ZNF306 antibody - N-terminal region (ARP33609_P050)
- Known as:
- ZNF306 (anti-) - N-terminal region (ARP33609_P050)
- Catalog number:
- arp33609_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZNF306 antibody - N-terminal region (ARP33609_P050)
Related genes to: ZNF306 antibody - N-terminal region (ARP33609_P050)
- Gene:
- ZKSCAN3 NIH gene
- Name:
- zinc finger with KRAB and SCAN domains 3
- Previous symbol:
- ZNF306, ZNF309
- Synonyms:
- Zfp47, ZF47, ZSCAN35
- Chromosome:
- 6p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-20
- Date modifiied:
- 2016-11-09
Related products to: ZNF306 antibody - N-terminal region (ARP33609_P050)
Related articles to: ZNF306 antibody - N-terminal region (ARP33609_P050)
- Growing evidence suggests that epilepsy and psychiatric disorders may share common genetic underpinnings, yet the precise etiological relationship remains unclear. Psychiatric comorbidities affect approximately 30% of individuals with epilepsy, a rate markedly higher than in the general population, with depression (∼23%) and anxiety (∼20%) being the most prevalent. This high comorbidity burden not only worsens prognosis but also complicates management, underscoring the need for genetic insights into their relationship. To address this gap, we aimed to systematically evaluate the genetic correlation, pleiotropy, and potential causal associations between epilepsy and 14 major psychiatric disorders. - Source: PubMed
Feng XiaYao HuanXiao Gui - Lung cancer (LC) is among the most prevalent cancers globally, posing a significant threat to human health. This study employed Mendelian randomization (MR) analysis to identify key drug targets for LC treatment. MR results from the inverse variance weighted (IVW) algorithm highlighted 352 expression quantitative trait loci (eQTLs) and 31 protein quantitative trait loci (pQTLs) causally associated with LC. Sensitivity and Steiger analyses confirmed that 305 eQTLs and 28 pQTLs exhibited a robust causal relationship with LC. Colocalization analysis further identified 20 eQTLs as potential drug targets for LC. Predictions were made for 257 drugs and 17 diseases, establishing a target-drug network that included PTGFR-D005557 and IREB2-C004925, among others. The drugs-diseases network revealed associations such as D007213 with Liver Cirrhosis and D013749 with Schizophrenia. Notably, the strongest binding interaction was observed between Valproic acid and eight genes (BRAT1, H2BC11, IREB2, MICAL1, MPHOSPH6, PTGFR, RHNO1, SERPING1), suggesting a significant molecular interaction. Ultimately, seven key drug targets (SERPING1, TDRD9, GBAP1, FAM241A, ZKSCAN4, ZKSCAN3, Z94721.1) were consistently identified across two MR studies and validated. These targets offer new avenues for LC treatment, highlighting their potential in therapeutic development. - Source: PubMed
Publication date: 2025/12/23
Huang YaweiGeng MengyaZhang Mukun - Ovarian cancer has the worst prognosis among major gynecological cancers. Current therapies include platinum, Taxol, angiogenesis inhibitors, and poly[ADP-ribose]polymerase (PARP) inhibitors. However, resistance develops in most ovarian cancer patients. Identification of more pro-tumor factors in ovarian cancer may provide insights into ovarian cancer biology and therapy. In this study, we find ZKSCAN3, a zinc-finger transcription factor, is overexpressed in ovarian cancer. We show that ZKSCAN3 promotes ovarian cancer cell proliferation. Through RNA-Seq and chromatin immunoprecipitation (ChIP)-seq, HSPB1 is identified as a target gene of ZKSCAN3. HSPB1 expression is significantly decreased upon suppressing ZKSCAN3 expression. Suppressing HSPB1 expression also inhibits ovarian cancer cell proliferation. In contrast, expressing exogenous HSPB1 partially rescues the cell proliferation in ZKSCAN3 knockdown cells, which supports HSPB1 as a functional target gene of ZKSCAN3. Collectively, our study uncovers a functional ZKSCAN3-HSPB1 axis that promotes ovarian cancer cell proliferation. - Source: PubMed
Publication date: 2025/11/28
