SMARCAD1 belongs to the SNF2_RAD54 helicase family. It contains 2 CUE domains, 1 helicase ATP-binding domain, and 1 helicase C-terminal domain. It is a probable ATP-dependent DNA helicase.
- Known as:
- SMARCAD1 belongs SNF2_RAD54 helicase family. contains 2 CUE domains, 1 helicase adenosine triphosphate-binding domain, 1 helicase C-terminal domain. a probable adenosine triphosphate-dependent Desoxyribonucleic acid helicase.
- Catalog number:
- 25-214
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- SMARCAD1 belongs the SNF2_RAD54 helicase family. contains 2 CUE domains 1 ATP-binding domain and C-terminal domain. probable ATP-dependent DNA helicase.
Related genes to: SMARCAD1 belongs to the SNF2_RAD54 helicase family. It contains 2 CUE domains, 1 helicase ATP-binding domain, and 1 helicase C-terminal domain. It is a probable ATP-dependent DNA helicase.
- Gene:
- SMARCAD1 NIH gene
- Name:
- SWI/SNF-related, matrix-associated actin-dependent regulator of chromatin, subfamily a, containing DEAD/H box 1
- Previous symbol:
- -
- Synonyms:
- ETL1, DKFZP762K2015, KIAA1122, DKFZp762K2015
- Chromosome:
- 4q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-29
- Date modifiied:
- 2015-01-28
Related products to: SMARCAD1 belongs to the SNF2_RAD54 helicase family. It contains 2 CUE domains, 1 helicase ATP-binding domain, and 1 helicase C-terminal domain. It is a probable ATP-dependent DNA helicase.
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- Uterine spiral artery remodelling (SAR) is a fundamental developmental process that facilitates optimal placental perfusion and supports fetal growth. Central to SAR is the phenotypic transformation of vascular smooth muscle cells (VSMCs) from a contractile to a synthetic state, directed by invasive trophoblast cells. To advance these findings, we sought to elucidate the epigenetic mechanisms governing trophoblast-induced reprogramming of VSMC identity, enabling plasticity required for uterine vascular adaptation. - Source: PubMed
Publication date: 2026/07/15
Sarkar PoulomiAin Rupasri - Genomic instability in high-grade serous tubo-ovarian carcinoma (HGSTOC) can generate fusion genes with potential roles in tumor evolution and clinical relevance. HGSTOCs commonly disseminate prior to diagnosis, but most studies analyze only one tumor sample per patient, limiting understanding of fusion gene dynamics. Here, RNA sequencing was performed on 108 tumor samples from multiple intra‑abdominal sites in 23 patients. A consensus approach involving three fusion callers identified 170 high-confidence fusion genes present in all samples from each patient, most of which were non‑recurrent and not in-frame. Protein kinases were significantly enriched among fusion partners, and commonly retained intact catalytic domains. Several of the kinase fusion genes may have oncogenic relevance, including AKAP8L::BRD4 (recurrent in three patients), GPBP1L1::MKNK1, SPAG16::ERBB4, UGP2::MAPK4, and STRN3::PRKD1. Four fusions involved homologous recombination-related genes, including FUT10::SPIDR, RAD54B::VIRMA, RAD54L::PLXNA2, and SMARCAD1::BOD1L1. Integration of these fusion genes with other somatic alterations in homologous recombination-related genes, deficiency signatures, and germline BRCA1/2 variants increased the involvement of the homologous recombination pathway to 15 HGSTOCs (65%). Overall, HGSTOC has a heterogeneous fusion gene landscape, and multi-site sampling with consensus calling offers a robust strategy for resolving fusion profiles. - Source: PubMed
Publication date: 2026/06/25
Panagopoulos IoannisStranger AneSveen AnitaJareid MieKidd Susanne GBischof KatharinaTaskén KjetilDørum AnneDavidson BenLothe Ragnhild ASkotheim Rolf IJohannessen Bjarne - Extrahepatic cholangiocarcinoma (eCCA) is characterized by marked molecular heterogeneity and limited therapeutic options. MicroRNAs (miRNAs) are key post-transcriptional regulators of cancer-related pathways, but their contribution to tumor adaptation in physiologically relevant models remains poorly understood. Three-dimensional (3D) tumor spheroids better mimic in vivo conditions than conventional two-dimensional (2D) cultures. - Source: PubMed
Publication date: 2026/06/22
Roncoroni LedaTerrazzan AnnaElli LucaAncona PietroOlaizola PaulaTabano SilviaColapietro PatriziaGamberini FilippoOrlandi ChiaraAguiari GianlucaTaccioli CristianDoneda LuisaBianchi Nicoletta - Tauopathies are neurodegenerative diseases characterized by the accumulation of misfolded tau protein and include Alzheimer's disease (AD) and related dementia disorders. Identifying new strategies to treat tauopathy remains an important gap in the field. Using forward and reverse genetic approaches in C. elegans, we identified smrd-1, the C. elegans homolog of SMARCAD1, as a potent modifier of tauopathy phenotypes in a transgenic model of tauopathy. Loss of smrd-1 function rescues tauopathy-associated neuronal dysfunction and neurodegeneration in C. elegans models of tauopathy. Loss or reduction of smrd-1/SMARCAD1 decreases phosphorylated and total tau protein levels by reducing tau mRNA transcripts in C. elegans and mammalian HEK-tau cells. Loss of smrd-1 rescues tau-driven abnormal H3K9me3 chromatin methylation. Immunohistochemistry in human postmortem AD brain tissue showed SMARCAD1 depletion in a subset of cases that also exhibit depletion of MSUT2. Loss of smrd-1/SMARCAD1 rescues tau-mediated neurodegeneration via a tau mRNA lowering mechanism accompanied by changes in chromatin conformation. - Source: PubMed
Jadhav Vaishnavi SKow Rebecca LBeale Asia DBaum MisaMcMillan Pamela JLatimer Caitlin SLiachko Nicole FKraemer Brian C - Replication stress is a major driver of genomic instability and contributes to diseases such as cancer. It triggers the S-phase checkpoint, a signaling pathway that coordinates the handling of replication obstacles with cell cycle progression. One prominent source of replication stress is the formation of DNA-protein crosslinks on the template, such as those induced by DNA topoisomerase I poisoning by camptothecin (CPT). Here, we investigated how the S-phase checkpoint responds to CPT-induced replication stress. We show that both activation and timely deactivation of checkpoint signaling are critical for DNA replication completion and cell viability. Using a locus-specific approach, we found that checkpoint signaling is actively dampened at lesion sites. Mechanistically, this attenuation involves the displacement of the checkpoint mediator Rad9 by the DNA repair factors Slx4 and Fun30. This local dampening not only promotes cell cycle progression, but also permits Exo1-dependent resection of replication forks stalled by Top1-DNA crosslinks. Controlled resection, in turn, allows homologous recombination factors to access and stabilize the forks, preventing their degradation. We propose that local checkpoint dampening by Slx4 and Fun30 at replication stress sites is a critical mechanism that promotes replication completion and preserves genome stability. - Source: PubMed
Courtes MathildeBoissière ThierryBarthe AntoinePasero PhilippePardo Benjamin