PATZ1 antibody Polyclonal Antibodies Primary antibodies
- Known as:
- PATZ1 (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100111
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- PATZ1 antibody Polyclonal Antibodies Primary antibodies
Related genes to: PATZ1 antibody Polyclonal Antibodies Primary antibodies
- Gene:
- PATZ1 NIH gene
- Name:
- POZ/BTB and AT hook containing zinc finger 1
- Previous symbol:
- ZNF278
- Synonyms:
- MAZR, dJ400N23, ZBTB19, ZSG, RIAZ, PATZ
- Chromosome:
- 22q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-20
- Date modifiied:
- 2016-02-10
Related products to: PATZ1 antibody Polyclonal Antibodies Primary antibodies
Related articles to: PATZ1 antibody Polyclonal Antibodies Primary antibodies
- PML nuclear bodies are cellular structures known to combat DNA viruses. In this study, how human bocavirus 1 (HBoV1), a respiratory pathogen, evades this defense was investigated. PATZ1, a host protein that constitutively regulates gene activity, is recruited by the viral NS1-70 protein to form concentrated clusters adjacent to PML bodies. These clusters bind to the viral DNA and suppress its ability to make new viral genes. To overcome this, the virus produces another protein, NS2, which disrupts the PATZ1 condensates and removes them from the viral DNA, allowing the virus to resume replication. This NS2-mediated antagonism also relieves PATZ1-dependent repression of certain host genes, facilitating viral DNA replication. Beyond HBoV1, PATZ1 also restricts other nuclear-replicating DNA viruses. Our study reveals an intrinsic antiviral mechanism centered on PATZ1-PML condensates and identifies NS2 as a viral antagonist that reprograms host transcription to promote infection. - Source: PubMed
Publication date: 2026/05/28
Tian ChuchuLiu HaibinWei YinFeng JiangpengYu BaochengZuo LiChen ZhenZhang XueyanHao HaojieXu HuanzhouGuan WuxiangSun Yuning - We report the clinicopathologic features of EWSR1-rearranged renal neoplasia from our institution. A retrospective cohort of 39 EWSR1-rearranged renal tumors was identified using fluorescence in situ hybridization (FISH) and RNA-based next generation sequencing (NGS). A final diagnosis of Ewing sarcoma (EWS) was established in 34 of 39 cases (87%), with the remaining cases diagnosed as desmoplastic small round cell tumor (DSRCT; n = 2), sclerosing epithelioid fibrosarcoma (SEF; n = 2), and thyroid-like follicular renal cell carcinoma (TLFRCC; n = 1). Fusion partners identified in EWS included FLI1 (n = 17) and ERG (n = 2). WT1 (n = 2), CREB3L1 (n = 1) and CREB3L2 (n = 1), and PATZ1 (n = 1) fusions were found in DSRCT, SEF, and TLFRCC, respectively. The mean age at EWS diagnosis was 31.4 years (range 6-73), with a similar sex distribution (18 females, 16 males), and a mean tumor size of 10.7 cm (range 3-24 cm). Both DSRCT cases occurred in males aged 6 and 29 years, diagnosed on renal biopsy and brain metastasis, respectively. The SEF cases involved primary tumors in 22-year-old and 43-year-old females. The one case of TLFRCC was identified in a 41-year-old female that underwent radical nephrectomy. Cases with available immunohistochemistry showed most EWS tumors (24/26, 92%) expressed a combination of CD99, FLI1, and ERG, while both SEF cases were positive for MUC4. Our results highlight the importance of molecular testing in providing an integrated diagnosis and are informative regarding the spectrum of renal neoplasia that harbor EWSR1 rearrangements, including EWS, DSRCT, SEF, and TLFRCC as these tumors can exhibit significant clinicopathologic heterogeneity. - Source: PubMed
Publication date: 2026/04/30