Ke QianLi ZhenyongFan LiLi NengSun LidongZhao HongboSong Tanjing - Psoriasis is a prevalent chronic skin disease. Cycloastragenol (CAG) has been shown to activate autophagy and alleviate epidermal keratinocyte hyperproliferation in psoriasis. This study aimed to clarify the mechanism of CAG-mediated autophagy in psoriasis-like models. We treated C57BL/6 mice with imiquimod cream and stimulated HaCaT cells with a cytokine mixture (C-mix) to establish mouse and cell models. Psoriasis area and severity index scores were used to evaluate pathological changes. Autophagy flux was monitored using a monomeric red fluorescent protein-green fluorescent protein-microtubule-associated protein 1 light chain 3 assay. The interaction between sirtuin 1 (SIRT1) and zinc finger containing Krüppel-associated box and SCAN domain 3 (ZKSCAN3), as well as ZKSCAN3 acetylation, was examined using co-immunoprecipitation. Our results found that CAG alleviated autophagy inhibition in the imiquimod-induced psoriasis-like mouse model and enhanced autophagy by upregulating SIRT1 expression. ZKSCAN3 inhibited autophagy in the C-mix-stimulated psoriasis-like cellular model, while SIRT1 reduced the nuclear localization of ZKSCAN3 through deacetylation. ZKSCAN3 overexpression reversed SIRT1-mediated autophagy enhancement, whereas CAG promoted autophagy by regulating the nuclear localization of ZKSCAN3. In conclusion, our findings demonstrate that CAG ameliorates autophagy inhibition by modulating the SIRT1/ZKSCAN3 axis in psoriasis. - Source: PubMed
Xia JieZhang DuZhang TengWang QingLiu Yong - Huntington disease (HD) is a neurodegenerative disease caused by the expression of a mutant form of HTT (huntingtin; mHTT), caused by an abnormal expansion of polyglutamine in HTT. In HD, macroautophagy/autophagy dysfunction can cause mHTT accumulation. Moreover, the promotion of autophagy is considered a therapeutic strategy for the treatment of HD. ZKSCAN3 (zinc finger with KRAB And SCAN domains 3) has been identified as a transcriptional repressor of TFEB (transcription factor EB), a master regulator of autophagy and lysosomal functions. In this study, we conducted CRISPR-Cas9-based gene ablation to disrupt ZKSCAN3 in HD animal models and HD patient-induced pluripotent stem cell (iPSC) -derived three-dimensional (3D) spheroids. In animal models of HD, targeted in vivo ablation via a single adeno-associated virus (AAV) mediated CRISPR-Cas9 approach resulted in reduced mHTT levels, leading to improvements in both behavioral symptoms and the brain environment. Furthermore, CRISPR-Cas9 mediated ablation of ZKSCAN3 in 3D spheroids from HD patient-derived iPSC resulted in increased autophagy and lysosomal function, along with reduced mHTT accumulation. Specifically, in iPSC-derived neurons from HD patients, ZKSCAN3-depleted neurons demonstrated increased lysosomal function and reduced oxidative stress compared to controls. Additionally, transcriptional analysis of ZKSCAN3-edited neurons revealed an increased expression of genes involved in synaptic function and transporter activity. Taken together, these results suggest that in HD treatment strategies for improving neuronal function and the brain environment, ZKSCAN3 downregulation in neurons by autophagy activation may improve the brain environment through neuronal self-repair. 2D: two-dimensional; 3D: three-dimensional; 4-HNE: 4-hydroxynonenal; AAV: adeno-associated virus; AD: Alzheimer disease; Aβ: beta-amyloid; DAPI: 4,6-diamidino-2-phenylindole; GFP: green fluorescent protein; HD: Huntington disease; HTT: huntingtin; IXMC: ImageXpress microconfocal high-content imaging system; Indel: insertion or deletion; iPSC: induced pluripotent stem cell; LAMP1: lysosomal-associated membrane protein 1; mHTT: mutant huntingtin; NPCs: neural precursor cells; RBFOX3/NeuN: RNA binding fox-1 homolog 3; PD: Parkinson disease; RNP: ribonucleoprotein; sgRNAs: single guide RNAs; ST: striatum; TFEB: transcription factor EB; TUBB3/Tuj-1: tubulin beta 3 class III; ZKSCAN3: zinc finger with KRAB and SCAN domains 3. - Source: PubMed
Publication date: 2025/10/10
Park Hyun JungKim JiYeonChoi JiwooRyou ChongsukShin EunjiLee Jae Young