SASH1 antibody
- Known as:
- SASH1 (anti-)
- Catalog number:
- orb29537
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- SASH1 antibody
Related genes to: SASH1 antibody
- Gene:
- SASH1 NIH gene
- Name:
- SAM and SH3 domain containing 1
- Previous symbol:
- -
- Synonyms:
- KIAA0790, dJ323M4.1, SH3D6A
- Chromosome:
- 6q24.3-q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-27
- Date modifiied:
- 2018-02-13
Related products to: SASH1 antibody
Related articles to: SASH1 antibody
- SASH1 is a signal adaptor protein involved in cell growth, apoptosis, and immune regulation, and has been increasingly studied in tumor and immune cells. Emerging evidence suggests that SASH1 plays an important role in inflammatory responses and cellular homeostasis, processes that are closely associated with the development of PE. This study aimed to determine whether SASH1 contributes to trophoblast apoptosis and inflammatory responses in PE and whether P-EXOS exerts protective effects through SASH1 regulation. In this study, three PE-related transcriptomic datasets (GSE75010, GSE10588, and GSE60438) were analyzed to identify shared differentially expressed genes (DEGs), followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Machine learning algorithms were further applied to screen key candidate genes, and single-cell RNA sequencing data were used to characterize cellular heterogeneity in placental tissue and to determine cell type-specific expression patterns. SASH1 was identified as a consensus candidate gene and was significantly upregulated in trophoblast cells from PE samples. In vitro, a hypoxia-treated HTR-8/SVneo trophoblast cell model was established, combined with SASH1 knockdown, SASH1 overexpression, and co-culture with P-EXOS. Functional experiments showed that knockdown of SASH1 significantly suppressed hypoxia-induced trophoblast apoptosis and reduced the secretion of pro-inflammatory cytokines, including IL-6, IL-1β, and TNF-α, whereas SASH1 overexpression promoted apoptosis and inflammatory responses. In addition, P-EXOS treatment markedly reduced SASH1 expression at both mRNA and protein levels and attenuated hypoxia-induced trophoblast injury, while SASH1 overexpression largely abolished these protective effects. Taken together, these findings indicate that SASH1 plays a critical role in trophoblast apoptosis and inflammatory responses in PE. P-EXOS may alleviate hypoxia-induced trophoblastic injury by suppressing SASH1 expression, providing new insights into the molecular mechanisms and potential therapeutic targets for PE. - Source: PubMed
Publication date: 2026/08/18
Gao JingLiu YongjuanZhang RanLiu FangfangWu Lixia - SASH1 (SAM [sterile alpha motif] and SH3 [SRC-homology-3] domain-containing protein 1) is a multidomain scaffold implicated in pigmentation, innate immunity, receptor signaling, cytoskeletal dynamics, vascular biology, and tumor suppression. Although genetic and expression studies link SASH1 dysfunction to diverse diseases, a unifying mechanistic framework has remained elusive. Here, we synthesize current knowledge of SASH1 structure, interaction networks, and biological functions across cell types and disease contexts. SASH1 contains an intrinsically disordered SPIDER (SLy Proteins Associated Disordered Region), an SH3 domain, two SAM domains, and multiple linear motifs; together, these elements mediate interactions with EphA8 (ephrin type-A receptor 8), β-arrestin 1, TRAF6 (TNF receptor-associated factor 6), CRKL (CRK-like proto-oncogene), IQGAP1 (IQ-motif-containing GTPase-activating protein 1), cortactin, and TNKS2 (tankyrase-2). We propose that SASH1 functions as a context-dependent multi-docking scaffold that organizes signaling architecture. Its modular domains, intrinsically disordered regions, and dual SAM domains enable flexible, multivalent interactions with partners that can be grouped into three functional modules: receptor regulation, intracellular signaling, and cytoskeletal organization. Notably, many SASH1 partners are themselves scaffold or adaptor proteins, allowing integration into pre-existing networks in a hierarchical 'scaffold-of-scaffolds' manner. Through selective partner recruitment, SASH1 links cell-surface receptor inputs to downstream signaling pathways and cytoskeletal remodeling. This model provides a mechanistic framework for how SASH1 drives diverse, cell-type-specific outputs across physiology and disease, while revealing broader principles by which multidomain scaffolds encode cellular behavior. - Source: PubMed
Publication date: 2026/08/06
Clements Christopher MRoney Md Saiful IslamShellman Yiqun G - Preeclampsia (PE), a pregnancy-specific pathological condition, has shown a growing incidence over recent decades. Disulfidptosis is a newly discovered mode of programmed cell death that differs from traditional cell death pathways in its molecular mechanisms. Numerous studies have reported the association between disulfidptosis and various diseases; however, the role of disulfidptosis in the pathogenesis of PE remains unknown. - Source: PubMed
Publication date: 2026/06/20
Chen XiangbeiChen XuemeiZhao BoenLv PingPang DongLai Lichuan - Meningiomas are the most common intracranial tumors. DNA methylation analysis in benign and aggressive meningiomas showed decreased methylation and overexpression of hsa-miR-21-5p in atypical and anaplastic tumors. Transcriptomic analysis of distinct WHO grade meningiomas showed multiple predicted hsa-miR-21-5p target genes as differentially expressed. They were mainly related to processes of intercellular and intracellular signaling. Intercellular communication in meningioma was investigated using the deposited scRNA-seq dataset and deconvolution of our RNA-seq data. We found WHO grade-related differences in the microenvironment including inverse correlation between the count of border-associated macrophages (BAM) and the level of hsa-miR-21-5p. Single-cell transcriptomics suggests the role of interleukin 6 in direct communication between tumor cells and BAMs. and are predicted targets of hsa-miR-21-5p downregulated in atypical/anaplastic meningiomas. IL6R downregulation was also confirmed by immunohistochemistry. Hsa-miR-21-5p enhanced proliferation and viability of KT21-MG1 meningioma cells and showed a regulatory effect on , and other predicted target genes , , , and by interacting with 3'UTRs. DNA hypomethylation-related overexpression of hsa-miR-21-5p contributes to aggressive meningioma growth by interaction with multiple target genes, and probably affects microenvironment communication between meningioma cells and BAMs by lowering the IL6R level in tumor tissue. - Source: PubMed
Publication date: 2026/05/15
Kober PaulinaBaluszek SzymonMossakowska Beata JoannaMyśliwy IzabellaTsegaye BiniyamOziębło ArturMandat TomaszBujko Mateusz - Laryngeal dysplasia and Reinke's edema (RE) are common vocal fold lesions associated with smoking. While the former is cancer prone, most cases of the latter do not undergo malignant transformation. Therefore, we proposed identifying biomarkers of smoking-induced benign-malignant transformation of vocal fold lesions. - Source: PubMed
Publication date: 2025/05/19
Liu Yun-YiZhuang Pei-Yun