PHF20 antibody - C-terminal region (ARP35917_P050)
- Known as:
- PHF20 (anti-) - C-terminal region (ARP35917_P050)
- Catalog number:
- arp35917_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- PHF20 antibody - C-terminal region (ARP35917_P050)
Related genes to: PHF20 antibody - C-terminal region (ARP35917_P050)
- Gene:
- PHF20 NIH gene
- Name:
- PHD finger protein 20
- Previous symbol:
- C20orf104
- Synonyms:
- dJ1121G12.1, TDRD20A
- Chromosome:
- 20q11.22-q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-17
- Date modifiied:
- 2018-02-13
Related products to: PHF20 antibody - C-terminal region (ARP35917_P050)
Related articles to: PHF20 antibody - C-terminal region (ARP35917_P050)
- Cutaneous squamous cell carcinoma (cSCC) is a common and aggressive skin cancer, with treatment options for advanced stages often limited by chemoresistance. Here, we observe a positive correlation between PHF20 expression and the malignancy and tumor grade of cSCC. Functional studies suggest that PHF20 promotes oncogenic phenotypes, including proliferation, invasion, and epithelial-mesenchymal transition. Notably, PHF20 depletion appears to sensitize cSCC cells to chemotherapeutic agents. Mechanistically, we show that PHF20 interacts with and promotes the ubiquitin-mediated degradation of GAS7. This downregulation of GAS7 is associated with nuclear F-actin assembly, a process that has been implicated in DNA damage repair (DDR). Consequently, PHF20 loss stabilizes GAS7, enhances nuclear F-actin assembly, and is accompanied by increased DNA damage accumulation. These in vitro findings were corroborated in vivo, where PHF20 knockdown suppressed tumor growth and increased DNA damage. Together, PHF20 may contribute to the regulation of DDR and chemotherapeutic response, highlighting its potential as a therapeutic target in poorly differentiated cSCC. - Source: PubMed
Publication date: 2026/05/29
Li YunqianWen HeZheng HanZhen YunyueJia JingLi Zhengjun - encodes plant homeodomain finger protein 20 (PHF20), a component of the KAT8-containing nonspecific lethal (NSL) complex that deposits acetylation on histone H4 to activate gene expression. We report two unrelated individuals with developmental delay, microcephaly, and distinctive facial features, in whom exome sequencing and chromosomal microarray analysis revealed a homozygous deletion of that segregated with the disease phenotype in their families. Breakpoint junction sequencing revealed an -mediated deletion event. Western blot in cells from an affected individual showed undetectable PHF20, while levels of other NSL complex subunits were unaltered. Transcriptomic and epigenomic analysis revealed significant downregulation of gene pathways related to cell projection and neuronal development, associated with reduced histone H4K16 acetylation at these genes. In conclusion, our data suggest that homozygous deletion of leads to a neurodevelopmental syndrome, potentially through targeted epigenetic dysregulation and altered gene expression essential for neuronal development. Identifying additional families with biallelic variants will further delineate the phenotypic spectrum, and molecular studies in neuronal cell lines will be essential for understanding the disease mechanism. - Source: PubMed
Publication date: 2025/12/22
Dagan Shira YanovskyXuan HongwenRips JonathanPaz-Ebstein EmunaBaer TaliaGross ShiraFrumkin AyalaShi XiaobingHarel Tamar - Pancreatic cancer has a high mortality rate and lacks early detection markers. Advanced methods, such as machine learning (ML) and network analysis, identify central cancer networks with potential diagnostic and prognostic biomarkers, leading to improved tumor targeting strategies - Source: PubMed
Publication date: 2025/09/20
Salihoglu RanaNieves JesusDandekar GudrunEbert ReginaRudert MaximilianDandekar ThomasBencurova Elena - Sarcopenia, a disease marked by a progressive loss of muscle mass, increases the risks of disability and metabolic disorders, and decreases quality of life. Current therapeutic options are limited. YY1 transcriptional activity is augmented through an interaction with PHF20 at its promoter region, suppressing muscle differentiation. This study screened sulfasalazine, a medication for managing inflammatory bowel diseases (IBD), using the PHF20-YY1 promoter assay in CC myoblasts from an FDA-approved drug library. Sulfasalazine effectively inhibited PHF20-induced YY1 promoter activity (IC = 24 μM), reducing YY1 expression and enhancing muscle-specific gene expression. In mouse models of muscle atrophy, sulfasalazine not only enhanced muscle strength and function but also mitigated muscle loss. Clinical data from patients with IBD revealed that those treated with sulfasalazine had a significantly higher TPI (total psoas index), used as a muscle mass marker, suggesting enhanced muscle preservation. In conclusion, this study suggests the potential for repurposing sulfasalazine to manage sarcopenia, especially associated with IBD. - Source: PubMed
Publication date: 2025/09/01
Park MeeheeCho SeungjuChoi SeonggyuLee HwayoungLee JandeeJo YoungsukPark JisooPark Jongsun - Over the last decade, the functions of PHD finger protein 20 (PHF20) in several signaling processes have been studied, including those of protein kinase B (PKB)-mediated phosphorylation, p53 regulation, muscle differentiation, and histone modification including histone H3 lysine 4 (H3K4) methylation. One PHF20 human mutation lacks the first nonspecific lethal complex of the component that binds to H3K4me2 to facilitate cancer cell survival. In carcinoma cells, PHF20 expression is regulated by PKB; PHF20 becomes phosphorylated when DNA is damaged, thus inhibiting the p53 activity that maintains cancer cell survival. Given this regulatory effect, PHF20 is usually expressed not only in gliomas but also in breast cancers, colorectal cancers, and other diseases associated with skeletal muscle osteoblastosis and osteoporosis. Thus, PHF20 dysregulation and its downstream effects enhance the abnormalities associated with cancers or other diseases and encourage disease progression. Moreover, PHF20 serves as a nuclear factor kappa-light-chain enhancer of B cell activation, thus increasing pro-inflammatory cytokine production, associated with crosstalk involving the mouse double minute 2 homolog that in turn reduces the normal p53 levels not only in cancers but also in damaged or otherwise injured normal tissues. Despite the findings of various studies, the roles of PHF20 in terms of prognosis, diagnosis, and targeting of disease therapies remain unclear and should be further explored. - Source: PubMed
Publication date: 2024/11/20
Juang UijinGwon SuhwanJung WoohyeongNguyen HuonggiangHuang QuingzhiLee SoohyeonLee BeomwooKwon So HeeKim Seon-HwanPark Jongsun