Ask about this productRelated genes to: PHF10 antibody
- Gene:
- PHF10 NIH gene
- Name:
- PHD finger protein 10
- Previous symbol:
- -
- Synonyms:
- FLJ10975, XAP135, BAF45a
- Chromosome:
- 6q27
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-01
- Date modifiied:
- 2014-11-19
Related products to: PHF10 antibody
Related articles to: PHF10 antibody
- Lesions and injuries to the extremities of the pig's body parts, like the tail and ears, are often associated with biting. However, lesion signs observed at birth and in 3-d-old piglets suggest that injuries may also result from swine inflammation and necrosis syndrome (SINS), which occurs without animal interaction. We aimed to investigate whether 1) there is a direct and maternal genetic effect on SINS; 2) we can use a proxy for different body parts for SINS and skin damage; 3) there is a genetic correlation between SINS and skin damage recorded in multiple time points; 4) there are genetic variants and important genes associated with both traits. We analyzed 7k female pigs born from February 2022 to June 2023 on three farms in the Netherlands. At birth, we scored SINS (no SINS = 0, and SINS = 1) on the ears, tail, and teats. Tail docking occurred after SINS phenotyping. We defined the Total_sins as the number of affected parts by SINS. The same animals were scored for skin damage (DMG on the ears, tail, and flank on average three times during the rearing phase (no DMG = 0, slight DMG = 1, severe DMG = 2, and very severe DMG = 3), resulting in 20k DMG records. We defined Sum_dmg as the sum of scores for DMG in the three body parts. Single and two-trait animal models were used to estimate heritabilities and genetic correlations. Direct (maternal) heritabilities for SINS ranged from 0.03 ± 0.01 (0.01 ± 0.00) to 0.08 ± 0.01 (0.06 ± 0.05); DMG ranged from 0.04 ± 0.01 to 0.09 ± 0.01. Although maternal heritability estimates were low and had high standard errors, likely reflecting limitations in separating direct and maternal effects, rather than the biological absence of maternal influence. Total_sins and Sum_dmg were highly genetically correlated (0.76). Our findings suggest that selection for reduced skin damage may be initiated earlier in life, based on SINS, and that piglets genetically less susceptible to SINS are more likely to experience improved welfare throughout the production system. Genomically, SINS was genetically associated with the genes DLL1, PHF10, WDR27, and THBS2, which are mainly related to embryonic and tissue formation, and warrant further investigation. - Source: PubMed
Oliveira Garcia AriellyGaloro Leite NataliaVogelzang RoosBretanha Rocha Renata de FátimaFacioni Guimarães Simone ElizaLourenco Daniela - The maternal-to-zygotic transition (MZT) is a reprograming process encompassing zygotic genome activation (ZGA) and the clearance of maternally-provided mRNAs. While some factors regulating MZT have been identified, there are thousands of maternal RNAs whose function has not been ascribed yet. Here, we have performed a proof-of-principle CRISPR-RfxCas13d maternal screen, in which we targeted mRNAs encoding kinases and phosphatases or proteins regulating them in zebrafish. This screen identified branched-chain ketoacid dehydrogenase kinase, Bckdk, as a novel post-translational regulator of MZT. Bckdk mRNA knockdown caused epiboly defects, ZGA deregulation, H3K27ac reduction and a partial impairment of miR-430 processing. Phospho-proteomic analysis revealed that Phf10/Baf45a, a chromatin remodeling factor, is less phosphorylated upon Bckdk depletion. Further, phf10 mRNA knockdown also altered ZGA, and expression of a phospho-mimetic mutant of Phf10 rescued the developmental defects observed after bckdk mRNA depletion, as well as restored H3K27ac levels. Altogether, our results demonstrate the competence of CRISPR-RfxCas13d screenings to uncover new regulators of early vertebrate development and shed light on the post-translational control of MZT mediated by protein phosphorylation. - Source: PubMed
