mProX™ Human LTK Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Published Data
Fig.1 LTK-F568L transforms BaF3 cells to cytokine-independence.
On Day 0, parental control cells (black circles) and BaF3 cells stably expressing LTK-F568L (red inverted triangles), LTK-R669Q (green triangles), or wildtype LTK (blue squares) were grown without IL-3. Using trypan blue exclusion, the total number of viable cells was calculated at each timepoint.
Ref: Roll, J. Devon, and Gary W. Reuther. "ALK-activating homologous mutations in LTK induce cellular transformation." PLoS One 7.2 (2012): e31733.
Pubmed: 22347506
DOI: 10.1371/journal.pone.0031733
Research Highlights
This is the first account of changes in LTK that have carcinogenic potential in malignancies. These findings suggest that lorlatinib may be used to treat NSCLC by targeting the CLIP1-LTK fusion.
Izumi, Hiroki, et al. "The CLIP1-LTK fusion is an oncogenic driver in non-small-cell lung cancer." Nature 600.7888 (2021): 319-323.
Pubmed:
34819663
DOI:
10.1038/s41586-021-04135-5
These results establish a physiological relationship between augmentor ligands and Ltk and show that specific augmentors can trigger iridophore development from neural crest-derived cells and pigment progenitor cells by activating Ltk in a tissue-specific setting.
Mo, Elizabeth S., et al. "Alk and Ltk ligands are essential for iridophore development in zebrafish mediated by the receptor tyrosine kinase Ltk." Proceedings of the National Academy of Sciences 114.45 (2017): 12027-12032.
Pubmed:
29078341
DOI:
10.1073/pnas.1710254114