STAT3 Human shRNA Lentiviral Particle (Locus ID 6774)
SKU
TL301348V
STAT3 - Human shRNA lentiviral particles (4 unique 29mer target-specific shRNA, 1 scramble control), 0.5 ml each, >10^7 TU/ml.
$1,731.00
2 Weeks*
Specifications
| Product Data | |
| Locus ID | 6774 |
|---|---|
| Synonyms | ADMIO; ADMIO1; APRF; HIES |
| Vector | pGFP-C-shLenti |
| E. coli Selection | Chloramphenicol (34 ug/ml) |
| Mammalian Cell Selection | Puromycin |
| Format | Lentiviral particles |
| Components | STAT3 - Human shRNA lentiviral particles (4 unique 29mer target-specific shRNA, 1 scramble control), 0.5 ml each, >10^7 TU/ml. |
| RefSeq | NM_003150, NM_139276, NM_213662, NM_003150.1, NM_003150.2, NM_003150.3, NM_213662.1, NM_139276.1, NM_139276.2, BC014482, BC014482.1, BC000627, BC008044, BC029783, BC067119, BC107775, NM_001369512, NM_001369513, NM_001369514, NM_001369516, NM_001369517, NM_001369518, NM_001369519, NM_001369520, NM_003150.4, NM_139276.3, NM_213662.2 |
| UniProt ID | P40763 |
| Summary | The protein encoded by this gene is a member of the STAT protein family. In response to cytokines and growth factors, STAT family members are phosphorylated by the receptor associated kinases, and then form homo- or heterodimers that translocate to the cell nucleus where they act as transcription activators. This protein is activated through phosphorylation in response to various cytokines and growth factors including IFNs, EGF, IL5, IL6, HGF, LIF and BMP2. This protein mediates the expression of a variety of genes in response to cell stimuli, and thus plays a key role in many cellular processes such as cell growth and apoptosis. The small GTPase Rac1 has been shown to bind and regulate the activity of this protein. PIAS3 protein is a specific inhibitor of this protein. This gene also plays a role in regulating host response to viral and bacterial infections. Mutations in this gene are associated with infantile-onset multisystem autoimmune disease and hyper-immunoglobulin E syndrome. provided by RefSeq, Aug 2020 |
| shRNA Design | These shRNA constructs were designed against multiple splice variants at this gene locus. To be certain that your variant of interest is targeted, please contact techsupport@origene.com. If you need a special design or shRNA sequence, please utilize our custom shRNA service. |
| Performance Guaranteed | OriGene guarantees that the sequences in the shRNA expression cassettes are verified to correspond to the target gene with 100% identity. One of the four constructs at minimum are guaranteed to produce 70% or more gene expression knock-down provided a minimum transfection efficiency of 80% is achieved. Western Blot data is recommended over qPCR to evaluate the silencing effect of the shRNA constructs 72 hrs post transfection. To properly assess knockdown, the gene expression level from the included scramble control vector must be used in comparison with the target-specific shRNA transfected samples. For non-conforming shRNA, requests for replacement product must be made within ninety (90) days from the date of delivery of the shRNA kit. To arrange for a free replacement with newly designed constructs, please contact Technical Services at techsupport@origene.com. Please provide your data indicating the transfection efficiency and measurement of gene expression knockdown compared to the scrambled shRNA control (Western Blot data preferred). |
| Storage | Store at -80°C |
| Shipping | Dry Ice |
Reviews
Documents
Resources
Citations
PD-L1 is overexpressed on breast cancer stem cells through notch3/mTOR axis
Mansour, Al-Mazrou, Al-Mohanna et al
Oncoimmunology (2020) 9 (1), 1729299 DOI: 10.1080/2162402X.2020.1729299
Mansour, Al-Mazrou, Al-Mohanna et al
Oncoimmunology (2020) 9 (1), 1729299 DOI: 10.1080/2162402X.2020.1729299
AI Summary: In this study, OriGene products including Notch3 shRNA (OriGene, Cat# TL313627) and mTOR shRNA (OriGene, Cat# TL314404) were used to specifically knock down Notch3 and mTOR expression, enabling the authors to demonstrate that PD-L1 overexpression on breast cancer stem-like cells is mediated through the Notch3/mTOR signaling axis.
PD-L1 is overexpressed on breast cancer stem cells through notch3/mTOR axis
Mansour, Al-Mazrou, Al-Mohanna et al
OncoImmunology (2020) 9 (1), 1729299 DOI: 10.1080/2162402X.2020.1729299
Mansour, Al-Mazrou, Al-Mohanna et al
OncoImmunology (2020) 9 (1), 1729299 DOI: 10.1080/2162402X.2020.1729299
AI Summary: OriGene products, specifically the STAT3 (TL301348V) and c-Myc (TL311323V) shRNA lentiviral vectors, were used to effectively knock down these genes in breast cancer cells, enabling the study of their roles in PD-L1 regulation and cancer stem cell properties.
Snippet: STAT3 and c-Myc were also downregulated using specific ShRNA from OriGene (USA) in lentiviral vectors, (TL301348V, and TL311323V, respectively, using pGFP-C-ShLenti vector) as previously described9 (supplementary Table 2). Among the four plasmids (A, B, C, and D) provided by the company for each gene knockdown, plasmids (B) were the most effective in downregulating c-Myc and STAT3 in MDA-MB-231 cells (supplementary figure 11)
Oncogenic transformation of human lung bronchial epithelial cells induced by arsenic involves ROS-dependent activation of STAT3-miR-21-PDCD4 mechanism
Pratheeshkumar, Son, Divya et al
Sci Rep (2016) 6, 37227 DOI: 10.1038/srep37227
Pratheeshkumar, Son, Divya et al
Sci Rep (2016) 6, 37227 DOI: 10.1038/srep37227
AI Summary: OriGene products, specifically the human catalase plasmid and STAT3 shRNA plasmid, were used in this study to manipulate gene expression in bronchial epithelial cells, enabling the researchers to investigate the roles of catalase and STAT3 in arsenic-induced oncogenic transformation.
Snippet: 5% CO2 in air. Plasmids and Transfection Plasmid DNA encoding human catalase and STAT3 shRNA was purchased from Origene (Rockville, MD). PDCD4 3′-UTR reporter plasmid was kindly provided by Dr. Yong Li (U
Hexavalent chromium induces malignant transformation of human lung bronchial epithelial cells via ROS-dependent activation of miR-21-PDCD4 signaling
Pratheeshkumar, Son, Divya et al
Oncotarget (2016) 7 (32), 51193-51210 DOI: 10.18632/oncotarget.9967
Pratheeshkumar, Son, Divya et al
Oncotarget (2016) 7 (32), 51193-51210 DOI: 10.18632/oncotarget.9967
Showing 1-4 of 4 papers.
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