment of AD. To uncover molecular insights into AsymAD, RNA sequencing (RNA-seq) datasets from two different consortia, ROSMAP (Religious Orders Study and Memory and Aging Project) and MSBB (Mount Sinai Brain Bank), were investigated. The individuals in the datasets were grouped into AD and AsymAD based on clinical and neuropathological criteria. Differentially expressed genes (DEGs), differentially expressed transcripts (DETs), and differentially used transcripts (DUTs) were identified between AD and AsymAD samples. The results were interpreted through functional enrichment analysis and compared with the predefined lists of AD-related and learning-memory-cognition-related genes, and genes from an independent mouse dataset. The genes from the list of DEGs, DETs and DUTs were mapped onto a human protein-protein interaction network, revealing subnetworks associated with AsymAD. This led to the discovery of biomarker candidate genes: NRXN3, DGKB, ADAMTS2, GNG4, ENPP5, PCOLCE, COL25A1, COL26A1, MRPL1, and MRPL30. This study introduces an innovative approach by including DETs and DUTs in the analyses, beyond the standard focus on DEGs, pointing out comprehensive insights into the molecular mechanisms of AsymAD. In addition, combining the results of the subnetwork analysis from DEGs, DETs, and DUTs provided a new perspective to AsymAD and resulted in the discovery of further important genes, which can pave the way for early detection and intervention of AD. - Source: PubMed
Publication date: 2026/02/22
Aksu RümeysaLüleci Hatice BüşraÇakır Tunahan - This study examined how insoluble corn-based fibrous coproducts (ICBF) affect gastrointestinal (GI) mucosal microbiota, gene expression, and intestinal morphology in growing pigs compared to fiber deprivation. Fifty-six gilts (26.7 ± 2.5 kg BW) were randomly assigned to one of seven semi-synthetic diets. Treatments included a fiber-deprived control (CTL;<1% insoluble dietary fiber [IDF]), and six diets where an ICBF replaced 30% of corn starch: dehulled degermed corn (DHDG; IDF = 1.7%), ground corn (COR; IDF = 4.7%), corn gluten meal (CGM; IDF = 5.2%), dried distillers grains (DDGS; IDF = 8.6%), high protein dried distillers grains (HP; IDF = 13.5%), and corn bran (BRN; IDF = 17.5%). Pigs were individually housed and limit-fed 2.4 times maintenance. On day 31, duodenum, jejunum, ileum, and colon tissues were collected. Microbial 16S rRNA sequencing of mucosal material, tissue transcriptomics, and histological analyses were conducted in various intestinal regions. Data were analyzed using mixed models with diet as a fixed effect and linear and quadratic contrasts to assess response IDF. A negative binomial model with FDR correction were used for operational taxonomic unit (OTU) analysis, and transcriptomics were evaluated with DESeq2 comparing ICBF sources to CTL (Q ≤ 0.05, |log2FC| ≥ 2). In the ileal mucosa, Shannon and Simpson diversity indices linearly increased with IDF%, while in the colon mucosa Chao1 and Shannon diversity responded quadratically (P < 0.05). Among the top 100 most abundant OTUs, 60 and 86 differed in ileal and colonic mucosa, respectively (Q < 0.05). In the ileum and colon, pigs fed low-ICBF diets (CTL, DHDG) had increased abundance of OTUs containing opportunistic or potentially pathogenic species (e.g., Enterobacteriaceae, Campylobacter, and Streptococcus). However, moderate-to-high ICBF diets, CGM, DDGS, and BRN, enriched mucosal-associated Lactobacillus, Bifidobacterium, and Akkermansia. In the duodenum and ileum, villous height had a positive quadratic relationship to increasing IDF, while the jejunum villous height linearly decreased (P < 0.05). Gene expression profiles revealed that moderate-to-high ICBF (DDGS, HP, and BRN) upregulated genes associated with cell structure and extracellular matrix (ECM) remodeling (TPPP3, MUC5AC, SERPINA1). Fiber-deprivation upregulated genes associated with ECM degradation (MMP9, MMP12) and collagen formation (COL26A1). Thus, both fiber deprivation and excessive ICBF can disrupt mucosal microbial and host homeostasis. - Source: PubMed
Miller Hannah ESasser Cassidy NHernandez M SebastianLegako Jerrad FAnderson Chiron JSchmitz-Esser StephanEricsson Aaron CBroadway Paul RBurdick Sanchez Nicole CCarroll Jeffery ACruz Penn Michael JPetry Amy L - Small cell lung cancer (SCLC) is a type of high-grade neuroendocrine malignancy with low gene mutation. Chemotherapy is the major treatment strategy, but long-term clinical application often leads to drug resistance. Etoposide is a first-line drug approved by the US Food and Drug Administration for SCLC treatment, but etoposide-resistance is a problem. In this study, a SCLC cell line with etoposide-acquired resistance, H1048-ER, was constructed through a concentration gradient increasing method, and its resistance to etoposide was investigated in vitro and in a zebrafish model. Through transcriptome sequencing, real-time reverse transcription-quantitative polymerase chain reaction, and bioinformatic analyses of H1048-ER vs. H1048 cells, 51 differentially expressed genes were found to be significantly enriched in "collagen degradation" and "MET/FAK signaling activation in ECM". Among them, six genes (COL11A1, COL26A1, COL4A3, COL4A4, LAMA4, and LAMC1) had strong correlations with the prognosis of lung cancer. They may be key factors in the acquired etoposide resistance of H1048-ER cells. H1048-ER cells showed cross-resistance to cisplatin but were sensitive to doxorubicin and temozolomide. Our study provides novel insights into etoposide resistance in SCLC and affords the potential treatment options after etoposide resistance. - Source: PubMed
Publication date: 2025/04/21
Fan Yan-WenLiu Mei-HuiXu Tao-JunFan Ruo-YueXiang JingWu Jia-QiHe Ming-Fang - Esophageal cancer is a major global health challenge with a poor prognosis. Recent studies underscore the extracellular matrix (ECM) role in cancer progression, but the full impact of ECM-related genes on patient outcomes remains unclear. Our study utilized next-generation sequencing and clinical data from esophageal cancer patients provided by The Cancer Genome Atlas, employing the R package in RStudio for computational analysis. This analysis identified significant associations between patient survival and various ECM-related genes, including IBSP, LINGO4, COL26A1, MMP12, KLK4, RTBDN, TENM1, GDF15, and RUNX1. Consequently, we developed a prognostic model to predict patient outcomes, which demonstrated clear survival differences between high-risk and low-risk patient groups. Our comprehensive review encompassed clinical correlations, biological pathways, and variations in immune response among these risk categories. We also constructed a nomogram integrating clinical information with risk assessment. Focusing on the TENM1 gene, we found it significantly impacts immune response, showing a positive correlation with T helper cells, NK cells, and CD8+ T cells, but a negative correlation with neutrophils and Th17 cells. Gene Set Enrichment Analysis revealed enhanced pathways related to pancreatic beta cells, spermatogenesis, apical junctions, and muscle formation in patients with high TENM1 expression. This research provides new insights into the role of ECM genes in esophageal cancer and informs future research directions. - Source: PubMed
Publication date: 2024/07/25
Wu YinghongHu WenjieJia ZhihongZhu QiyingXu JinghuiPeng LiangWang Renjie