Colef Robert GPujari Ganesh PSill Daniel RPitel Beth AZhang PingchuanTekin BurakLucas Peter CWhaley Rumeal DHerrera Hernandez LorenJimenez Rafael EErickson Lori ACheville John CKipp Benjamin RHalling Kevin CGreipp Patricia TGupta Sounak - The dynamics of chromatin accessibility that regulate oogenesis for the establishment of the female ovarian reserve in mammals have not been explored in reptiles with lifelong continuous oogenesis. Assays for transposase-accessible chromatin with high-throughput sequencing (ATAC-seq) were conducted to generate a chromatin accessibility landscape from gonadal samples from three critical stages of oogenesis in female Chinese alligators, which revealed a pronounced global decrease in chromatin accessibility across these developmental stages. Functional enrichment analysis demonstrated that differentially accessible regions were associated with genes involved in cell cycle regulation, meiosis, RNA binding, and cellular metabolism. Transcription factor footprinting identified krüppel-like factor (KLF) and specificity protein (SP) family members, POZ/BTB and AT-hook containing zinc finger protein 1 (PATZ1), and the nuclear transcription factor Y (NF-Y) complex (including subunits NFYA, NFYB, and NFYC) as core regulatory factors, with NF-Y binding sites exhibiting marked dynamic changes during development. Further analysis showed that NF-Y target genes are significantly enriched in critical processes such as cell cycle, mitosis, and meiosis, including key regulators Aurora Kinase A (AURKA) and AURKB. Experimental validation confirmed widespread ovarian expression of NFYA, NFYB, and NFYC, with AURKB expression strongly correlated with NF-Y protein levels. Dual-luciferase reporter assays demonstrated that NFYA significantly enhances AURKB promoter activity through two CCAAT-box elements near the transcription start site. This research depicts the chromatin accessibility dynamics during oogenesis of the Chinese alligator and pinpoints NF-Y as a crucial regulator of AURKB, thereby providing a mechanistic foundation for understanding reproduction and advancing conservation in this endangered species. - Source: PubMed
Publication date: 2026/04/29
Li PengfeiNi YutingWen YueCao XiaojingLi JinZhou YongkangYi PingsiWu XiaobingNie Haitao - Fatty acid metabolism (FAM) is essential for cancer cell proliferation and progression, contributing to membrane synthesis, energy storage, and signaling molecule production. However, effective therapeutic strategies targeting FAM are yet to be established in clinical practice. This study aimed to develop a novel FAM-related prognostic signature for bladder cancer (BLCA) and investigate its biological and clinical significance. - Source: PubMed
Publication date: 2026/02/27
Yu HuiLei QingqiangYang WenyongCao MinZhang MiaoyuWang TaisongDong JunhaoChen XueruiSu XuHuang YiXu HeZhuo HuiLin Liangbin - Kaposi's sarcoma-associated herpesvirus (KSHV) establishes lifelong latency in the host but can reactivate in the lytic cycle under specific pathophysiological conditions. The replication and transcription activator (RTA) serves as the master regulator of this latent-to-lytic switch. Although RTA is well known as a potent viral transcriptional activator and E3 ubiquitin ligase, its role in modulating host gene expression remains incompletely understood. In this study, we identified eukaryotic translation elongation factor 1δ (EEF1D) as a previously unrecognized host inhibitory factor that inhibits KSHV reactivation. Functional analyses revealed that ectopic expression of EEF1D suppressed viral lytic replication, whereas EEF1D depletion enhanced viral reactivation. KSHV RTA counteracts this inhibition through two complementary mechanisms: interaction with EEF1D protein to promote its ubiquitin-proteasome-mediated degradation and, more prominently, repression of transcription through promoter silencing. Dual-luciferase reporter assays further revealed that this transcriptional repression is conserved among primate γ-herpesviruses, including KSHV, rhesus rhadinovirus, and Epstein-Barr virus, but is absent in murine γ-herpesvirus 68. Mechanistically, RTA induces DNMT3A-dependent hypermethylation of the promoter, a process facilitated by the transcription factor, PATZ1. Collectively, these findings reveal a previously unrecognized repressive function of RTA on the host gene , highlighting an additional layer of viral strategy to promote lytic reactivation. - Source: PubMed
Publication date: 2026/03/10
Xiang MinYu LeiHan ChunyanHuang LiangDong LianghuiBai LeiWu ShuwenLan Ke