Publication date: 2025/11/18
Hernández-Huertas LuisMoreno-Sánchez IsmaelCrespo-Cuadrado JesúsVargas-Baco Anada Silva Pescador GabrielZhang YingWen ZhihuiFlorens LaurenceSantos-Pereira José MBazzini Ariel AMoreno-Mateos Miguel A - Keap1 mutations mainly caused NRF2-dependent anti-oxidative stress responses, yet whether there are other downstream substrates and pathways remains unknown. This study aimed to uncover the role of Keap1 mutations in regulating PHF10-NRF2 axis in NSCLC and ferroptosis evasion. - Source: PubMed
Publication date: 2025/11/03
Lu XuanKang NingningChen YajunZhao XinruZhu DonglinYang JunYang YongXie Hongya - Chemoresistance represents a major threat to the treatment of human cancers, including cholangiocarcinoma (CHOL). Aberrant epigenetic events contribute most to the progression of CHOL and chemotherapy efficacy. PHF10, one subunit of SWI/SNF complex, expressed highly in tumours that correlated with tumorigenesis. However, the roles of PHF10 in CHOL remains unclear. Here, we utilised the bioinformatic analysis to reveal that PHF10 expressed lowly in CHOL samples relative to normal tissues. Functionally, we demonstrated that PHF10 deficiency enhanced cell proliferation, migration and self-renewal capacities of CHOL cells. PHF10 ablation further enhanced the chemoresistance of CHOL cells. The transcriptome analysis revealed that PHF10-KO could notably alter several oncogenic crosstalk, including the NF-kB signalling. As the top hit, HMGB1 mRNA expressions had the sharpest increase upon PHF10 deficiency. PHF10 coordinated with Setdb1 to mediate the H3K9me3 modifications on the HMGB1 promoter to suppress its expressions. Low PHF10 relied on HMGB1 to promote the progression of CHOL cells in vitro and in vivo. Furthermore, EZH2 mediated the H3K27me3 enrichment on the PHF10 promoter region that contributes to its low expressions. Lastly, the HMGB1 inhibitor (Glycyrrhizin) decreased proliferation rate of PHF10-deleted cells in vitro and in vivo. Targeting HMGB1 rendered PHF10 CHOL re-sensitive to chemotherapy. Collectively, this study demonstrated that PHF10 functions as a tumour suppressor in CHOL, and is a novel target to predict and overcome chemoresistance. - Source: PubMed
Yin QiushiLin DaningZeng WeiqianGu ShijingZhu ChuangshiLiang ChangfuYang Yan - Gastric cancer (GC) is characterized with differentiation disorders, the precise mechanisms of which remain unknown. Our previous study showed that PHF10 exhibits oncogenic properties in GC, with its histological presentation indicating a potential role in the modulation of differentiation disorders in GC. This study reveals a significant upregulation of PHF10 in GC tissues, showing a negative correlation with differentiation level. PHF10 was found to impede the differentiation of GC cells while promoting their stemness properties. This was attributed to the formation of a positive feedback loop between PHF10 and E2F1, resulting in dysregulated expression levels in GC. Additionally, PHF10 was found to mediate the transcriptional repression of the target gene DUSP5 in GC cells through the assembly of the SWI/SNF complex, leading to an elevation in pERK1/2 levels. In GC tissues, a negative association was noted between the expression of E2F1 or PHF10 and DUSP5, whereas a positive correlation was observed between the expression of E2F1 or PHF10 and pERK1/2. Additional rescue experiments confirmed that the inhibitory effect on differentiation of GC cells by PHF10 is dependent on the DUSP5-pERK1/2 axis. The signaling cascade involving E2F1-PHF10-DUSP5-pERK1/2 was identified as an important player in regulating differentiation and stemness in GC cells. PHF10 emerges as a promising target for differentiation induction therapy in GC. - Source: PubMed
Publication date: 2024/08/10
Fan ZhiyuanYan WenjingLi JianfangYan MinLiu BingyaYang ZhongyinYu Beiqin