PHF16 antibody - middle region (ARP34331_P050)
- Known as:
- PHF16 (anti-) - middle region (ARP34331_P050)
- Catalog number:
- arp34331_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- PHF16 antibody - middle region (ARP34331_P050)
Related genes to: PHF16 antibody - middle region (ARP34331_P050)
- Gene:
- JADE3 NIH gene
- Name:
- jade family PHD finger 3
- Previous symbol:
- PHF16
- Synonyms:
- KIAA0215, JADE-3
- Chromosome:
- Xp11.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-08-08
- Date modifiied:
- 2014-11-18
Related products to: PHF16 antibody - middle region (ARP34331_P050)
Related articles to: PHF16 antibody - middle region (ARP34331_P050)
- Diffuse large B-cell lymphoma (DLBCL) is an aggressive and common subtype of non-Hodgkin lymphoma (NHL). Despite the availability of several risk stratification tools, substantial room for improvement in personalized prognostic prediction still exists. Furthermore, considering the heterogeneity of DLBCL, how to select an appropriate treatment in a personalized manner remains a clinical challenge. In this study, we developed a random survival forests model by integrating clinical and gene expression data from 677 DLBCL case in Gene Expression Omnibus (GEO) database. Our model predicted overall survival with high concordance between training and validation datasets (C-index: 0.832 and 0.758, respectively), outperforming the consistency predicted by common prognostic markers such as Cell-Of-Origin Subtype, IPI score and Ann Arbor stage. Time-dependent ROC curves also showed good predictive performance for 1-year, 3-year, and 5-year survival in training and validation cohorts, the models are accessible via an open-access website. Survival analysis demonstrated that the group receiving the optimal treatment showed a more favorable survival association. Furthermore, we also used Kaplan-Meier curves, multivariate analysis and penalized Cox regression model to identify six genes (C2CD5, CD163, JADE3, BIRC3, TMEM200A, and LINC00877) related to the prognosis of DLBCL. In conclusion, we developed a machine learning model integrating clinical characteristics and gene expression profiles, providing a reliable decision-support tool for DLBCL prognosis and treatment selection. - Source: PubMed
Publication date: 2026/02/21
Lin JunweiLv WeifengCai HuixingNie QianyingZeng JinxiangLin KunLin QiWen XiaoqianLi YaoSu Rong - Although sex differences have been reported in patients with clear cell renal cell carcinoma (ccRCC), biological sex has not received clinical attention and genetic differences between sexes are poorly understood. This study aims to identify sex-specific gene mutations and explore their clinical significance in ccRCC. We used data from The Cancer Genome Atlas-Kidney Renal Clear Cell Carcinoma (TCGA-KIRC), The Renal Cell Cancer-European Union (RECA-EU) and Korean-KIRC. A total of 68 sex-related genes were selected from TCGA-KIRC through machine learning, and 23 sex-specific genes were identified through verification using the three databases. Survival differences according to sex were identified in nine genes (ACSS3, ALG13, ASXL3, BAP1, JADE3, KDM5C, KDM6A, NCOR1P1, and ZNF449). Female-specific survival differences were found in BAP1 in overall survival (OS) (TCGA-KIRC, p = 0.004; RECA-EU, p = 0.002; and Korean-KIRC, p = 0.003) and disease-free survival (DFS) (TCGA-KIRC, p = 0.001 and Korean-KIRC, p = 0.000004), and NCOR1P1 in DFS (TCGA-KIRC, p = 0.046 and RECA-EU, p = 0.00003). Male-specific survival differences were found in ASXL3 (OS, p = 0.017 in TCGA-KIRC; and OS, p = 0.005 in RECA-EU) and KDM5C (OS, p = 0.009 in RECA-EU; and DFS, p = 0.016 in Korean-KIRC). These results suggest that biological sex may be an important predictor and sex-specific tailored treatment may improve patient care in ccRCC. - Source: PubMed
Publication date: 2024/07/09
Hwang JiaLee Hye EunHan Jin SeonChoi Moon HyungHong Sung HooKim Sae WoongYang Ji HoonPark UnsangJung Eun SunChoi Yeong Jin - The innate immune system features a web of interacting pathways that require exquisite regulation. To identify novel nodes in this immune landscape, we conducted a gain-of-function, genome-wide CRISPR activation screen with influenza A virus. We identified both appreciated and novel antiviral genes, including Jade family PHD zinc finger 3 (JADE3) a protein involved in directing the histone acetyltransferase histone acetyltransferase binding to ORC1 complex to modify chromatin and regulate transcription. JADE3 is both necessary and sufficient to restrict influenza A virus infection. Our results suggest a distinct function for JADE3 as expression of the closely related paralogs JADE1 and JADE2 does not confer resistance to influenza A virus infection. JADE3 is required for both constitutive and inducible expression of the well-characterized antiviral gene interferon-induced transmembrane protein 3 (IFITM3). Furthermore, we find JADE3 activates the NF-kB signaling pathway, which is required for the promotion of IFITM3 expression by JADE3. Therefore, we propose JADE3 activates an antiviral genetic program involving NF-kB-dependent IFITM3 expression to restrict influenza A virus infection. - Source: PubMed
Publication date: 2024/03/09
Munir MoizEmbry AaronDoench John GHeaton Nicholas SWilen Craig BOrchard Robert C - The purpose of this study is to explore the potential biological role and prognostic significance of chromatin regulators (CRs) in low-grade gliomas (LGGs). - Source: PubMed
Publication date: 2023/11/30
Wang BoFeng YuLi ZhengweiZhou FanLuo JieYang BinLong ShengrongLi XinyiLiu ZhenyuanLi XiangChen JincaoWang LeiWei Wei - The innate immune system features a web of interacting pathways that require exquisite regulation. To identify novel nodes in this immune landscape we conducted a gain of function, genome-wide CRISPR activation screen with influenza A virus. We identified both appreciated and novel antiviral genes, including JADE3 a protein involved in directing the histone acetyltransferase HBO1 complex to modify chromatin and regulate transcription. JADE3 is both necessary and sufficient to restrict influenza A virus infection. Interestingly, expression of the closely related paralogues JADE1 and JADE2 are unable to restrict influenza A virus infection, suggesting a distinct function of JADE3. We identify both shared and unique transcriptional signatures between uninfected cells expressing JADE3 and JADE2. These data provide a framework for understanding the overlapping and distinct functions of the JADE family of paralogues. Specifically, we find that JADE3 expression activates the NF-kB signaling pathway, consistent with an antiviral function. Therefore, we propose JADE3, but not JADE1 or JADE2, activates an antiviral genetic program involving the NF-kB pathway to restrict influenza A virus infection. - Source: PubMed
Publication date: 2023/09/29
Munir MoizEmbry AaronDoench John GHeaton Nicholas SWilen Craig BOrchard Robert C