Transfected Stable Cell Lines
Reliable | High-Performance | Wide Rage
Precision reporter, kinase, immune receptor, biosimilar, Cas9, and knockout stable cell lines for diverse applications.
| Cat.No. | Product Name | Price |
|---|---|---|
| CSC-DC005195 | Panoply™ Human FADS1 Knockdown Stable Cell Line | Inquiry |
| CSC-SC005195 | Panoply™ Human FADS1 Over-expressing Stable Cell Line | Inquiry |
| CSC-RT1460 | Human FADS1 Knockout Cell Line-HeLa | Inquiry |
| CLKO-1310 | FADS1 KO Cell Lysate-HeLa | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| AD05714Z | Human FADS1 adenoviral particles | Inquiry |
| LV12111L | human FADS1 (NM_013402) lentivirus particles | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| SHH288709 | shRNA set against Human FADS1 (NM_013402.4) | Inquiry |
| SHH288713 | shRNA set against Mouse FADS1 (NM_146094.2) | Inquiry |
| SHH044377 | shRNA set against Rat Fads1(NM_053445.2) | Inquiry |
| SHH288717 | shRNA set against Rat FADS1 (NM_053445.2) | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| CDCR062212 | Human FADS1 ORF clone (NM_013402.4) | Inquiry |
| CDFH006278 | Human FADS1 cDNA Clone(NM_013402.4) | Inquiry |
| CDFR013184 | Rat Fads1 cDNA Clone(NM_053445.2) | Inquiry |
| MiUTR1R-01814 | FADS1 miRNA 3'UTR clone | Inquiry |
| MiUTR4H-TG03235 | FADS1 miRNA 3'UTR clone | Inquiry |
| CDCB192248 | Rabbit FADS1 ORF clone (XM_008274405.1) | Inquiry |
| CDCG001308 | Mouse FADS1 ORF clone(NM_146094.2) | Inquiry |
| CDCR380271 | Rat Fads1 ORF Clone(NM_053445.2) | Inquiry |
| CDCS413446 | Human FADS1 ORF Clone (BC007846) | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| CC-492 | FADS1 Easy KO Kit (Mouse) | Inquiry |
| CC-493 | FADS1 Easy KO Kit (Human) | Inquiry |
Fatty acid desaturase 1 is a key rate-limiting enzyme responsible for converting dihomo-gamma-linolenic acid (DGLA) to arachidonic acid (AA), and dysregulated expression of FADS1 was found in many cancers, moreover, FADS1 knockdown can not only inhibit cancer growth and migration but also sensitize the cytotoxicity of chemotherapy.
It is hard to catch hidden mechanism of laryngeal squamous cell carcinoma (LSCC) even though dysregulated metabolism is pronounced in its whole progression. The key rate-limiting enzyme of polyunsaturated fatty acids (PUFAs), Fatty acid desaturase 1 (FADS1), demonstrates the ability of catalyzing dihomo-gamma-linolenic acid (DGLA) to arachidonic acid (AA) and upregulated expression in LSCC, which has close linkage with advanced clinical features and poor prognosis of the recurrent LSCC patient after chemotherapy. The greater conversion rate of DGLA to AA may be an indicator of increased activity of FADS1 or FADS1 overexpression. Similarly, there is also an elevated level of prostaglandin E2 (PGE2) and downstream metabolite of AA in cancerous laryngeal tissues. Bioinformatic analysis-based microarray data revealed AKT/mTOR signaling can be activated by FADS1 and its further validated by in vivo and in vitro assays. So those results underpin the viewpoint of FADS1 acting as promoter in LSCC progression and set basis of figuring out more dietary supplementation interventions targeting FADS1/AKT/mTOR pathway for LSCC treatment. PGE2 is a downstream metabolite of arachidonic acid (AA) with high abundance in various kinds of human malignancies used to predict poor prognosis, and activate its downstream signaling pathway by binding to G double protein receptors (EP1, EP2, EP3, and EP4), which have engagement in cancer development, proliferation, apoptosis, angiogenesis, immunosuppression, tumor invasion, and metastases. Previous studies indicated that PGE2 could increase AKT, p70S6K, and S6 phosphorylation and AKT/mTOR pathway via EP2/4 receptors. Measurement of PGE2 concentration in LSCC tissue and cell revealed positive relation between PGE2 and FADS1 expression, thus further confirmed the concept of PGE2 acting as trigger for AKT-mTOR signaling.
Cardiovascular diseases (CVDs) are serious threat to human life and health, and polyunsaturated fatty acid (PUFA) is widely known for its preventive effect on CVDs. Series of researches about illustrating molecular mechanism of how PUFA works on CVDs have aroused a big number of interests. Among those researches, a pair of genes with negative correlation, miRNA(miRNA-193a-5p) and FADS1, were screened to exam if they are the potential factors matter polyunsaturated fatty acids synthesis. Dual luciferase reporter assays further confirmed the targeted relationship between miRNA-193a-5p and FADS1 in bovine mammary epithelial cells (BMECs).
Fig 1. Metabolic disease influenced by balancing pro-inflammatory and pro-resolving lipid mediators via FADS1 (J. Mark Brown et al. 2020)
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