Gene: Fat1
Official Full Name: FAT atypical cadherin 1provided by MGI
Gene Summary: Involved in epithelial cell morphogenesis; establishment of epithelial cell apical/basal polarity involved in camera-type eye morphogenesis; and lens development in camera-type eye. Acts upstream of or within actin filament organization; cell-cell adhesion; and establishment or maintenance of cell polarity. Located in cell junction; filopodium; and lamellipodium. Is active in apical plasma membrane. Is expressed in several structures, including alimentary system; central nervous system; embryo ectoderm; embryo mesenchyme; and sensory organ. Used to study facioscapulohumeral muscular dystrophy and nephrotic syndrome. Human ortholog(s) of this gene implicated in colorectal cancer; esophagus squamous cell carcinoma; lung non-small cell carcinoma; lung small cell carcinoma; and oral squamous cell carcinoma. Orthologous to human FAT1 (FAT atypical cadherin 1). [provided by Alliance of Genome Resources, Apr 2025]
Catalog Number | Product Name | Species | Gene | Passage ratio | Mycoplasma testing | Price |
---|---|---|---|---|---|---|
KO01911 | FAT1 Knockout cell line (HeLa) | Human | FAT1 | 1:3~1:6 | Negative | Online Inquiry |
KO01912 | FAT1 Knockout cell line (HCT 116) | Human | FAT1 | 1:2~1:4 | Negative | Online Inquiry |
KO01913 | FAT1 Knockout cell line (HEK293) | Human | FAT1 | 1:3~1:6 | Negative | Online Inquiry |
KO01914 | FAT1 Knockout cell line (A549) | Human | FAT1 | 1:3~1:4 | Negative | Online Inquiry |
Fat1 Gene Knockout Cell Lines are specifically engineered cellular models that have had the Fat1 gene disrupted, providing researchers with vital tools to study the functional roles of this gene in various biological processes. The Fat1 gene encodes a member of the cadherin superfamily, which is essential for cell adhesion and signaling pathways. By employing CRISPR-Cas9 genome editing technology, these knockout cell lines allow for the precise alteration of the Fat1 gene, facilitating the investigation of its contributions to cell morphology, migration, and differentiation.
The primary function of these cell lines lies in their ability to reveal the mechanistic underpinnings of Fat1's role in cellular processes, particularly in cancer biology and neural development. The loss of Fat1 has been linked to alterations in cellular adhesion and the regulation of both epithelial and mesenchymal states, making these models valuable in research contexts that explore tumor progression or developmental disorders.
The scientific importance of Fat1 Gene Knockout Cell Lines extends into both basic and translational research. These cell lines can be utilized not only for fundamental studies but also for drug screening and toxicity testing, making them pivotal in the quest for novel therapeutic strategies. Furthermore, the stability and reproducibility of these cell lines contribute to their reliability in experimental designs.
Compared to alternative methods such as transient knockdown techniques, which often yield inconsistent results, the knockout phenotype provides a permanent and stable model for long-term studies. This durability ensures that researchers can conduct comprehensive investigations across varied time points and conditions without the variability associated with transient systems.
Research institutions, biotechnology firms, and clinicians seeking to deepen their understanding of cell signaling pathways, tumorigenesis, or developmental biology will find immense value in using Fat1 Gene Knockout Cell Lines. Their unique offerings contribute significantly to the advancement of knowledge in these critical fields.
Our company, with its rich background in genetic engineering and cellular biology, is dedicated to providing high-quality biological products that empower researchers and clinicians. We pride ourselves on our commitment to innovation and excellence, ensuring that our customers are equipped with the best tools for their research endeavors.
Please note that all services are for research use only. Not intended for any clinical use.
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