Ask about this productRelated genes to: TXNDC15 Blocking Peptide
- Gene:
- TXNDC15 NIH gene
- Name:
- thioredoxin domain containing 15
- Previous symbol:
- C5orf14
- Synonyms:
- 2310047H23Rik, FLJ22625
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-27
- Date modifiied:
- 2016-12-12
Related products to: TXNDC15 Blocking Peptide
Related articles to: TXNDC15 Blocking Peptide
- Diabetic foot diseases (DFD) severely impair quality of life, yet specific biomarkers and effective therapies remain limited. Identifying causal molecular targets is critical to address this unmet need. - Source: PubMed
Publication date: 2026/07/21
Fang ManLei YitianFan PengjuWu Hong - Chronic kidney disease (CKD) significantly increases the risk of coronary artery disease (CAD), but the causal plasma proteins linking these conditions are poorly understood. This study aimed to identify genetically validated plasma biomarkers and therapeutic targets for this cardiorenal link. - Source: PubMed
Publication date: 2026/06/16
Huang HaiQuanLiu WenkangYan YaNanCao JuanWang JiePengFang ChaoYi - Lung adenocarcinoma (LUAD) is characterized by high heterogeneity and insidious early-stage progression, leading to a dismal clinical prognosis and posing a formidable challenge in current oncological research. Although the Thioredoxin domain-containing (TXNDC) family is involved in various cancers, the role of TXNDC15 in LUAD remains unclear. Here, we show that TXNDC15 is downregulated in LUAD and predicts better survival. Functional assays reveal that TXNDC15 suppresses proliferation by inducing G2/M phase arrest. Mechanistically, TXNDC15 interacts with the mitotic kinase NEK4, thereby orchestrating the G2/M checkpoint circuitry to restrict malignant progression. These findings highlight the TXNDC15-NEK4 factor as a pivotal regulatory node in LUAD progression. - Source: PubMed
Publication date: 2026/05/20
Wang YingFeng XinYuan LeiXiao Wenming - Biological systems face a constantly changing environment and must swiftly respond to stimuli, yet how cells sense and adapt to environmental and physiological cues is incompletely understood. Short-lived proteins can be rapidly induced upon perturbation, enabling swift activation of adaptive cellular responses. Leveraging genome-wide data on protein-transcript correlation, we systematically searched for rapid proteolysis substrates whose abundance reflects the activity of the underlying proteolytic machinery. Here, focusing on the candidate substrate ABHD2, we employed CRISPR-based functional screens to dissect its degradation and identified as an essential factor in MARCHF6-mediated ER-associated protein degradation (ERAD). Unexpectedly, TXNDC15 supports substrate exit and degradation from the ER via a catalysis-independent mechanism. Loss of remodels the ER proteome and lipid homeostasis. Together, our work defines a missing component of ERAD and provides a generalizable strategy to decode post-translational regulatory circuits. - Source: PubMed
Publication date: 2026/04/02
Liu YuyangYaochai Michelle YinfeiLiu ShanshanAlwaseem HananBirsoy Kivanc - Pigs are vital to global agriculture, and infectious diseases cause significant economic losses. Leukocytes provide a critical window into the genetic regulation of pig immune traits. However, understanding of these mechanisms within specific immune cell types remains insufficient. Here, we integrate 11 immune traits and systematically map the regulatory landscapes of expression quantitative trait loci (eQTLs), splicing QTLs (sQTLs), and alternative polyadenylation QTLs (apaQTLs) in porcine peripheral blood mononuclear cells (PBMCs) and neutrophils to uncover cell type-specific patterns. These molecular QTLs (molQTLs) exhibit strong cell-type specificity and preferentially regulate genes involved in cross-cell communication that are linked to core immunity, thereby shaping immune phenotypes through intercellular networks. Furthermore, we identify 588 molQTLs that colocalize with genome-wide association study signals for phagocytic capacity. Among these, 60.3% of apaQTLs independently modulate immune traits, including the variant rs330263631. Experiments confirm that rs330263631 modulates mRNA stability and expression levels of the TXNDC15 by dynamically selecting polyadenylation sites and altering the length of the 3' untranslated region. This work systematically delineates the PBMC- and neutrophil-specific genetic architecture underlying immune regulation in pigs and provides a molecular foundation for deciphering the genetic mechanisms of porcine immune traits. - Source: PubMed
Publication date: 2026/02/11
Yang JinyanChen SiqianTang YongjieWang XiniWang LuluLiu HuataoMa FupingZhao QingyaoXing KaiYu YingWang Chuduan