S100A13, human, recombinant, full length
- Known as:
- S100A13, H. sapiens, Rec., length
- Catalog number:
- 201SA13
- Product Quantity:
- 100ug
- Category:
- -
- Supplier:
- ProtEra
- Gene target:
- S100A13 human recombinant full length
Related genes to: S100A13, human, recombinant, full length
- Gene:
- S100A13 NIH gene
- Name:
- S100 calcium binding protein A13
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-30
- Date modifiied:
- 2016-10-05
Related products to: S100A13, human, recombinant, full length
Related articles to: S100A13, human, recombinant, full length
- Frontotemporal dementia (FTD) is a genetically and clinically heterogeneous neurodegenerative disorder with no disease-modifying treatments. Plasma proteomic signatures offer a promising avenue for uncovering disease mechanisms and developing targeted interventions. - Source: PubMed
Publication date: 2026/07/25
Yao YuanZou QinChen Ke - S100A13, a calcium-binding protein containing two EF-hand motifs, contributes to intracellular calcium homeostasis, a key determinant of mitochondrial quality control. We previously showed that S100A13 modulates mitochondrial membrane potential (ΔΨm) in patient-derived skin fibroblasts carrying S100A13 (p.I80Gfs*13 and S100A3 (p.R77C) mutations. However, its role in regulating mitochondrial dynamics remains unclear. Here, we investigated whether S100A13 regulates mitochondrial fusion-fission balance in human bronchial epithelial cells (BEAS-2B) using Myc-tagged wild-type or p.I80Gfs*13 S100A13 constructs. The S100A13 p.I80Gfs*13 mutant markedly attenuated bradykinin- and ionophore-induced intracellular calcium transients and reduced ΔΨm compared with wild-type S100A13 ( < 0.05). These alterations were associated with severe mitochondrial ultrastructural abnormalities, disrupted cristae organization, and increased mitochondrial fragmentation ( < 0.05). Interestingly, both wild-type and p.I80Gfs*13 mutant S100A13 increased expression of the mitochondrial fusion-associated proteins MFN1/2 and OPA1 while reducing expression of the fission mediator MFF. However, despite these apparently pro-fusion molecular changes, the S100A13 p.I80Gfs*13 mutant failed to maintain mitochondrial fusion competency, suggesting a functional uncoupling between fusion protein abundance and mitochondrial fusion competency. Collectively, these findings identify S100A13 as an important regulator of intracellular calcium-dependent mitochondrial dynamics and demonstrate that C-terminal truncation disrupts calcium-dependent regulation of mitochondrial fusion and cristae integrity in lung epithelial cells. - Source: PubMed
Publication date: 2026/06/04
Alqattan SomayaAlonazi MonaAlmutairy EidRaveendran Vineesh VAlamri AbdulazizAl-Mohanna Futwan - An accumulation of evidence underscores the critical importance of both hypoxia and the immune microenvironment in driving the progression of osteosarcoma. Despite advancements in therapeutic strategies, osteosarcoma continues to pose a formidable challenge due to its aggressive nature and high metastatic potential. Nonetheless, the identification of reliable gene signatures that combine information on hypoxia and immune status to predict osteosarcoma prognosis remains an unmet need. - Source: PubMed
Publication date: 2026/06/20
Xie ShangfangYu WenyaoLin RunyeXin Songjian - Osteosarcoma (OS), the most prevalent primary malignant bone tumor with a dismal prognosis, exhibits significant heterogeneity in programmed cell death (PCD) pathways, but its subtype-specific functional mechanisms remain poorly characterized. This study integrated PCD-related gene signatures to delineate molecular subtypes in OS via consensus clustering, successfully defining four distinct subtypes with divergent prognostic outcomes and immune microenvironments. Differential expression, functional enrichment, and protein-protein interaction (PPI) network analyses revealed subtype-specific PCD pathway associations (e.g., lysosome-dependent cell death, apoptosis, pyroptosis and anoikis), while comparative immune profiling and clinical characterization further refined subgroup identities. A robust prognostic risk model incorporating five pivotal genes (, , , , and ) and metastasis status demonstrated superior predictive performance in both training and external validation cohorts. These findings not only elucidate the functional architecture of PCD across OS molecular subtypes but also establish a clinically actionable model for precision risk stratification and tailored therapeutic strategies. - Source: PubMed
Publication date: 2026/04/11
Zou XinyiRu Yuanfang - Cerebral small vessel disease (SVD), manifesting as white matter hyperintensities (WMH), lacunar infarctions, and cerebral microbleeds on magnetic resonance imaging (MRI), has been linked to developmental epigenetic alterations. This study aimed to identify and validate gene-specific promoter methylation changes as epigenetic markers associated with SVD, using MRI-defined imaging features and blood inflammatory cells. - Source: PubMed
Publication date: 2026/03/12
Kim JeeyeonPark JihyeKang KeunsooLee Young HoShin Byoung-SooKim Dae-HyunShin Dong-IckAhn Seong HwanKim Jae GukKang Hyun GooJeong HyeseonYum Kyu SunChae Hee-YunKim Do-HyungKim Jei