IGF1R Knockout A-549 Cell Line
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Cat.No.:
EDC07941
Species:
Human
Cell Name:
A-549
Gene:
IGF1R
Gene ID:
3480
Size:
1×10⁶cells
IGF1R Knockout Cell Line (A549) is an exclusive upgraded CRISPR/Cas9 system-mediated gene knockout cell, with the advantages of Optimized Strategy Design, Efficient Cell Transfection, High-Performance Cas9 Protein and Hassle-Free Cell Selection.
| Cat.No. | EDC07941 |
|---|---|
| Product Name | IGF1R Knockout A549 Cell Line |
| Cell Line | A-549 |
| Cellosaurus ID | CVCL_0023 |
| Cell Line Synonyms | A 549, A549, NCI-A549, A549/ATCC, A549 ATCC, A549ATCC, hA549 |
| Gene | IGF1R |
| NCBI Gene ID | |
| Gene Synonyms | CD221|IGFIR|IGFR|JTK13 |
| Summary |
This receptor binds insulin-like growth factor with a high affinity. It has tyrosine kinase activity. The insulin-like growth factor I receptor plays a critical role in transformation events. Cleavage of the precursor generates alpha and beta subunits. It is highly overexpressed in most malignant tissues where it functions as an anti-apoptotic agent by enhancing cell survival. Alternatively spliced transcript variants encoding distinct isoforms have been found for this gene. [provided by RefSeq, May 2014]
|
| Associated Diseases | Non-Small Cell Lung Carcinoma |
| Morphology | Adherent |
| Passage Ratio | 1/5-1/4 ,2days |
| Complete Culture Medium | F-12K + 10% FBS |
| Freezing Medium | 95% Complete culture medium + 5% DMSO |
| QC | Indels validated by Sanger sequencing; sterility confirmed via microbial testing. |
* For research use only. Not intended for use in humans or animals, including clinical, therapeutic, or diagnostic purposes.
| Loci | STR Info (Sample Cell) Sample Cell Line: A-549 | STR Info (Cell bank) Cell Line: A-549 | ||
| Allele1 | Allele2 | Allele1 | Allele2 | |
| Amelogenin | X | Y | X | Y |
| CSF1PO | 10 | 12 | 10 | 12 |
| D2S1338 | 24 | 24 | ||
| D3S1358 | 16 | 16 | ||
| D5S818 | 11 | 11 | ||
| D7S820 | 8 | 11 | 8 | 11 |
| D8S1179 | 13 | 14 | 13 | 14 |
| D13S317 | 11 | 11 | ||
| D16S539 | 11 | 12 | 11 | 12 |
| D18S51 | 14 | 17 | 14 | 17 |
| D19S433 | 13 | 13 | ||
| D21S11 | 29 | 29 | ||
| FGA | 23 | 23 | ||
| Penta D | 9 | 9 | ||
| Penta E | 7 | 11 | 7 | 11 |
| TH01 | 8 | 9.3 | 8 | 9.3 |
| TPOX | 8 | 11 | 8 | 11 |
| vWA | 14 | 14 | ||
| D6S1043 | 11 | 13 | ||
| D12S391 | 18 | 18 | ||
| D2S441 | 10 | 13 | 10 | 13 |
* STR authentication data of this cell line matches with that of cell lines sourced from ATCC, DSMZ, JCRB, and RIKEN databases.
Conclusion: The STR identification of this cell is correct.
Conclusion: The STR identification of this cell is correct.
FAQ
Which is better for studying IGF1R function, IGF1R Knockout A-549 Cell Line or IGF1R overexpression A-549 Cell Line?
The choice depends on whether you are studying IGF1R's role in lung cancer biology or modeling EGFR-TKI resistance mechanisms involving IGF1R signaling. The Knockout line is the standard tool for asking whether IGF1R is required for lung cancer proliferation and survival in NSCLC context — IGF1R amplification, autocrine IGF-1/IGF-2 signaling, and IGF1R-mediated resistance to EGFR-targeted therapy have been characterized in lung cancer. Overexpression is useful for studying IGF1R amplification effects in lung cancer.
