CASZ1 antibody - middle region (ARP33139_P050)
- Known as:
- CASZ1 (anti-) - middle region (ARP33139_P050)
- Catalog number:
- arp33139_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CASZ1 antibody - middle region (ARP33139_P050)
Related genes to: CASZ1 antibody - middle region (ARP33139_P050)
- Gene:
- CASZ1 NIH gene
- Name:
- castor zinc finger 1
- Previous symbol:
- -
- Synonyms:
- FLJ20321, ZNF693, castor, cst, SRG
- Chromosome:
- 1p36.22
- Locus Type:
- gene with protein product
- Date approved:
- 2005-05-13
- Date modifiied:
- 2014-11-19
Related products to: CASZ1 antibody - middle region (ARP33139_P050)
Related articles to: CASZ1 antibody - middle region (ARP33139_P050)
- The CASZ1 gene expresses a cardiomyocyte transcription factor implicated in early heart morphogenesis. CASZ1 variants have been associated with the development of dilated cardiomyopathy (DCM) and noncompaction cardiomyopathy (NCCM), although reported cases are limited. - Source: PubMed
Publication date: 2026/06/01
Sekiguchi LaurenNguyen-Truong MichaelLin Kristy YChan David P - : Lung adenocarcinoma (LUAD) is the most common type of lung cancer and a major cause of cancer death. Zinc finger proteins (ZNFs) have been implicated in LUAD progression, functioning either as oncogenes or tumor suppressors. Therefore, an in-depth investigation of ZNFs may contribute to the development of novel diagnostic and therapeutic strategies for LUAD. : Transcriptomic and clinical data were obtained from the TCGA and GEO databases. Prognosis-related ZNF genes were identified using univariate Cox, LASSO, and multivariate Cox regression analyses. An eight-gene ZNF-based prognostic signature was constructed and validated in two independent external cohorts (GSE50081 and GSE26939). A nomogram integrating independent prognostic factors was developed. Immune infiltration, somatic mutation profiles, and drug sensitivity were systematically analyzed. We further focused on FGD3, a key gene from the signature, examining its expression in LUAD cells and tissues, including lorlatinib-resistant models. : The prognostic signature comprising TRIM6, TRIM29, CTCFL, FGD3, GATA4, CASZ1, TRAF2, and ZNF322 effectively stratified patients into distinct risk groups with significantly different overall survival ( < 0.05). The risk score, together with T and N stage, served as independent prognostic predictors ( = 500, < 0.05). High-risk patients exhibited an immune-desert phenotype, increased tumor mutational burden, and distinct drug sensitivity patterns. Notably, FGD3 expression was downregulated in LUAD tissues ( = 14, < 0.0001) and lorlatinib-resistant cells, and its restoration suppressed resistant cell proliferation and partially reversed drug resistance. : This study establishes a promising ZNF-based prognostic model for LUAD, providing a potential tool for risk stratification and individualized therapeutic decision-making. The identification of FGD3 as a potential mediator of drug resistance highlights its promise as a candidate biomarker and therapeutic target in LUAD. - Source: PubMed
Publication date: 2026/05/14
Sun JiayueYang YueHuang XiaoyiXue DinglongLi JiazhuangHuang YaruMeng Qingwei - Lymphedema is a chronic condition characterized by the accumulation of fluid due to impaired lymphatic drainage, frequently occurring secondary to chronic venous insufficiency (CVI), malignancy, or obesity. Despite known environmental and clinical risk factors, the genetic contributors to lymphedema and CVI have been understudied. - Source: PubMed
Publication date: 2026/04/22
Peloso Gina MAdhikari NimishYoung Melissa MCho KellyKinlay Scott - Endothelial cells (ECs) are essential components of the vertebrate circulatory system; however, a comprehensive atlas characterizing how ECs acquire organ-specific transcriptomic heterogeneity has not been established. Here, we generated a time-series endothelial resource covering the entirety of mouse embryonic development, including 26 time points and 8 organs. Time-series multi-organ comparison revealed emergence timing and lineage trajectory of organotypic ECs together with organ-specific genes and pathways. Using these resources, we found that most ECs showed distinguishable organ specificity before late gestation. The organotypic EC-enriched genes were associated with vascular function in the organs. Human and mouse pulmonary ECs underwent an evolutionarily conserved transcriptional transition. Endothelial-specific knockout of Casz1, a pulmonary EC-enriched transcription factor, resulted in impaired vascular growth, disturbed pulmonary endothelial organotypic differentiation, and deficient epithelial-EC crosstalk. Our work provides a powerful endothelial resource that reveals fundamental principles of organ-specific EC differentiation and uncovers previously unknown molecular mechanisms governing lung-specific vascular development. - Source: PubMed
Publication date: 2026/02/16
Lin LihuiZhong JingJiang FuqingWang Yu-XiangMa Lan-YueYang Jia-XinLi Yu-YanGao Rong-RongFeng HuijianCai BaomeiFeng ZiyuZhou XinShu Ya-HaiChen PanWu XueCai Chen-LengWang QiangWu GuangmingPei DuanqingCao ShangtaoLiu YangPeng GuangdunChen JiekaiChen Qi - We reported a rare case of 1p36 deletion syndrome diagnosed using whole-exome sequencing (WES) in a Tunisian neonate, and to highlight the utility of WES in detecting structural variants, particularly in resource-limited settings. - Source: PubMed
Kerkeni NesrineKharrat MaherKraoua LiliaAchour AhlemMaazoul FaouziMrad RidhaTrabelsi Mediha