Homo sapiens,Human,ZIC5,Zinc finger protein of the cerebellum 5,Zinc finger protein ZIC 5
- Known as:
- Homo sapiens,Human,ZIC5,Zinc finger protein cerebellum 5,Zinc finger protein ZIC 5
- Catalog number:
- EIAAB47183
- Category:
- -
- Supplier:
- EIAab
- Gene target:
- Homo sapiens Human ZIC5 Zinc finger protein the cerebellum 5 ZIC
Related genes to: Homo sapiens,Human,ZIC5,Zinc finger protein of the cerebellum 5,Zinc finger protein ZIC 5
- Gene:
- ZIC5 NIH gene
- Name:
- Zic family member 5
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 13q32.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-30
- Date modifiied:
- 2016-10-05
Related products to: Homo sapiens,Human,ZIC5,Zinc finger protein of the cerebellum 5,Zinc finger protein ZIC 5
Related articles to: Homo sapiens,Human,ZIC5,Zinc finger protein of the cerebellum 5,Zinc finger protein ZIC 5
- The Foxi3 transcription factor, expressed in the neural plate border at the end of gastrulation, is necessary for the formation of posterior placodes and is thus important for ectodermal patterning. We have created two knock-in mouse lines expressing GFP or a tamoxifen-inducible Cre recombinase to show that Foxi3 is one of the earliest genes to label the border between the neural tube and epidermis, and that Foxi3-expressing neural plate border progenitors contribute primarily to cranial placodes and epidermis from the onset of expression, but not to the neural crest or neural tube lineages. By simultaneously knocking out Foxi3 in neural plate border cells and following their fates, we show that neural plate border cells lacking Foxi3 contribute to all four lineages of the ectoderm - placodes, epidermis, crest and neural tube. We contrast Foxi3 with another neural plate border transcription factor, Zic5, the progenitors of which initially contribute broadly to all germ layers until gastrulation and gradually become restricted to the neural crest lineage and dorsal neural tube cells. Our study demonstrates that Foxi3 uniquely acts early at the neural plate border to restrict progenitors to a placodal and epidermal fate. - Source: PubMed
Publication date: 2023/10/09
Thawani AnkitaMaunsell Helen RZhang HongyuanAnkamreddy HarinarayanaGroves Andrew K - For pre-clinical drug development and precision oncology research, robust cancer cell models are essential. Patient-derived models in low passages retain more genetic and phenotypic characteristics of their original tumors than conventional cancer cell lines. Subentity, individual genetics, and heterogeneity greatly influence drug sensitivity and clinical outcome. - Source: PubMed
Publication date: 2023/05/09
Andus IngoPrall FriedrichLinnebacher MichaelLinnebacher Christina S - This study aims to explore the mechanism of microRNA (miR)-101-3p-mediated SOX2/ZIC5 axis in the progression of cisplatin resistance of nasopharyngeal carcinoma (NPC). ZIC5 expression was analyzed with a bioinformatics database and detected in NPC cell lines. Cisplatin-resistant cells (HNE-1/DDP and C666-1/DDP) were transfected with sh-ZIC5, sh-SOX2, sh-SOX2 + pcDNA3.1-ZIC5, or miR-101-3p Agomir + pcDNA3.1-SOX2. MiR-101-3p, SOX2, and ZIC5 expression was assessed after transfection, and cancer associated phenotypes were evaluated after cisplatin treatment. The potential relationships among miR-101-3p, SOX2, and ZIC5 were analyzed. A xenograft mouse model of NPC was established with HNE-1 cells stably transfected or not transfected with oe-ZIC5 and subjected to tail vein injection of miR-101-3p Agomir and intraperitoneal injection of cisplatin. Overexpression of ZIC5 was found in cisplatin-resistant NPC cells. Downregulating ZIC5 in NPC cells decreased cell viability, promoted apoptosis, and reduced cisplatin resistance. SOX2 had a binding site on ZIC5, and SOX2 promoted proliferation, migration, and cisplatin resistance and inhibited cell apoptosis by up-regulating ZIC5. Mechanistically, miR-101-3p was decreased in cisplatin-resistant NPC cells and negatively targeted SOX2. Overexpression of miR-101-3p inhibited tumor growth and cisplatin resistance in xenograft mouse model, which was reversed by ZIC5 overexpression. In conclusion, the miR-101-3p/SOX2/ZIC5 axis was implicated in cancer associated phenotypes and cisplatin resistance in NPC. - Source: PubMed
Publication date: 2023/02/09
Li TieqiZhang GehouLi WeiXiao JianZhou ZhengTan GuolinAi Jingang - Chromosome 13q deletion syndrome shows variable clinical features related to the different potential breakpoints in chromosome 13q. The severely malformed phenotype is known to be associated with the deletion of a critical region in 13q32. However, esophageal atresia is a rare symptom and the relevant region is unknown. Thus, determining the association between accurate breakpoints and new clinical features is essential. - Source: PubMed
Publication date: 2022/12/27
Kotani TomomiTsuda HiroyukiIto YumikoNakamura NoriyukiUshida TakafumiImai KenjiIitani YukakoFuma KazuyaMuramatsu YukakoHayakawa MasahiroKajiyama Hiroaki - Cervical cancer is one of the major malignancies causing morbidity and mortality in women in developing countries. ZIC5 has been found to be associated with a variety of cancers, yet the expression and molecular function of ZIC5 in cervical squamous cell carcinoma (CESC) is unknown. - Source: PubMed
Publication date: 2022/12/05
Jia QinggeSong JunyangXu TianqiLiu JinChai JiaYang YanruLi LingfeiLi MingyangYang Xinyuan