For lung cancer research, the EDITGENE IGF1R Knockout in A-549 is highly relevant — A-549 is an NSCLC cell line, and IGF1R signaling has been implicated in NSCLC progression and treatment resistance. This product complements the parallel IGF1R Knockout in HEK293 (also available); A-549 is preferred for lung cancer-relevant studies, HEK293 for systematic biochemistry. Rescue with wild-type or kinase-dead IGF1R is the standard specificity control. The knockout is valuable for studying IGF1R-EGFR signaling crosstalk, EGFR-TKI resistance mechanisms, and IGF1R-targeted therapy in lung cancer.
What are the application scenarios for this model?
Primary applications:
• Lung cancer proliferation: cell growth kinetics and apoptosis assays given IGF1R's role in NSCLC survival.
• EGFR-TKI resistance: gefitinib, erlotinib, osimertinib resistance studies given IGF1R-mediated EGFR-TKI resistance mechanisms.
• IGF-1 autocrine signaling: IGF-1 secretion analysis and autocrine signaling characterization in NSCLC context.
• Combination therapy: IGF1R inhibitor + EGFR-TKI combination studies for overcoming resistance.
EDITGENE recommends this A-549-based model for researchers investigating IGF1R lung cancer biology, EGFR-TKI resistance mechanisms, and IGF1R-targeted combination cancer therapy.
Is this IGF1R Knockout A-549 Cell Line compatible with overexpression rescue experiments?
Yes. IGF1R rescue experiments in A-549 are well-suited for lung cancer research:
• Construct design: use a codon-modified IGF1R sequence with a small intracellular C-terminal tag (FLAG, HA). Preserve α2β2 tetramer architecture.
• Surface localization validation: confirm plasma membrane localization before functional assays.
• Kinase-dead rescue: K1003A mutation abolishes catalytic activity.
• EGFR-TKI resistance studies: rescue with wild-type IGF1R in A-549 enables assessment of IGF1R contribution to EGFR-TKI resistance.
• Functional readout: rescue should restore IGF-1-induced IGF1R signaling and lung cancer proliferation.
A-549 transduces efficiently with lentivirus and supports stable rescue line generation.
* Research Use Disclaimer: Content is generated from publicly available research data, bioinformatic resources, and computational analyses for research reference only.
Related Publications
The mechanism of plasma exosome miR-15a-5p targeting the CF-modified protein IGF1R to regulate alveolar epithelial autophagy and influence pulmonary interstitial fibrosis.
IF=4.7
Non-coding RNA research
Aims:This study investigates how plasma exosomal miRNAs regulate core fucosylation (CF)-modified targets to influence autophagy and fibrosis in idiopathic pulmonary fibrosis (IPF), aiming to identify novel therapeutic strategies targeting dysregulated alveolar epithelial cell (AEC) autophagy. Materials and methods:Plasma exosomes from IPF patients and healthy controls were isolated via ultracentrifugation, validated by TEM, nanoparticle tracking analysis (NTA), and Western blot (CD9/CD81). Exosomal miRNA profiling employed high-throughput sequencing, with TargetScan/miRanda predicting target genes. A549 and MLE-12 cells assessed exosome uptake (PKH67 labeling) and miRNA-mRNA interactions (dual-luciferase assays). CF modification was analyzed via immunoprecipitation/Western blot. In vivo validation used bleomycin (BLM)-induced fibrosis models in alveolar epithelial-specific FUT8-knockout (CKO) mice. Key findings:IPF plasma exosomes suppressed autophagy and exacerbated fibrosis in AECs. miR-15a-5p was markedly downregulated in IPF exosomes. Overexpression of miR-15a-5p reversed BLM-induced autophagy inhibition and fibrosis. Mechanistically, miR-15a-5p directly targeted IGF1R, a CF-modified protein. Reduced miR-15a-5p elevated IGF1R expression, activating PI3K/AKT to inhibit autophagy and promote fibrosis. Significance:This study identifies miR-15a-5p as a critical regulator of CF-modified IGF1R in IPF pathogenesis. Its downregulation drives PI3K/AKT-mediated autophagy suppression, accelerating fibrosis. Restoring miR-15a-5p or targeting IGF1R/PI3K/AKT signaling may offer novel therapeutic avenues for IPF.
Required Accessories
Cell Culture Optimization Series
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